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Low, high birth weights increase risk for fatty liver, fibrosis in children
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Low birth weight and high birth weight were associated with the development of non-alcoholic fatty liver disease in children and both appear to increase the risk for more severe diseases such as non-alcoholic steatohepatitis or advanced fibrosis, according to a recently published study.
“What our research found is that low birth weight and high birth weight were both associated with the severity of liver disease, but in different ways,” Jeffrey B. Schwimmer, MD, professor of pediatrics at University of California San Diego School of Medicine and director of the Fatty Liver Clinic at Rady Children’s Hospital-San Diego, said in a press release. “Children with low birth weight were more likely to develop severe scarring of the liver. However, children with high birth weight were more likely to develop the hepatitis form of fatty liver disease.”
The multicenter, cross-sectional study comprised 538 children with NAFLD. Mean patient age was 13 years, median BMI was 32 kg/m2 and 71% were boys. The children were categorized as having had low birth weight (1,500-2,499 g), normal birth weight (2,500-3,999 g) or high birth weight (4,000 g). Fifty children had low birth weight, 408 had normal birth weight and 80 had high birth weight. NASH was present in 26.6% of the children.
There were no significant differences in age, sex or ethnicity among the children. At the time of NAFLD diagnosis, however, there was a significant difference between height and weight by birth weight category (P < .001). The distribution of low and high birth weight categories was significantly higher in the study group compared with general U.S. population of children (P < .0001).
Forty-one of the children in the high birth weight category had severe steatosis, representing 1.82-fold greater odds of having more severe steatosis compared with children in the normal birth weight category (OR = 1.82; 95% CI, 1.15-2.88).
“Although obtaining maternal health information was beyond the scope of this investigation, previous studies have shown that mothers with elevated BMI and diabetes are prone to have children born large for gestational age, and that hepatic steatosis is more likely to be present at birth in these infants,” the researchers wrote. “Importantly, in our study, the children with [high birth weight] not only had more severe steatosis, but also had greater odds of having NASH. Thus, [high birth weight] may be an early marker for imprinting that predisposes a child to NAFLD itself as well as for more severe disease in the form of steatohepatitis.” NASH was present in 15 children with low birth weight, 96 with normal birth weight and 32 with high birth weight (P < .01). The odds of children with high birth weight having NASH were 2.03-fold greater compared with children with normal birth weight (OR = 2.03; 95% CI, 1.21-3.4).
Advanced fibrosis was present in 12 children with low birth weight, 52 with normal birth weight and 13 with high birth weight (P = .09). The odds of children with low birth weight having advanced fibrosis were 2.23-fold greater compared with children with normal birth weight (OR = 2.23; 95% CI, 1.08-4.62).
“This is the first study to show that extremes of weights on either side of the normal spectrum are connected to an increased risk for NAFLD,” Schwimmer said. “Children who are born with low birth weight or high birth weight may merit closer attention to their metabolic health to help prevent obesity, liver disease and diabetes.”– by Talitha Bennett
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Philip Rosenthal, MD
The study by Newton and colleagues expands our knowledge on the role of birth weight on the development of fatty liver and fibrosis in children. Both low birth weight and high birth weight were associated with increased risk for developing NAFLD. Maternal and in utero factors may have significant effects and long-lasting consequences. Low birth weight was associated with increased fibrosis and high birthweight with increased fatty liver and inflammation.
We cannot completely control maternal and in utero factors that have now been shown to influence risks for NAFLD. While the authors speculate that increased attention to metabolic issues may be warranted in individuals with low or high birth weights, there presently are no studies demonstrating that interventions early on can alter the course of persons at risk for NASH development due to their birth weight. We still do not know what causes NAFLD. Is the maternal microbiome the cause? Are there genetic factors that are the cause? It is curious that both malnutrition and obesity both can lead to fatty liver. The same phenomenon occurs with low or high birth weight. Is nature trying to tell us that it is best to be in a normal range? Not too heavy and not too lean? Further work is necessary to use this new finding in our management and prevention of NAFLD.
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