Letter to the Editor: Influence of maternal NAFLD on infant weight—the real precursor to NAFLD in offspring?

To the editor, We read with enthusiasm the publication by Amadou et al.1 demonstrating that within a large French cohort, extremes of birthweight increased the risk for NAFLD in adulthood. On mediation analysis, findings for low birthweight were explained by prematurity. As the authors’ highlight, an important limitation was unavailable maternal data, including maternal weight. Beyond maternal obesity, there remains a knowledge gap regarding the in-utero influence of maternal NAFLD on infant outcomes. NAFLD rates in pregnancy have nearly tripled over the past decade, and NAFLD cirrhosis is also rising in pregnant women.2,3 In pediatric populations, NAFLD can develop even in utero, and by school-age 10% of all children, and 30%–40% of those with obesity have NAFLD.4 Thus, there is an urgent need to identify early and modifiable risk factors in pregnant women with NAFLD and their offspring. Though prior data link maternal obesity to childhood NAFLD, the influence of maternal NAFLD on long-term metabolic outcomes has not been elucidated. In a large US study we evaluated NAFLD in pregnancy and maternal and perinatal outcomes at delivery.2 Importantly, maternal NAFLD increased risk for both large-for-gestational age infants (adjusted OR of 1.8, 95% CI: 1.4–2.5) and preterm birth (adjusted OR: 1.60, 95% CI: 1.3–2.0), independent of maternal metabolic comorbidities. Likewise, in our Canadian study of cirrhosis in pregnancy, maternal NAFLD independently increased arge-for-gestational age risk as compared with other etiologies of cirrhosis (RR: 1.6, 95% CI: 1.3–2.1).3 These data suggest a direct influence of in utero NAFLD exposure as a contributor to prematurity and arge-for-gestational age infants, key risk factors for long-term NAFLD risk in offspring as demonstrated by Amoudou and colleagues. Although the underlying mechanisms have not been elucidated, independent of diabetes and obesity the liver plays a critical role in the regulation of glucose and lipid metabolism. NAFLD-specific effects beyond the liver include peripheral insulin resistance, systemic inflammation, and dysregulated lipid metabolism, which may help to explain our findings of increased arge-for-gestational age risk in infants of mothers with NAFLD. In summary, we applaud the work by Amadou and colleagues and emerging literature evaluating early influencers of NAFLD. An even earlier focus on preconception through postpartum periods may further define contributors to NAFLD in offspring, and support interventions among expectant mothers to help mitigate rising NAFLD rates in young populations.

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