ESPE Yearbook of Paediatric Endocrinology

Brief Summary: This longitudinal study describes the long-term effects of prenatal alcohol exposure on early childhood development. The results clearly show that prenatal alcohol exposure impairs growth and IGF-1 levels in children, highlighting the need for public health interventions to prevent alcohol consumption during pregnancy, especially in low-resource settings.

This study assessed the long-term consequences of prenatal alcohol exposure (PAE) on early childhood development in Leyte, Philippines. It provides insights into strategies for the timely identification of cases and potential mechanistic pathways of an often underrepresented issue in global health research. (1). It followed a cohort of 296 mother-infant couples (32% cases and 68% controls) from early gestation through 24 months of age, measuring child’s auxological parameters, IGF-I, leptin and serum phosphatidylethanol (PEth), a direct biomarker of alcohol metabolism of mothers and infants (2).

Children exposed to alcohol in utero had impaired growth trajectories compared to their non-exposed peers, in particular in height-for-age z-score. The effect appeared between 4 and 6 months of age and continued through 12-24 months, together with a decreased rate of mid-upper-arm circumference growth from birth to 12 months. This finding is consistent with previous studies but adds depth by linking these growth impairments to both nutritional status and levels of IGF-I that were significantly lower at birth and 6 months in children with PAE (3-4). The association between PAE and lower IGF-I levels suggests a possible mechanism through which PAE may lead to stunting (5).

These findings could drive future interventions aimed at mitigating the effects of PAE, such as nutritional supplementation or targeted therapies to boost IGF-1 levels in affected children. Furthermore, this study draws attention to the broader public health implications of alcohol abuse during pregnancy, particularly in settings where malnutrition and poor health infrastructure pose significant threats to child development.

References: 1. Burd L. Fetal alcohol spectrum disorder: complexity from comorbidity. Lancet. 2016 Mar 5;387(10022):926-927. doi: 10.1016/S0140-6736(15)01346-X. Epub 2016 Jan 6. PMID: 26777271.2. Bakhireva LN, Leeman L, Savich RD, Cano S, Gutierrez H, Savage DD, Rayburn WF. The validity of phosphatidylethanol in dried blood spots of newborns for the identification of prenatal alcohol exposure. Alcohol Clin Exp Res. 2014 Apr;38(4):1078-85. doi: 10.1111/acer.12349. Epub 2014 Feb 11. PMID: 24511895; PMCID: PMC4412471.3. Savage MO, Burren CP, Rosenfeld RG. The continuum of growth hormone-IGF-I axis defects causing short stature: diagnostic and therapeutic challenges. Clin Endocrinol (Oxf). 2010 Jun;72(6):721-8. doi: 10.1111/j.1365-2265.2009.03775.x. Epub 2009 Dec 29. PMID: 20050859.4. Ni Q, Tan Y, Zhang X, Luo H, Deng Y, Magdalou J, Chen L, Wang H. Prenatal ethanol exposure increases osteoarthritis susceptibility in female rat offspring by programming a low-functioning IGF-1 signaling pathway. Sci Rep. 2015 Oct 5;5:14711. doi: 10.1038/srep14711. PMID: 26434683; PMCID: PMC4592973.5. Han VK, Lund PK, Lee DC, D’Ercole AJ. Expression of somatomedin/insulin-like growth factor messenger ribonucleic acids in the human fetus: identification, characterization, and tissue distribution. J Clin Endocrinol Metab. 1988 Feb;66(2):422-9. doi: 10.1210/jcem-66-2-422. PMID: 2448331.