# Cobalamin Status Among Patients with Fetal Alcohol Spectrum Disorder (FASD)—A Preliminary Study

## TL;DR

This study explores vitamin B12 levels in individuals with fetal alcohol spectrum disorder and finds no significant differences compared to healthy controls.

## Contribution

The study investigates the role of vitamin B12 in fetal alcohol spectrum disorder for the first time.

## Key findings

- Patients with fetal alcohol spectrum disorder had higher vitamin B12 intake than controls.
- No significant differences in serum vitamin B12 or related metabolites were found between groups.
- Correlations between vitamin B12 and its metabolites differed in fetal alcohol spectrum disorder patients.

## Abstract

Background/Objectives: Fetal alcohol spectrum disorder comprise a range of neurodevelopmental disorder caused by prenatal alcohol exposure. Recent investigations have revealed that among patients with neurodevelopmental disorders, serum cobalamin (vitamin B12) levels are substantially higher than those of healthy controls. Patients with fetal alcohol spectrum disorder similarly present with higher levels of cobalamin, yet the significance of cobalamin in the pathogenesis of fetal alcohol spectrum disorder remains to be established. This study aimed to examine cobalamin and other cobalamin status markers in patients with fetal alcohol spectrum disorder in comparison with healthy controls. Methods: In total, 80 patients were enrolled in the study—41 diagnosed with fetal alcohol spectrum disorder and 39 healthy controls. The diet history method was used to assess vitamin B12 intake for three days preceding blood sampling. Total vitamin B12 (cobalamin), holotranscobalamin, methylmalonic acid and soluble transcobalamin receptor (CD320) were measured in serum samples. Results: The daily intake of vitamin B12 was higher in patients with fetal alcohol spectrum disorder compared to controls, both in the simple analysis and after adjusting for age (OR for patients with FASD: 1.82; 95% CI: 1.16–2.87). An elevated serum cobalamin level was noted in some patients from the group with fetal alcohol spectrum disorder. No statistically significant differences were found between the groups in serum levels of cobalamin, holotranscobalamin, CD320 or methylmalonic acid. However, the correlations between cobalamin and its metabolites differed in fetal alcohol spectrum disorder as compared to those in the control group. Conclusions: Our study did not find any deficits of vitamin B12 and its metabolites in patients with fetal alcohol spectrum disorder. Further studies to investigate the role of vitamin B12 in the pathogenesis of fetal alcohol spectrum disorder should be established given the fact that both high and low levels of vitamin B12 may have negative health impacts.