Children with fetal alcohol spectrum disorder (FASD) are often not identified until their school years or even their teens, when behavioural and learning issues escalate. By then, the window for early intervention has long closed.
But new research by Michael Kobor and colleagues is raising hopes that FASD may have a biomarker that could identify vulnerable children much earlier in life.
Kobor is a senior fellow in CIFAR’s program in Child & Brain Development, professor of medical genetics at the University of British Columbia in Vancouver, an investigator at BC Children’s Hospital, and Canada Research Chair in Social Epigenetics.
His team analyzed DNA samples from more than 200 children between the ages of five and 18, collected through the UBC-based Kids Brain Health Network (formerly NeuroDevNet). About half of the children had been diagnosed with FASD or were known to have had significant prenatal alcohol exposure. The other half were controls.
The team found differences in more than 600 individual DNA methylation marks between the two groups, with 41 sites showing the biggest changes, and thus being most likely to have biological impact. DNA methylation is a tiny chemical tag that when added to a gene regulatory region often reduces or eliminates its expression.
This heatmap above shows the 50 most significant up- (top) and down-methylated (bottom) probes in control (left, gray) versus FASD cases (right, blue). (Credit: Epigenetics & Chromatin)
“It was a fairly robust effect, in the same ballpark as what people have reported in similar studies of autism,” Kobor says. “It’s a first step to potentially developing a biomarker.”
FASD is an umbrella term for a group of cognitive, physical and behavioural deficits in people whose mothers drank alcohol during pregnancy. It includes fetal alcohol syndrome, the most severe condition; partial fetal alcohol syndrome; and alcohol-related neurodevelopmental disorder.
The most common effects of FASD involve problems with attention, speech, social communication, memory, coordination and learning, and an increased risk of depression and anxiety.
While there’s no cure for FASD, there is evidence that early intervention programs such as behaviour modification, speech therapy, parent training and social services can help.
“The hope would be, if you have a child at risk, you could do a test at, say, six months. It could show, in combination with other things we see, that this child may be at risk of developing FASD, so let’s think about how we can help with targeted interventions and programs,” Kobor says.
The team is now working on replicating the study with a second cohort of children. Kobor notes that several of the genes associated with the DNA methylation mark changes are also involved in brain development.
“This work could go beyond biomarkers and be a blueprint for further studies in trying to understand other neurodevelopmental disorders in children,” he says.