BRISBANE, Australia — Autism spectrum disorder is three times more common in boys than girls. Now, researchers in Australia have a new theory as to why there is such a gap. A team from Queensland University say maternal vitamin D deficiency may be the culprit.
Among a group of lab rats, vitamin D deficiency among pregnant females led to higher levels of testosterone in the brains of their developing sons.
“The biological cause of autism spectrum disorder (ASD) is unknown but we have shown that one of the many risk factors—low vitamin D in mothers—causes an increase in testosterone in the brain of the male fetuses, as well as the maternal blood and amniotic fluid,” Professor Darryl Eyles explains in a university release. “In addition to its role in calcium absorption, vitamin D is crucial to many developmental processes.”
“Our research also showed that in vitamin D-deficient male fetuses, an enzyme which breaks down testosterone was silenced and could be contributing to the presence of high testosterone levels,” the study author adds.
Vitamin D’s vital role during pregnancy
Prior projects led by Prof. Eyles revealed that vitamin D is very important for the developing mind. For example, vitamin D supplements given to pregnant rodents successfully eliminated any autism-like traits in their children.
Moreover, it’s suspected but not yet confirmed that exposing the developing brain to sex hormones (testosterone) causes autism.
“Vitamin D is involved in pathways controlling many sex hormones,” says study co-author Dr. Asad Ali. “When the rat mothers were fed a low vitamin D diet, it caused male fetal brains to have high levels of exposure to testosterone.”
This is the first report to show that a known risk factor for ASD raises testosterone levels in fetal brains.
“We have only studied one risk factor for ASD — vitamin D deficiency during development — our next step is to look at other possible risk factors, such as maternal stress and hypoxia – lack of oxygen – and see if they have the same effect,” Prof. Eyles concludes.
The study is published in Molecular Autism.