Zinc deficiency during pregnancy linked to autism in babies
Babies who don’t get enough zinc while in the womb may be more likely to develop autism, a new study claims.
Scientists still don’t have a definitive answer for what causes autism, but the vast majority of research shows it is down to a combination of ‘environmental factors’ and genetic defects.
In a new paper published Monday, United States (U.S.) and German scientists say they have evidence that zinc levels may be one of the defining environmental factors that sew the seeds of the behavioral disorder.
More research is needed to confirm whether there could be a causal link, but the team says they have defined a possible mechanistic link.
They found zinc shapes the connections or ‘synapses’ between brain cells that form during early development, via a complex molecular machinery encoded by autism risk genes.
However they caution research is at its early stage and the findings does not mean pregnant women should start taking zinc supplements to prevent autism.
Senior author Dr. Sally Kim of Stanford University School of Medicine in California said: “Autism is associated with specific variants of genes involved in the formation, maturation and stabilisation of synapses during early development.
“Our findings link zinc levels in neurons – via interactions with the proteins encoded by these genes – to the development of autism.”
Zinc helps with making new cells and enzymes, processing carbohydrate, fat and protein in food and wound healing.
Foods rich in the mineral include meat, shellfish, dairy foods such as cheese, bread and cereals.
Experts said most people get enough zinc from their diet and should not take more than 25mg of zinc supplements a day unless advised to by a doctor.
Too much reduces the amount of copper the body can absorb, which can lead to anaemia and weakening of the bones.
The study published in the journal Frontiers in Molecular Neuroscience found when a signal is transferred via a synapse, zinc enters the target neuron where it can bind two such proteins – Shank2 and Shank3.
These proteins in turn cause changes in the composition and function (‘maturation’) of adjacent signal receptors, called ‘AMPARs’, on the neuron’s surface at the synapse.
Experiments showed the mechanism of zinc-Shank-mediated AMPAR maturation in developing synapses.