Zinc deficiency during pregnancy linked to autism in babies

Babies who do not get enough zinc while in the womb may be more likely to develop autism, a new study claims.

Scientists still do not 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 today, US 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 a possible 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 must consider taking 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 stabilization 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.'

Co-senior author Professor Craig Garner of the German Center for Neurodegenerative Diseases added: 'Currently, there are no controlled studies of autism risk with zinc supplementation in pregnant women or babies, so the jury is still out.

'We really can not make any conclusions or recommendations for this supplementation, but this work has not been done.

Nevertheless, zinc deficiency – or disrupted handling of zinc in neurons – might contribute to autism.

Zinc helps with making new cells and enzymes, carbohydrate processing, fat and protein in food and wound healing.

Foods rich in the mineral include meat, shellfish, dairy foods such as cheese, bread and cereals.

The NHS said most people get enough zinc from their diet and should not take any more.

Too much reduces the size of the body, which can lead to anemia and weakening of the bones.

The study published in the journal Frontiers in Molecular Neuroscience found when a signal is transmitted via a synapse, where it binds 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.

Lead author Dr. Huong Ha Researcher at Stanford Explained: 'In developing rat neurons, we found that shank 2 and 3 accumulate at synapses in parallel with a switch to mature AMPARs.

Adding extra zinc accelerates the switch – but not when we reduce the accumulation of Shank 2 or 3.

'Furthermore, our study shows mechanistically how Shank2 and 3 work in concert with zinc to regulate AMPAR maturation, a key developmental step.'

Co-senior author Professor John Huguenard, also of Stanford added in other words, zinc shapes the properties of developing synapses via Shank proteins.

Prof. Huguenard concluded: 'This suggests that a lack of zinc during early development could contribute to autism through impaired synaptic maturation and neuronal circuit training.

'Understanding the interaction between zinc and Shank proteins could lead to diagnosis, treatment and prevention strategies for autism.'

• Note to readers: Speak to your doctor before altering your diet