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DIABETIC DIET MAY HELP AUTISM


By Bradley J. Fikes

Autism symptoms can be reduced in an animal model with low glycemic index diets, similar to those diabetics follow to control blood sugar levels, according to a new study.
The study by Salk Institute scientists found that the brains of mice fed diets with a high glycemic index accumulated more activated immune cells called microglia, along with signs of inflammation. The mice also exhibited more autistic type behaviors, such as impaired social interactions, and apparently purposeless activities.
Mice fed low glycemic index diets showed improved behavior.
There's good evidence for immune system dysfunction in autism spectrum disorder, the study said, and it appears to be environmentally caused. While genetic influences predispose certain people to autism, the environment helps determine how the symptoms manifest.
The study was published June 9 in the journal Molecular Psychiatry. Pamela Maher was senior author; Antonio Currais, also of the Salk, was first author.
A growing body of evidence suggests that autism starts during pregnancy. But that doesn't rule out an environmental role, according to a scientist not involved in the Salk study.
Autism in its various forms is a complex condition, and many different contributing factors appear to be involved. There appear to be two main types of autism, according to a recent study led by UC San Diego researcher Eric Courchesne.
Brains of mice fed a high glycemic index diet have greater numbers of activated immune cells (shown in red and green) called microglia. — Salk Institute for Biological Studies
Researchers such as Courchesne have found evidence of a prenatal origin of autism in post-mortem studies of the brains of young people with autism. According to other research, maternal antibodies that apparently attack brain structures in developing babies are responsible for about one-quarter of all autism causes.
The new study provided the different diets both pre- and post-natally, because autism is thought to arise from influences before and after birth. So it can't distinguish between the effects on autism diet has in each time frame. This will be addressed in future studies.
The study found evidence that high-glycemic index diets change the composition of the gut microbiota, the population of bacteria that live in the gastrointestinal system. Moreover, it found that genes associated with inflammation were more activated in the brains of mice given the high-glycemic diet than those given low-glycemic diets.
The study gives a reasonable interpretation of a dietary influence, said Tiziano Pramparo, an associate research scientist in the Autism Center of Excellence headed by UCSD's Courchesne and Karen Pierce.
"It is indeed plausible to think that diet-related changes may be included in a broader picture of gastrointestinal issues with alterations in the composition and total biomass of the gut microbiota," Pramparo said by email.
"In turn, these alterations may ultimately be leading to epigenetic changes in stress-related genes or the release of metabolites or even antigens that are permeable to the blood-brain barrier. These elements are hypothesized to alter behavior, stress response, brain processes and biochemistry."
Epigenetics is the field that studies how genes are turned off or on by chemical modifications that don't alter the underlying genetic sequence. These modifications are known to be influenced by environment.
Moreover, other research suggests the role for diet in autism, Pramparo said.
"The consequences of the increase in inflammatory signals described in this mouse study converge with brain alterations we have seen in human studies affecting neurogenesis, neuronal maturation and synaptic functions," he said. "Ultimately, these alterations together with behavioral abnormalities appear to be ameliorated by a diet poor in glycemic index."

For followup studies, the Salk scientists plan to analyze the microbiome and autism symptoms more directly. They will also study how inflammation affects the growth of new neurons.