Babies whose moms lived within a mile of crops treated with widely used pesticides were more likely to develop autism, according to new research published today.

The study of 970 children, born in farm-rich areas of Northern California, is part of the largest project to date that is exploring links between autism and environmental exposures.

The University of California, Davis research – which used women’s addresses to determine their proximity to insecticide-treated fields – is the third project to link prenatal insecticide exposures to autism and related disorders.“The weight of evidence is beginning to suggest that mothers’ exposures during pregnancy may play a role in the development of autism spectrum disorders,” said Kim Harley, associate director of University of California, Berkeley's Center for Environmental Research and Children's Health. She was not involved in the new study.

Dusty Sweeney faces more obstacles than the average 16 year old. Diagnosed with autism at age 2, Dusty has limited verbal communication skills, and he will likely never be able to live on his own or hold a job.

But, Dusty has picked up one habit that his mother, Katie Sweeney, hopes will make his life a little better – and a little healthier.

“When he runs, he runs with a smile on his face,” Sweeney, who runs with Dusty every week in New York City’s Central Park, told FoxNews.com.

Dusty was first introduced to running by Achilles International, a group that aims to allow people with all types of disabilities to participate in mainstream athletic events. Now, Achilles has received a grant from the Cigna Foundation to initiate a study on how running can help children with autism, like Dusty.

Autistic-like behaviors and decreased cognitive ability may be associated with disruption of the function of the Adenomatous Polyposis Coli (APC)gene. When Tufts researchers deleted the gene from select neurons in the developing mousebrain, the mice showed reduced social behavior, increased repetitive behavior, and impaired learning and memory formation, similar to behaviors seen in individuals withautismand intellectual disabilities. This study is the first to evaluate how the loss of APC from nerve cells in the forebrain affects brain development, learning, and behavior. The research team, led by Michele Jacob, Ph.D., engineered a new mouse model for studying cognitive and autistic-like disabilities. The study was published online today inMolecular Psychiatry.

In addition to observing autistic-like behaviors and cognitive impairments in the mice, researchers found significant molecular changes in the brain. Eliminating APC chiefly from the excitatory neurons in the forebrain led to altered levels of specific proteins that regulategene expressionand influenced the structure, number, and function of synapses.

Some of these molecular changes have not been seen in other genetic mouse models of cognitive and autistic-like disabilities, but are likely relevant to the human disorders based on recently identified risk genes. The researchers propose that APC tightly regulates particular protein levels, maintaining them within a range that is critical to normal learning and memory consolidation.

"What makes this study interesting is that although there are hundreds of risk genes implicated in autism, the removal of this single gene produced a multi-syndromic disorder similar to that seen in individuals with both cognitive deficits and autism. The APC-deficient mice are noticeably different from normal mice in their impaired learning, poor memory consolidation, repetitive behaviors, and reduced social interest," said co-first author Jonathan Alexander, a Ph.D. candidate in neuroscience at the Sackler School of Graduate Biomedical Sciences at Tufts and a member of the Michele Jacob lab at Tufts University School of Medicine.

"This APC knock-out mouse is different because APC is eliminated from a specific type of cell in the brain during a critical period of development. This leads to deregulation of key signaling pathways and produces the cognitive and behavioral changes that we observed," explained co-first author Jesse Mohn, Ph.D., a graduate of the Sackler School and now a scientist at Galenea Corp....

More and source: http://www.news-medical.net/news/20140617/Autistic-like-behaviors-linked-with-disruption-of-Adenomatous-Polyposis-Coli-gene.aspx

Compounds derived from cow’s milk may have a similar ability to the analgesic morphine to alter important biochemical processes implicated in autism including those affecting gene function. That was the finding from new research by Malav Trivedi and colleagues* based at Northeastern University in the United States and Ghent University in Belgium.

A laboratory based study looking at morphine and various food-derived morphine-like compounds – opioid peptides – extracted from foods containing gluten, the primary protein found in wheat and other cereal crops, or casein found in mammalian dairy sources, researchers examined the effects on cell lines. They concluded that the addition of opioid peptides to cells may interfere with the uptake of cysteine, an important precursor of the cellular antioxidant glutathione, something already quite consistently found to be perturbed in at least a subgroup of people on the autism spectrum. Researchers further demonstrated that opioid peptides derived from both cow and human milk may also have the ability to increase genome wide methylation levels in the transcription start site region “with a potency order similar to their inhibition of cysteine uptake” so potentially affecting gene functions.

Although still the source of discussion and debate in science and lay circles, the use of a gluten- and casein-free (GFCF) diet in cases of autism spectrum disorder (ASD) continues to enjoy some following. The experimental evidence for such an approach is still relatively weak. There is also a continued dearth of knowledge about why such an approach could affect the behavioural presentation of autism outside of the presence of comorbidities such as lactose intolerance or coeliac (celiac) disease appearing alongside cases of autism.

One of the earliest hypothesis put forward to attempt to explain the positive effects reported for some children and adults following a GFCF diet relied on the appearance of opioid peptides following the breakdown of gluten and casein. Coupled with reports of increased intestinal permeability – the so-called leaky gut – the suggestion was that a state of opioid excess allowed transport of these peptides into the central nervous system (CNS) to exert an effect. Other studies looking at the use of medications designed to block opioid receptors such as the drug naltrexone in case of autism to some extent corroborated the hypothesis.

The results from Trivedi and colleagues offer an alternative explanation for how foods containing casein may be implicated in other processes previously reported as being present in cases of autism. The idea that DNA methylation may also be affected by such food by-products also taps into the increasingly important area of autism research known as epigenetics, where changes to gene function rather than structural changes to the genome may be important.

The authors note however that their study requires further replication. Their focus on a particular cell line represents a preliminary examination of the effects of opioid peptides and may not necessarily translate into real effects in real people. They add however that their results “provide a novel antioxidant-based biochemical pathway linking gut and brain function via the diet” and source for further investigations.

More and source: http://www.autismdailynewscast.com/another-piece-of-the-gluten-and-casein-free-gfcf-diet-for-autism-puzzle/12306/paulwhiteley/

Air pollution is not only detrimental for the environment, it is also bad for people's health. According to some studies, excessive exposure to air pollution can be linked to respiratory diseases. In a new study, researchers experimented on mice models and found that air pollution could increase one's risk of autism and schizophrenia.

The research team headed by Deborah Cory-Slechta, Ph.D., professor of Environmental Medicine at the University of Rochester conducted three sets of experiments. In each set, the mice were exposed to varying levels of air pollution that were comparable to the levels emitted during rush hour in mid-sized U.S. cities. Mice were first exposed two weeks after birth for four hours in two four-day sections.

The researchers found that all of the mice had inflammation throughout the brain. Specifically, the lateral ventricles, which contain cerebrospinal fluid, were double to triple their normal size. The team added that these problems were still noticeable in mice that were examined 40 and 270 days after exposure. The team concluded that the damage was permanent.

"When we looked closely at the ventricles, we could see that the white matter that normally surrounds them hadn't fully developed," said Cory-Slechta. "It appears that inflammation had damaged those brain cells and prevented that region of the brain from developing, and the ventricles simply expanded to fill the space."

The researchers reported that the mice also had increased levels of glutamate, which is a neurotransmitter tied to autism and schizophrenia in humans. Overall, the effects of air pollution were more noticeable in male mice than female mice. Exposed mice performed worse on testes that measured short-term memory. They also had poorer learning ability and impulsivity.

"I think these findings are going to raise new questions about whether the current regulatory standards for air quality are sufficient to protect our children," said Cory-Slechta.

The study was published in the journal, Environmental Health Perspectives.

More and source: http://www.counselheal.com/articles/9987/20140605/3pm-mice-study-finds-link-between-air-pollution-and-autism-schizophrenia.htm

Levels of the toxic metals lead and mercury were 30-40% higher in analysed samples from children diagnosed with autism compared with an asymptomatic control group. That was one of the primary findings published in new research from Altaf Alabdali and colleagues* based in Riyadh, Saudi Arabia.

Authors also reported that measured levels of important compounds involved in detoxification mechanisms, glutathione-s-transferase (GST) and vitamin E, were decreased in children with autism and correlated with autism severity. The cumulative effects from these findings suggested that an accumulation of toxic metals and impaired means of metabolising such compounds may contribute to the onset or perpetuation of symptoms seen in autism.

Supported by a growing body of research suggestive of a more combined model of genetic and environmental factors potentially at work in relation to autism, the authors focused on compounds and biological systems previously cited in the autism research literature. Metals such as lead and mercury are already well-known pollutants, exposure to which in high enough doses carries various adverse effects on biology and behaviour. Although some controversy still exists around the source(s) of exposure to such metals, the Alabdali results hint that further investigations are required for at least some children on the autism spectrum. Lower levels of GST also noted in the autism group adds to a substantial body of work implicating this important pathway in relation to autism.

The authors conclude that further work is required into whether or not supplementation with antioxidants may prove beneficial for some on the autism spectrum in order to remove the “toxicity burden” as and when identified.....

More and source: http://www.autismdailynewscast.com/higher-toxic-metal-burden-associated-with-autism/11815/paulwhiteley/