Some of the most fascinating theories of what causes autism focus on the womb. There’s the idea that the disorder stems from maternal flu exposure during pregnancy, for example, or from too much prenatal testosterone, or from not enough prenatal folate.
The trouble is, for now these hypotheses leave us with more questions than answers. At what stage of pregnancy does a flu infection confer the most risk? Do these prenatal conditions lead to a range of developmental disorders, or specifically autism? How much does genetic predisposition come into play?
On Tuesday, researchers from four U.S. institutions launched a huge study that sets out to unpack some of this complexity. The Early Autism Risk Longitudinal Investigation (EARLI) will follow 1,200 pregnant women who already have a child with autism.
The researchers are collecting enormous amounts of data. They will gather blood and urine samples during pregnancy, and once the baby’s born, they’ll get tissue from the umbilical cord, placenta, and baby stool. They’ll collect more biological samples from the child, and test for language and developmental abilities, every few months until age 3.
A few other longitudinal studies are also studying infant siblings of children with autism, to discover early behaviors that might be used to diagnose the disorder. But these data won’t reveal much about prenatal risk factors.
Scandinavian medical registries hold loads of information about pregnancy complications and psychiatric diagnoses, and even samples of amniotic fluid. But the data are spotty and old, and weren’t necessarily collected to study autism.
EARLI is measuring changes starting from the first days of pregnancy and looking specifically for measures that may be relevant to understanding autism. I’m eager to see what new associations the data pinpoint, and of course whether they back those previously proposed hypotheses. Preliminary analyses are slated for 2012.

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June 12, 2009 at 10:07 am
republicofhealth
It should be obvious by this point that autism is caused by vaccines…
…because vaccines contain chemicals like formaldehyde, mercury, and genetically modified human and animal tissue. These toxic substances cause an auto immune response in the body that leads to diabetes, autism, and seizures.
Check out my blog for more information at http://RepublicofHealth.wordpress.com
June 17, 2009 at 9:49 am
Robert Jensen
The EARLI studies are not likely to prove anything. Unfavorable events in the pre, peri and neonatal period have been consistently reported over many decades. The problem, as you state, is that none of these events are specific to autism (nor are the genetic variants described as candidate autism genes).
http://pediatrics.aappublications.org/cgi/content/full/107/4/e63#T1
The most important research underway is in twin studies. I correspond with the PI’s of three twin studies currently underway. All of them will raise questions about the strength of the most cited twin study in autism research history:
http://www.ncbi.nlm.nih.gov/pubmed/7792363?
All three studies are reporting a high rate of concordant DZ twins ranging from 14% to 37% depending on what diagnostic schemes were used and nowhere near the ’90% heritable’ claims made by genetic theorists based on the Bailey et al twin study..
1. Autism IAN has a study in press that will show a 60% concordance rate for MZ twins and a 14% concordance rate in DZ twins.
2. The Wisconsin twin study(TAPS) has preliminary results that were presented at the 2009 IMFAR conference last month. They are reporting that concordance rates in MZ twins are nowhere near 100% and concordance rates in DZ twins is nowhere near zero.
3. The California Autism Twin Study (CATS) is recruiting some 300 pairs of twins. The AUTISM IAN twin study which is reporting a 60% concordance rate is consistent with the 60% concordance rate reported in the Bailey et al study.The CATS study will for the first time be collecting chorion type data where available. Since 60 to 66% of MZ pregnancies are monochorionic (single placenta) the 60% concordance rate in MZ twins may be the consequence of a shared prenatal environment. MZ twins who develop in seperate placenta (1/3) do not share the same prenatal environment. Preliminary results are unlikely for several years since they are still in the recruitment phase.
Significantly higher concordance rates in monochorionic MZ twins compared to MZ dichorionic twins will be the first evidence that there is an unrecognized prenatal environment component and that autism etiology primarily involves gene environment interactions. No signifcant differences in the two types of MZ twins will be the most powerful evidence ever produced for the concept of autism as a gene-gene interaction disorder.
The results of this study, when replicated, will determine the direction of autism research for decades to come.