It's unfortunate but true that we tend to fall for all manner of woo, that we do a poor job of weeding out nonsense from sense. People will believe just about any crazy thing, especially if the person selling it makes really outlandish claims. I can’t tell you the number of times I’ve seen booths selling the special magnetic bracelets or the salt crystal rocks that are supposed to heal everything. There’s a sucker out there for every con man, as long as the con man is willing to act like a fisherman and cast a wide net.<?xml:namespace prefix = o /?>

It’s no wonder, either. Even well-intentioned, decent people who try to think, who reject some woo, can badly misunderstand the science that’s out there, and when the media takes scientific findings and inflates them and has a willing researcher to go along for the ride (think autism piss test), it’s no wonder people walk around thinking all manner of things, certain of their correctness (think Dunning-Kruger effect), and it’s no surprise that all manner of woo goes over so easily.

There’s a new study out, and it’s not a bad one, overall, that tells us there’s a slightly greater risk of a child having special education needs (to include autism) if the child is born between 37 and 39 weeks or after 40 weeks. Now, that really shouldn’t come as a shocker to most folks. The researchers “conducted a population-based, retrospective study by linking school census data on the 407,503 eligible school-aged children resident in 19 Scottish Local Authority areas (total population 3.8 million) to their routine birth data. SEN was recorded in 17,784 (4.9%) children; 1,565 (8.4%) of those born preterm and 16,219 (4.7%) of those born at term. The risk of SEN increased across the whole range of gestation from 40 to 24 wk: 37–39 wk adjusted odds ratio (OR) 1.16, 95% confidence interval (CI) 1.12–1.20; 33–36 wk adjusted OR 1.53, 95% CI 1.43–1.63; 28–32 wk adjusted OR 2.66, 95% CI 2.38–2.97; 24–27 wk adjusted OR 6.92, 95% CI 5.58–8.58. There was no interaction between elective versus spontaneous delivery. Overall, gestation at delivery accounted for 10% of the adjusted population attributable fraction of SEN. Because of their high frequency, early term deliveries (37–39 wk) accounted for 5.5% of cases of SEN compared with preterm deliveries (37 wk), which accounted for only 3.6% of cases.

This seems fairly cut and dried to me, after reading the entire study. The conclusion seems to be that it’s reasonable, where births are elective, to shoot for the 40th week, as this confers the least risk overall.

Note: this study didn’t say that gestational age at birth caused autism. Autism was incorporated in the broad pool of special educational needs. Now, Medical News Today for some reason felt the need to sensationalize this study’s findings into this headline: “Babies Born At 37 To 39 Weeks Have Higher Risk Of Autism And Special Educational Needs.” That’s a bit much, don’t you think?

And, of course, people are running with it and reaching conclusions nowhere near what the study found, or rejecting it because their child was born on time and was autistic, or autism is genetic so gestational age can’t have anything to do with it. I take back the idea that no one thought autism was purely genetic. Apparently there are indeed people who don’t understand that most things, most things, most things are a rich interplay of genetics and environment, but I assure you this, they aren’t following the science on autism when they play that gambit, and I think they’re almost as deep into inaccurate information and faulty reasoning as the vaccine-induced folks are.

Another new study on the genetics of autism is out, and its findings are fascinating. Will the findings connect with people who think they have all the answers on autism, either because their child is their science or because they’ve read the studies. I assure you, if you think you’ve read all the science on autism, you’re wrong. There is so much information out there, so many hundreds of studies being done worldwide each year that no one person can have read it all. And if you’ve misinterpreted reading some studies as meaning you have rock-solid answers, especially as it relates to cognition and autism or brain anatomy and physiology and autism, again, let me assure you, you’re wrong.

Pinto et al. (2010) conclude:

“Our findings provide strong support for the involvement of multiple rare genic CNVs, both genome-wide and at specific loci, in ASD. These findings, similar to those recently described in schizophrenia26, suggest that at least some of these ASD CNVs (and the genes that they affect) are under purifying selection27. Genes previously implicated in ASD by rare variant findings have pointed to functional themes in ASD pathophysiology628. Molecules such as NRXN1, NLGN3/4X and SHANK3, localized presynaptically or at the post-synaptic density (PSD), highlight maturation and function of glutamatergic synapses. Our data reveal that SHANK2SYNGAP1 and DLGAP2 are new ASD loci that also encode proteins in the PSD. We also found intellectual disability genes to be important in ASD29. Furthermore, our functional enrichment map identifies new groups such as GTPase/Ras, effectively expanding both the number and connectivity of modules that may be involved in ASD. The next step will be to relate defects or patterns of alterations in these groups to ASD endophenotypes. The combined identification of higher-penetrance rare variants and new biological pathways, including those identified in this study, may broaden the targets amenable to genetic testing and therapeutic intervention.”

Autism is a behaviorally defined spectrum, with what appears to be a tremendously varied and variable genome. On blogs, people decry the genetic research for fear that it will result in a prenatal test. With so many genes playing a role in the manifestation of such a broad spectrum of behaviors we currently term autism, I think that the possibility of such a test anytime in the near future is unlikely, and as we begin to see that these genes may also be found in family members who experience no impairment, it’s even less likely to happen.

Our knowledge base is expanding rapidly; it’s impossible for anyone individual to consume all the knowledge being gained in even a small subset of a field. The media has an obligation to work harder at accuracy in reporting. School systems need to work better at teaching critical thinking skills, and it’d be nice to see high schools and all college programs require a basic statistics course if consumers are going to regularly consume scientific literature. Because it really isn’t pretty to watch a group of well-meaning, well-intentioned people butcher beyond recognition a study like the one on the risk of a special educational needs child being greater for children born before or after 40 weeks, to see them decry the statistical analysis because for some reason they’ve decided that scientists look only at the large number, the sample number and compare directly that number instead of the percentage of children with an SEN at 37 weeks compared to the percentage of children with an SEN at 40 weeks, for example. It doesn’t matter what the overall number of children was at either week (as long as the numbers are large enough to meet statistical significance).

Bad enough as that is, it’s even worse when you see people take a study with a small sample size, say of 12 (like Wakefield) or 10 in the mirror neuron study that supposedly debunked that theory (it didn’t, by the way), and run with it as if it represented every single autistic person out there.

The Nature study “analysed the genome-wide characteristics of rare (1% frequency) copy number variation in ASD using dense genotyping arrays. When comparing 996 ASD individuals of European ancestry to 1,287 matched controls, cases were found to carry a higher global burden of rare, genic copy number variants (CNVs) (1.19 fold, P = 0.012), especially so for loci previously implicated in either ASD and/or intellectual disability (1.69 fold, P = 3.4 × 10-4).” 

In The Independent, one of the researchers commented:

"Our results substantiate the importance of genes as susceptibility factors in autism. Our results will lead to a paradigm shift when it comes to understanding the root causes of autism," said Stephen Scherer, of the Hospital for Sick Children in Toronto one of the lead authors of the study published in Nature. "We find that the genetic variations we discovered are actually rare in their frequency, meaning that most individuals with autism are actually probably genetically quite unique, each having their own genetic form of autism."

They found a rich array of genetic information, information that certainly swamps what postmortem studies of a few people or brain imaging studies of a dozen or so tell us, just as a study that looks at over 400,000 children tells us far more than what your personal experience of having your child does. I get it, I do. It’s so hard to weight your personal experience appropriately against abstract science. However, it’s the science that’s more likely to have the more accurate lock on reality.