risk – ASF Weekly Science Podcasts

Don’t be fooled, not all the studies on this week’s podcast focus on the DSM5.  But the first one, a review of a meta analysis and review of the dozens of publications that have emerged in the past 5 years around the DSM5 leads us off.  There are some people that weren’t captured by either DSM5 or Social Communication Disorder that need a diagnosis, and that should be the focus of future research.  A new topic of diagnosis is also explored by a large collaboration is addressed:  diagnosis in cousins.  They do show a higher probability of an autism diagnosis, but not as high as first degree siblings.  Finally, a new tool called JAKE in monitoring  treatment effectiveness is presented.  This could be used not just in the clinic but at home.  It includes monitoring of biological and behavioral features, and might be the next big thing in outcomes for treatment studies.

https://www.ncbi.nlm.nih.gov/pubmed/30852784

https://www.ncbi.nlm.nih.gov/pubmed/30851399

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6402449/

This week, two studies from the large CDC funded study called the Study to Explore Early Development were published that examines probability of having a child with autism after infertility treatments (first paper) and long or short times between pregnancies (second paper).  These studies put to rest some of the questions moms have been interested in.  First, it’s infertility not infertility treatments that is linked to autism, and second, spacing pregnancies too close together or too far apart is also associated with an increased probability of having a child with severe autism symptoms.  This podcast explains what the studies mean and what parents should know.  The references are here:

https://www.ncbi.nlm.nih.gov/pubmed/29164825

https://www.ncbi.nlm.nih.gov/pubmed/28900768

Every time you turn around there is another study contradicting the last on antidepressant use and autism risk.  An answer on why there are differences across different studies may be found in a new analysis published by University of Washington and SSM Dean Medical Group in Wisconsin this week.  They showed that autism severity (not risk) is increased only with both a likely gene disruption AND following antidepressant exposure in pregnancy together.  This suggests a double hit model similar to other complex neuropsychiatric disorders like depression.  It also suggests that findings from other chemicals, like PBDE’s, may be dependent on gene / environment interactions too.  After all, a new systematic review showed PBDE’s during pregnancy are bad for the IQ of the child.  This provides insight on ASD risk and subtype given the multitude of possible genetic / environmental combinations out there.

Advanced paternal age is one of the more replicated risk factors for autism – but maybe not autism as it as seen as a disorder.  Recent studies by Mount Sinai School of Medicine and Kings College of London show in both animal models and in epidemiological studies that advanced age in fathers is associated with the “active but odd” phenotype and PDD NOS.  In people, older (but not “old”) age in fathers led to increased IQ and social aloofness that led to higher academic achievement.  Is this autism?  Or just a subtype of autism where the outcomes are adaptive rather than maladaptive?  There are lots of questions about the nature of autism in these findings.