The ASF Travel Grantees have been tasked with sharing some of the most interesting tidbits from the 2012 IMFAR Conference. This is the knowledge gained from day 1.
Kadi Luchsinger – Communicating Autism Research: Make sure you develop your communication plan with three key points and three supporting statements in a family friendly context. Remember the rule of threes.
Emily Willingham – Wiggins Phenotypic Profiles: Study comparing various endpoints for children with and without ASD and who had developmental disability and ASD. The bottom line was that they identified a lot of overlap in various parameters–including social responsiveness, co-morbidities, and some screening tool scores, suggesting an overlapping etiology.
Melissa Shimek – Ruth Feldman Presentation: I am interested in the emphasis findings on the effect of oxytocin in persons with ASD. I would like to think eventually therapies could include OT, but I have reservations when I consider the use of dopamine in individuals with Parkinson’s. And, if not dosed correctly individuals may experience psychosis. All considerations with the idea of the least harm is essential.
Eric Hogan – Smaller Trials, Treatment Factors: As a person starting Autistic Advancement, I was exposed to other cutting-edge job placement services for individuals with ASD through this conference.
Debra Dunn – Clinical Phenotype-Assessing Diagnostic Criteria: Predicting Developing Course of ASDs: Study from the Netherlands re-evaluated 170 adolescents who had been diagnosed with “high-functioning” ASD (avg IQ was greater than 90) during childhood. Of these, 26% no longer met DSM-IV criteria at 12-19 years old. The 26% were distinguished from those who remained on spectrum in that, as children, they had less pragmatic language difficulties, more social contact and less orientation problems. However, event though they no longer meet ASD criteria, 34% move to another psychiatric diagnosis.
Eric Hogan – Friendship in ASD through the Life Span: As a person with Asperger’s, I realized the researchers know what they are talking about, based upon my experiences.
Emily Willingham – Simon Baron-Cohen and Fetal Testosterone Levels: Looked at hormone profiles in amniocentesis samples, first from a small cohort and then from a larger collection of samples in a Danish databank. They were expecting to see elevated fetal testosterone levels in pregnancies that resulted in children who later received an autism diagnosis. Instead, they found elevated levels of all four hormones along the pathway from cholesterol to testosterone (starting with progesterone). They say repeatedly that these results will require replication for confirmation.
Melissa Shimek – Awards Ceremony: I felt especially engaged by two things during the awards ceremony. Being a mother of twin girls with ASDs, I definitely will look into more work by Susan Folstein. Also, it was fantastic to hear Temple Grandin call for more research on sensitivity issues. As a woman with ASD, I can personally say to any thoughts of socialization and communication are immediately trumped by something as simple as someone near me wearing too much scented powder or hearing the sound of a rustling paper bag. Any thoughts at all can be interrupted by such sensor issues. I can see the same happening when my daughter freezes, covers her ears, and shuts down in a large noisy crowd. I hope researchers listen.
Mark Shen – Thursday Keynote Dr. Ruth Feldman, Bar Ilan University: This morning’s keynote speaker, Dr. Ruth Feldman from Bar-Ilan University in Israel, demonstrated how administering oxytocin to a parent can increase emotional interactions, touch, gaze synchrony, and promote closer relationships and attachment between a parent and their infant. The infant’s own oxytocin levels increase and, in turn, the infant will reciprocate the positive interaction with the parent. Dr. Feldman discussed the promise of using oxytocin, which is benign and has no side effects, as a potential therapeutic intervention in ASD.
Emily Willingham – Teheri’s Talk Regarding DSM-IV vs V Comparisons: Various results reported in this brief talk, among them that no children currently diagnosed with ASD or PDD-NOS under IV criteria would meet all of DSM-V criteria. Only 20% would meet proposed criteria B2 and B3. Further, only 18% of children with current PDD-NOS diagnosis under DSMIV would receive ASD diagnosis under DSMV criteria. They also found an inverse correlation between IQ and meeting DSMV diagnostic criteria, with 90% of those with IQ less than 30 meeting DSM V but only 21% of those with IQ greater than 70 doing so. Finally, they found that the proposed criteria may “miss autistic symptoms in more capable children” or children with milder severity.
Eric Hogan – Cultural Diversity Networking Luncheon: I made excellent contacts with professionals from other countries who have similar goals, employing individuals with autism.
Marjorie Madfis – Observations from Thursday: Focus on social development of babies through adults. Friendship is a critical development to enable a person to be whole and functioning…from infancy with parents takes place, to school years where coaching can help to adult years where support is in greatest need.
Catherine Blackwell – Thoughts from Thursday -Well-known sex differences in autism call for research on developmental androgenic activity and a potential link to autism spectrum disorders. Fetal testosterone may cause differences in sociability and pattern detection. Baron-Cohen et al found fetal testosterone is inversely correlated with eye contact, social skills, vocabulary size, and empathy in later childhood. Subjects who later developed autism had elevated levels of 4 measured sex steroids compared to controls (Baron-Cohen). Hollier confirmed a negative effect of biologically active testosterone and language in males. Hollier did not find this effect in females, and actually noted the possibility of a protective effect of elevated fetal androgens, but this needs further data. Baron-Cohen noted the possibility that, “autism may be an extreme form of the male developmental profile.”
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OmGggggg. THANK YOU Hollier! My brain has been trying to resolve that one for yeeeeeears!!
Wonder if that has something to do genetically in leptin expression M/F (possibly mediating or mediated by mTOR) and why protocols when it comes to testosterone enhancing/decreasing elements had such differential responses? Even when testosterone (brain developmentally)-driven at the core as brains can be intersexed and hormonally driven develpomental pathways (grey matter expression)? I had wondered that when that seemed to be the experience. Men lowering or blocking T, (which contrarily can be increased by estrogen exposure like BPA), whilst women responded with increasing/balancing aspects of in some direct or indirect raising, which seemed weird and contradictory to me, but figured there had to be a layer impacting the variation which creates such contradiction in predictable patterns) … interesting exploration, looking forward to hearing and seeing more from Baron-Cohen and Hollier.
Leptin and mTOR: partners in metabolism and inflammation.
http://www.ncbi.nlm.nih.gov/pubmed/18583936
Genetics of leptin expression in baboons
http://www.nature.com/ijo/journal/v27/n7/full/0802310a.html
Brief report: plasma leptin levels are elevated in autism: association with early onset phenotype?
http://www.ncbi.nlm.nih.gov/pubmed/17347881