In the summer 2014, I was fortunate to receive the Autism Science Foundation Undergraduate Summer Research Fellowship to work with Dr. Sara Jane Webb at the University of Washington. During my summer research, I was able to complete my honors thesis: A Study of Twins of Individuals with Autism: Heritability of Pragmatic Language Ability in Autism Spectrum Disorder. I was also involved in two other projects in the lab: one focusing on brain activity and genetics in girls with autism, and the other to identify a potential biomarker for treatment response in adults with ASD.
For my ASF research and honors thesis, I studied language in twins with and without autism and found that twins who both had ASD had more difficulty grammar and pronunciation compared to twin pairs where both did not have ASD. If one of the twins had ASD, their language ability was not as impaired, but still not to the levels seen in those without autism. Also, the better social communication skill in the twin with ASD predicted better language ability in his or her twin non ASD twin. These results show that the genetic determinants of language may be shared by social communication. It opens up new areas of study to look at social communication skills as a target of interventions for language. I presented these data (A Study of Siblings of Individuals with ASD: Comparison of Pragmatic Language Ability) as first author at the International Meeting for Autism Research in Salt Lake City in May 2015. I was also awarded, the University of Washington (UW) Undergraduate Research Conference Travel Award and the UW Psychology Honors Travel Award.
In June, I graduated with a B.S. in Psychology with Honors. I am currently working with Dr. Wendy Stone, also at the University of Washington. I will be primarily working on research projects that focus on early detection and intervention for children with autism. I hope to pursue a Ph.D. in Child Clinical Psychology in order to continue research on intervention for social communication skills in children with autism, and potentially incorporating EEG to look at the effectiveness of the intervention.
The ASF Undergraduate Summer Research Fellowship made a huge impact on my career. It opened the doorways to additional opportunities in research, and has advanced my professional goals. The presentation, the travel award, and my direction in autism research would not have been possible at all without the support from ASF and the mentorship by Dr. Webb. I am very excited to contribute what I have learned from this experience. Thank you, ASF, for supporting my research, and thank you, Dr. Webb, for your sincere and continuous mentorship!
One of the more radical changes to the autism classification within the DSM-5 was the elimination of the category “Asperger’s Disorder” and inclusion of those who would have met that criteria under the name “autism spectrum disorder”. Some families of individuals with Asperger’s and those diagnosed with Asperger’s opposed this change for fear that being a member of the ‘autism’ group would force them to live with a more stigmatized label and subjugate them to further social and academic pressures. In order to address whether this was the case, researchers designed studies to understand the public perception of the word “autism” vs. “Asperger’s”. Coincidentally, two studies were published this week which examined the impact of clinical labels on stigma and treatment attitudes. Does an autism spectrum disorder label conjure a more unpleasant disposition when compared to an Asperger’s Disorder label? These studies also asked whether there was a difference in peer responses to overt ASD behaviors if a clinical label was disclosed.
The first report, authored by Ohan et al., examined the responses of 465 adults who were presented with a vignette of a 9 year old who displayed symptoms characteristic of someone who would have received a diagnosis of Asperger’s Disorder. Participants were then asked to rate levels of discomfort, compassion, and irritation towards the child based on a definition of stigma that included: negative beliefs (stereotypes), emotions (prejudice), and behaviours (discrimination). Statistical analyses showed stigma ratings were not dependent on the clinical label – Asperger’s or ASD. Post hoc tests also revealed participants were less likely to seek out medical treatment for the vignette child if they were unaware of any label due to the assumption that treatment would be ineffective for an undiagnosed condition.
Another study conducted in the UK, authored by Brosnan and Mills, analyzed the responses of 120 college students to two male vignettes, both exhibiting behavior characteristic of an individual with Asperger’s Disorder. Participants were informed that one of them had a clinical disorder (AS, ASD, or schizophrenia) while in the control scenario, they were told that the individual was a typical university student above average intelligence. More positive responses were found towards the clinical disorder vignette and like the first study, the type of clinical label used did not influence the student’s response.
Due to stigma surrounding mental disorders, the name of the clinical diagnosis itself can be powerful enough to deter an individual from seeking or completing treatment. Yet these studies indicate a changing attitude towards mental health, one that encourages people to be more open about an ASD diagnosis. However, it is also important to note that both studies set out to collect data from societies that were more willing to accept, even celebrate, differences and thus dedicate research and education to raising awareness about mental health problems. What happens if we take a look at the responses of cultures who have not accepted the term “autism” let alone the concept of mental health? How can we build on those existing foundations to foster inclusion for the autism community?
Ohan JL, Ellefson S, Corrigan PW. Brief Report: The Impact of Changing from DSM-IV ‘Asperger’s’ to DSM-5 ‘Autistic Spectrum Disorder’ Diagnostic Labels on Stigma and Treatment Attitudes. Journal of autism and developmental disorders. June 5 2015; doi: 10.1007/s10803-015-2485-7
Brosnan M, Mills E. The effect of diagnostic labels on the affective responses of college students towards peers with ‘Asperger’s Syndrome’ and ‘Autism Spectrum Disorder’. Autism. June 8, 2015; doi: 10.1177/1362361315586721
The autism community is constantly bombarded with potential treatments, cures, and other claims for products that have no scientific evidence. Even worse, some of these products are known to be harmful and there have been reports of deaths after such treatments, like chelation. Unfortunately, another one of these non-evidence-based, potentially-harmful compounds, has made its way into the mainstream media, potentially confusing families and individuals with autism about the promise or potential of such treatments.
In March, investigators at the Los Angeles Biomedical Research Institute in California published the rationale and methodology for a new study investigating the effectiveness of MDMA or 3,4-methylenedioxymethamphetamine for the treatment of social anxiety in adults with autism.1 This drug has shown some promise for the treatment of post-traumatic-stress disorder. This recent publication, which presented no data, went mostly unnoticed or ignored in the scientific community until the mainstream media picked up on the idea and it has since ended up in the newsfeed. MDMA is the main ingredient in the drug commonly known as Ecstacy or Molly, which was added to the DEA Controlled Schedule list in 1985. The authors claim it is safer because in the pure form because it does not include any additives or fillers that may be included in the street form of the drug. However, this theory has a problem.
One important point that the authors of this publication completely failed to mention is the potent neurotoxicity of MDMA. This scientific fact is in stark contrast to the image the authors portray of it being a benign substance which opens the mind and promotes closeness. It is a form of amphetamine which has been proven to cause long lasting loss of neurons for serotonin in the cortex of animals exposed to MDMA2. As these animals age, some of the neurons start to grow back, but with shorter or absent dendritic spines3. In humans, MDMA exposure produces a similar pattern of neurotoxicity and leads to cognitive problems, sleep issues, and psychiatric issues.4-6 MDMA also induces an increase in body temperature, and has shown to be toxic on cardiac and liver tissues.7,8 According to scientific evidence a less-pure form of Ecstacy may actually be safer than the pure unaltered compound. Therefore, the claim that the version given in this study is ‘safer’ is misleading.
There is no known safe dose in humans. In fact, in non-human primates, one dose was sufficient to produce long lasting deficits in serotonergic functioning.9 Serotonin is associated with mood, emotion, and cognitive ability, so it is not really a surprise that MDMA use causes deficits in these areas of behavior. Evidence using post-mortem brain tissue shows that people with autism have neurons that are already disorganized, misplaced, and irregularly shaped10. Therefore, giving this compound to individuals with ASD may be especially dangerous.
For those who were intrigued by this news story, concentrate on safe, non-toxic, evidence-based interventions. While the study received IRB approval, this is a dangerous compound that should be avoided. To see a comprehensive list of evidence and non-evidence based treatments, please go to our website. The autism community deserves better than to have money wasted on a study using a drug that is known to be toxic and in some cases, lethal.
Danforth AL, Struble CM, Yazar-Klosinski B, Grob CS. MDMA-assisted therapy: A new treatment model for social anxiety in autistic adults. Progress in neuro-psychopharmacology & biological psychiatry. Mar 25 2015.
Sarkar S, Schmued L. Neurotoxicity of ecstasy (MDMA): an overview. Current pharmaceutical biotechnology. Aug 2010;11(5):460-469.
Williams MT, Skelton MR, Longacre ID, et al. Neuronal reorganization in adult rats neonatally exposed to (+/-)-3,4-methylenedioxymethamphetamine. Toxicology reports. 2014;1:699-706.
Parrott AC. Human psychobiology of MDMA or ‘Ecstasy’: an overview of 25 years of empirical research. Human psychopharmacology. Jul 2013;28(4):289-307.
Benningfield MM, Cowan RL. Brain serotonin function in MDMA (ecstasy) users: evidence for persisting neurotoxicity. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. Jan 2013;38(1):253-255.
Gerra G, Zaimovic A, Ferri M, et al. Long-lasting effects of (+/-)3,4-methylenedioxymethamphetamine (ecstasy) on serotonin system function in humans. Biological psychiatry. Jan 15 2000;47(2):127-136.
Turillazzi E, Riezzo I, Neri M, Bello S, Fineschi V. MDMA toxicity and pathological consequences: a review about experimental data and autopsy findings. Current pharmaceutical biotechnology. Aug 2010;11(5):500-509.
Baumann MH, Rothman RB. Neural and cardiac toxicities associated with 3,4-methylenedioxymethamphetamine (MDMA). International review of neurobiology. 2009;88:257-296.
Mueller M, Yuan J, McCann UD, Hatzidimitriou G, Ricaurte GA. Single oral doses of (+/-) 3,4-methylenedioxymethamphetamine (‘Ecstasy’) produce lasting serotonergic deficits in non-human primates: relationship to plasma drug and metabolite concentrations. The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum. May 2013;16(4):791-801.
Hutsler JJ, Zhang H. Increased dendritic spine densities on cortical projection neurons in autism spectrum disorders. Brain research. Jan 14 2010;1309:83-94.