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Blogging IMFAR: Exceprts Of An Interview With David Mandell, ScD

21 May

So I set out blog about the first full day at IMAR, and quickly realized I’d bitten off way more than I can chew. I had tons of scribbled notes after attending most of the epidemiology track this morning, perusing the research posters, and listening to some presentations on specific “treatments”, which were essentially, although very different from one another, targeted educational strategies in many cases. There’s just so much at IMFAR, it’s really impossible to provide any great detail about any one thing. The presentations move very quickly, at about 12 minutes each, with 2-3 questions at the end, and it seems like there’s really only time to hear about the “what” the research is about.

 If this were to be successfully blogged with any depth beyond what’s contained in the abstracts (which anyone can view online), it would probably require about 8-10 people, holding more in-depth discusssions with several research teams, just to provide spotty coverage. If you’ve ever heard the complaint that there just isn’t enough autism research taking place, IMFAR is a pretty good example of the fact that such complaint may not be based in reality. So what to do about this?

Since I have the opportunity to be here, and see and hear what’s taking place, what can I provide to readers that can’t be here? Sure, there is a little additional detail provided by the presenting researchers (their abstract presentations often contain slides that are helpful in barely understanding the abstract’s material details), but the truth is, what’s seen and heard here is actually quite similar to exactly what’s in the abstracts. So where to, from here?

I don’t expect everyone to agree, but I think it might be of at least a little value, to simply meet some of the people who are here. And there are some fascinating people here. Perhaps some would find it informative if I (we) have an opportunity to hear from someone who is heavily interleaved with the inside scene of the science of IMFAR? We don’t have to talk all science. Perhaps we could find out more about them. You know? Get to know ’em a little more than we did before.

So, here we go. Meet David Mandell, ScD.

(Incidentally, Sullivan has written about some research that has his name on it here at LBRB).

Dr. Mandell is a researcher himself, and the Associate Director of the Center for Autism Research, at The Children’s Hospital of Philadelphia. He’s also this year’s Scientific Program Chair for IMFAR. Although he has the help and participation of several collaborative teams in varying disciplines in the field of autism research, it’s essentially his responsibility to put together the scientific program that really makes IMFAR what it is this year.

My first-impression, and lay opinion, is that he seems way too young to be as accomplished as he appears to be. Looks can be deceiving though. He’s friendly, yet scientifically earnest. He sits down with me for half an hour, simply to share some of his take on, and enthusiasm for the autism research and IMFAR. I won’t agree with everything he says, but his points are thoughtful, and clearly communicated. Let’s meet Dr. Mandell, and learn a little more about his take on IMFAR along the way, shall we? So that you, dear readers, can share a little in this IMFAR experience with me, and get something that you couldn’t otherwise get from the book of abstracts, let’s chat with David Mandell ScD.

Exceprts of an interview with David Mandell ScD

LBRB: How did you become involved in IMFAR? How did you go from being a researcher to chairing such a large scientific thing like this?

DM: My first IMFAR was in 2001. It was maybe the first or second one, yeah the second, and I was a post-doc. My training was as a psychiatric epidemiologist. I had originally come to the University of Pennsylvania to work on a CDC study to do surveillance – to look at the number of kids with autism, and it was actually at IMAR that one of the keynote speakers set my research agenda for the rest of my life.

LBRB: Who was that?

DM: It was Peter Mundy, who’s now at the Mind Institute (at the University Of Miami before that). There was a lot of talk about screening instruments, and the MCHAT was of great interest to people, and: How early can we recognize these kids? How can we find the ones that we’re missing? And, you know, we are getting better and better at identifying these kids with autism, and the communities in which we’re identifying them, are completely unprepared to meet their needs. And what are we going to do about that?

LBRB: Speaking of identification and missing kids, you’ve done some research with ethnic disparity. Are those missing groups what got your interest in epidemiology? Or, was there other stuff?

DM: I sort of came at it backwards, and I came to autism sort of late. I knew from about the time I was twelve that I wanted to be a child psychologist. I thought that’s what I wanted to do. I had always worked at camps. I worked with underpriveleged kids. I knew I wanted to work with kids, and I was particularly interested in working with kids with emotional and behvioral problems. I spent most of my college years, and after college, working in psychiatric hospital, working with Guatemalan refugee children (preparing them for entry into the public school system), and I worked with adolescents who had psychiatric disorders, and who’d abused substances. And it was at one of my jobs, sort of later in that path, that I was working for a place called the Chidren of Alcoholics Foundation, and I worked developing curricula for professionals who were working with children from addicted families. So, we were developing these programs, we were training teachers in recognizing when there may be problems at home and what to do about it, helping pediatricians address very sensitive topics during the very brief pediatric visit and what to do when they uncover problems. And so we developed these programs, we’d get them published, and I’d go out and I’d do all these trainings, and we’d ask for evaluations, and the evaluations would always come back with, “yes everybody loved the training”. We had no idea if what we were doing was making any difference in any kid’s life. There was no follow-up. There was no evaluation – and I became very interested in evaluation.

LBRB: So, actually measuring results?

DM: Measuring change. How do we know what we’re doing works? Some of the members of our scientific advisory board at the Children of Alcoholics Foundation, who I worked very closely with in developing the curricula, suggested that I go back to graduate school, and they suggested a masters in public health – with a focus on program evaluation (which was my interest).

LBRB: And you said, “sure, why not”?

DM: I applied to schools, and I thought, “that’s great”. All of my essays were about how I was going to take the skills that I learned in the program and bring them back to the front line work that I had been doing. And as it turned out, I couldn’t afford the masters program. It was very expensive and there were no scholarships, but if I switched my application to the doctoral program, and I got in, they would cover my tuition give me a stipend.

LBRB: That seems worthwhile.

DM: Yes. So I ended up in the doctoral program instead of the masters program.

LBRB: So where does your research interest take you today?

DM: So my interests are not very distant from where they were when I started.

LBRB: Epidemiology?

DM: Well, no. Epidemiology is a set of tools. Epidemiology is literally the study of the health and illness, and its distribution in a population. You can do that with any health condition. But, it also teaches a systematic set of tools for evalutating – the association of different variables. Sometimes we think about those variables as risk factors. So there’s a lot of discussion at IMFAR this year about… there’s several studies on, prematurity, and fertility problems, and fertility treatment, and its association with autism. So those are large scale epdiemiological studies. They’re looking at different variables in the population. But you can also use those same tools to look at positive outcomes associated with treatment. So I take that skillset, those tools that you learn in epidemiology and apply them to looking at treatment and other supports that children with autism and their families get, and what the associated outcomes are.

LBRB: You mentioned in yesterday’s press conference that a theme in this year’s research was treatment research beginning to make a real difference. Where do you see that “real difference” translating into everyday life for families or schools?

DM: So let me give you one example. One of the huge challenges we have in the U.S. is that we can’t get insurance companies to pay for treatment for children with autism. The reason the insurance companies give is that treatments don’t have the level of evidence to support them that those insurance companies often require. And the highest level of evidence for them, is a randomized trial. One of the really exciting things about the treatment studies that are being presented here, is a dramatic increase in the number that use randomization as part of their model. And so these are treatment studies, that when published, then become the standard of care. They can be used as a level of evidence to support changes to the decision rules that insurance companies have. And I’m already getting calls from insurance companies about, “How do we think about restructuring and financing, so that we can support these kinds of interventions?” That’s one, I think probably the most obvious real world example.

LBRB: Tell me more about your role with IMFAR? How did you get so involved?

DM: Well, I’m the local boy. So a lot of it is, you know, I’m from Philadelphia, from the University of Pennsylvania…meeting chair and program director..

LBRB: So you were elected this year?

DM: Yeah,  that’s right.

Bob Schultz is the director of the Center For Autism Research, and is the immediate past president of IMFAR, and he had just come from Yale to the Children’s Hospital of Philadelphia, and he’d asked me to be the associate director of the center. He also asked me if I would chair the meeting.

LBRB: It’s a one year appointment?

DM: Yes. I think he saw it as something that would be beneficial to me. But it’s exhausting.

LBRB: I’ll bet. The program is huge.

DM: I read nine hundred and eighty-seven abstracts.

LBRB: You read every abstract?

DM: I read every abstract. You manange the program committee. You manange the reviewers. The people on the program committee are brilliant, and very dedicated to the field. So a huge part of it is via learning from them what’s important in their particular discipline. And the second thing is by reading all the abstracts, you really begin to see the themes that are emerging in the science.

What’s really exciting to me about this IMFAR is that the really exiciting science is happening in between the traditional disciplinary boundaries. So we used to think about there are the genetics ones, and there are the animal models ones, right, and there’s a biological mechanisms in humans one, and there was pharmacological treatment, and there’s behavioral treatment. And then, sort of here over on the side, there’s epidemiology and services research, and policy type stuff. These were very separate tracks, with very little crossover. And now I think the message, or at least one of the messages at IMFAR is that these disciplines have to talk to each other. It’s by collaborating, and it’s by training new investigators who have expertise in at least two of those disciplines where we’re going to see the most exciting science.

LBRB: So this is a huge program. What are you going back to? What’s next for you after IMFAR?

DM: So I have two things. My particular interest is how you take evidence-based interventions and implement them in communities so that they are effective and they sustain. My group is presenting tomorrow on our study, the autism structural methods study. We partnered with the school disctrict of Philadelphia, we trained teachers in 50 classrooms in evidence-based interventions and in looking at outcomes for kids. So part of my research agenda is expanding that, expanding it up and down the age span, and also thinking about what the next steps are.

LBRB: That sounds heavily educational. Do you consider that autism “treatment”?

DM: I call it what the funder needs it to be called. So this sort of gets to the other half of my research. The other half is actually going much more biological. Which is, we have kids who are phenomenal responders to the behavioral intervention, and then we have kids who aren’t. Why? What is changing in their brains as a result of the intervention; because any behavior you observe has a correlate in brain function. If we can find those correlates, like Eric Courchesne was presenting, it is going to help us understand how to better target our behavioral strategies, and it’s going to give us earlier markers… So I want to connect the behavioral interventions to the biology. Because I think ultimately what we’re going to see, is that we will find systems in the brains of children with autism that are not functioning that way we would hope they might, and that we might have biological interventions (like medication). A medication may help correct that system, but that child still has to learn. And so I think the most exciting interventions are going to come from pairing mecdications with the different strategies for learning. So that’s the other direction my research is going.

LBRB: Does any of this leave you any free time? What do you like to do on a Saturday? Do you take time off from research?

DM: I take my kids to dance class on Saturdays. And, I fence.

LBRB: That’s not something you hear too often…

DM: That’s my evening activity.

LBRB: I don’t know anything about fencing, is that good exercise?

DM: Yeah, it is good exercise. But the thing about academics in general is that you never turn it off. I definitely keep a notebook by my bed. You wake up in the middle of the night with an idea, and it gets written down. You never really turn it off, but like with any job, you have to make time for yourself and your family. I think people do that with varying degrees of success.

LBRB: Are you pretty good with that?

Pretty good. I have a six year-old and a four and a half year-old. They go to bed at seven.

LBRB: Wow! That’s early. You’ll have to share your secret with me for that?

DM: My secret is my wife.

Dr. Mandell had much more to share about what he considers success in autism research, and explained personal reward from succcess and  small change at local Philadelphia schools.  I’d really have loved to share more, but learned a valuable lesson during writing this post – I really suck at transcription. I hope you enjoyed hearing from Dr. Mandell though. I know enjoyed hearing his take on the IMFAR science in person, and I thank him for making a little time for LBRB.

(Disclosure: my attendance at IMFAR was funded in part, by a travel grant from the Autism Science Foundation.)

NIH Workshop on Nonverbal School-Aged Children with Autism

20 May

The U.S. National Institutes of Health recently held a workshop on nonverbal school-aged children with autism. The sponsoring Institutes were:

National Institute on Deafness and Other Communication Disorders

National Institute of Mental Health

Eunice Kennedy Shriver National Institute of Child Health and Human Development

The scope of the workshop was:

In April 2010, the National Institutes of Health (NIH) convened a multidisciplinary workshop to discuss the state of the empirical knowledge about, and research opportunities regarding, the substantial subgroup of children with autism spectrum disorders (ASD) who have not developed functional verbal language by five years of age. The discussants reviewed the current state of scientific knowledge, highlighted critical gaps in our knowledge, and identified research opportunities to address knowledge gaps. A series of presentations and group discussions addressed the three major topics of the workshop.

The topics included

Topic 1: Who are these children? What do we know about their developmental trajectories?

Topic 2: How can we assess their skills and knowledge across different domains, with special reference to those abilities relevant to language acquisition (e.g., verbal comprehension, sensory and motor skills, apraxia)?

Topic 3: What treatments/interventions are effective in improving spoken language and communication in these children (augmentative and non-augmentative methods)?

and

Research Gaps and Opportunities

The workshop summary is very interesting. It reinforces what is probably an obvious point: any language, no matter how small, is a big leap forward. Any verbal language by age 5, echolalic or otherwise, is a big indicator of verbal language gains later. Apraxic kids with autism are very diverse, just as all autistic people comprise a very diverse group.

Most of the apraxic/autistic kids who will become verbal start in the 5-7 age bracket. There is an example of a child attaining verbal language at age 13.

Dr. Cathy Lord discussed the characteristics which are related to whether an apraxic/autistic child becomes verbal:

* Intellectual disability
* Little desire or motivation to communicate
* Poor socialization scores (Vineland)
* Presence of challenging behaviors
* Impaired joint attention
* Impaired imitation of sounds and movements
* Specific language and other motor factors

Dr. Barry Gordon discussed the characteristics of those children who transition from verbal to nonverbal nonverbal to verbal:

# Age (most children who started speaking were between 5 and 7)—none over age 13.
# Some conceptual and semantic abilities.
# Strong motivation to communicate via oral speech.
# Specific training in the formation of sounds and words. Such training needs to be very intensive (often ABA approaches) and highly flexible, taking into consideration individual child abilities.
# With intervention, 70% acquired production of words, only 30% developed phrase speech

What is not noted is how many children acquired production of words without intervention. This is not an experiment I would propose (at all), but it would be good to have that baseline number to compare to this 70% number. Obviously, it would be good to see what interventions work and with which groups of children. There was discussion of various methodologies (ABA, PRT, PECS, as well as augmentative communication methods)

One point made, and this is very important, there is very little research that concentrates on the nonverbal school-age group. My guess is that there is even less research on nonverbal adults.

This is something that needs to change. I appreciate that the NIH held this workshop, but unless research funding is allocated to apraxic/autistic kids, there will continue to be huge gaps in the knowledge base.

Dr. Andrew Wakefield to join Dr. Arthur Krigsman in clinic independent of Thoughtful House?

20 May

Dr. Andrew Wakefield gives an interview in a recent story in the Austin Statesman, Censured doctor says he’ll resume autism research in Austin.

Dr. Wakefield is the primary doctor behind the idea that the MMR vaccine causes autism. His initial paper suggesting this link has been retracted by The Lancet, and the General Medical Council ruled that he was dishonest in his research efforts and showed a callous disregard for his subjects. He expects to lose his license when the GMC finishes the second phase of their action against him next Monday.

According to Dr. Wakefield, this will be the “final effort by the mainstream medical establishment to silence him and stop his research.”

I am at a loss for how this could silence him or stop his research. Dr. Wakefield resides in the United States and has for some time. Even when he was doing research in the United Kingdom, he was not working in a capacity to use his medical license (at least to my understanding).

The interview continues–

“Now that they have come to their determination, I will make absolutely sure the truth comes out,” Wakefield said. “I think I am in a position to encourage people to take a more serious look at the kinds of projects I am considering,” such as researching the long-term health of children who have been vaccinated and those who have not been vaccinated.

Again, I am at a loss. Why has Dr. Wakefield waited until he lost his license, something which he does not use, to make sure that the truth comes out? I would also question whether he is in a position to be taken seriously.

Dr. Wakefield is further quoted:

“Vaccine safety is built upon the confidence of the public u2026 and I’m not prepared to (compromise) that,” he said Wednesday, adding that he hopes people will read the book and “make up their own minds about what is real and what isn’t real.”

Dr. Wakefield is not prepared to compromize the public’s confidence in vaccines?

I am, yet again, at a loss for words.

On the subject of Dr. Wakefield’s future efforts:

Wakefield said he resigned from Thoughtful House so he wouldn’t be a distraction from its work. He said Thoughtful House was getting away from a focus on gastrointestinal issues and autism. Krigsman posted a message to former Thoughtful House patients saying their records would be forwarded to him, and they could see him at a “new, independent” office in Austin where Wakefield said he would do research similar to what he did at Thoughtful House.

Blogging IMFAR: Autism And Divorce Debunked, Among Others

20 May

Autism And Divorce Debunked

Does anyone really believe that whopper of an urban-legend that goes something like this – “The divorce rate among families with autistic children is 80%!”?

Sure, many people do believe it, and I wrote about this topic when the Easter Seals Living with Autism survey results were released a little over a year ago, here. You probably won’t be surprised, but the often repeated 80% statistic looks like pure online mythology. Sullivan has the early notes here. And some of the more mainstream media have the story as well.

As pointed out previously by other LBRB commenters, and in addition to the Easter Seals “Living With Autism” survey, there is some existing science on the subject that essentially shows that autistic children are no more likely to live in divorced households than non-ASD children.

– Montes & Halterman, Psychological Functioning and Coping Among Mothers of Children With Autism: A Population-Based Study, Pediatrics 2007;119;e1040-e1046

– Montes & Halterman, Characteristics of school-age children with autism in the United States, J Dev Behav Pediatr. 2006;27:379–385

Well, now there’s a much larger research study heading for publication. I had the opportunity to sit down with Brian Freedman PhD, from the Kennedy Krieger Institute’s Center For Autism And Related Disorders in Baltimore, MD (the study’s lead author).

When asked about how he became interested in pursuing researching the 80% divorce rate urban legend, he explained that as a result of hearing concern about family stressors and divorce from families that he works with, he wanted to find the original source of the statistic. Freedman went on to explain that he set out locate a scientific source for the statistic, but that the science to support it just wasn’t out there.

On the topic of working with families regularly, Freedman also shared that, “an important consideration in providing information to families, is that the information provided is correct, and evidence-based”.

The results of the study were stated as follows at the press conference:

The weighted unadjusted percentage of children with ASD belonging to a family with two married biological or adoptive parents was 64%, as compared to 65.2% for children who do not have an ASD.

In fact, in addition to finding “no consistent evidence of an association between a child having an ASD diagnosis and that child living in a traditional vs. non-traditional family”, the abstract from Freedman’s research goes on to say that once variables of co-occurring psychiatric disorders are controlled for,
“our results show that a child with an ASD is slighty more likely than those without ASD to live in a traditional household”.

How does that translate to the 80% divorce rate myth? It blows it out of the water. The 80% divorce rate myth predicts that only 20% percent of autistic children would live with married parents (or at least it allows for that perception). Based on this research, reality would appear to dictate that 64% of autistic children live with two married parents, pretty much just like non-ASD kids.

Interestingly, and although no research is ever free of any limitations, this seems to be a large, and probably fairly population-representative study. The data for children originated with the National Survey for Child Health (Blumberg et al., 2009), which is not only very recent, it’s inclusive of over 77,000 children aged 3-17.

What? Low levels of “quality indicators” on autism websites?

Really?

Okay, so no one is going to be surprised by this one, at least LBRB readers aren’t anyway. An abstract presented at today’s press conference details research by a team at the Yale Child Study Center.

122.001 Pressence of Quality Indicators On Autism Websites. B. Reichow*1, J. Halpern2 and F. R. Volkmar3, (1)Yale Child Study Center, (2)Fordham University, (3)Yale School of Medicine

See page 452 of the online abstract book for the rest of the study detail, but I’ll save you some time, and share with you that if autism websites in general were being graded on the presence of some selected objective indicators of website quality, the majority would be getting an “F”. Most people probably wouldn’t eat in restaurants with failing health grades, why would they apparently seek information about autism from the internet? Perhaps that “why”, or even the implied assertion on my part that this is where people do get information about autism, will have to go undiscussed. The fact is, the websites that are out there (that turn up for very generic searches in popular search engines), are really lacking when it comes to quality indicators.

Results: On average, the 164 websites analyzed for this study suggested autism related websites contained less than 6 of 8 quality indicators. Nearly 1 in 5 websites offered a product or service for purchase, and/or promoted a miracle cure. These websites were also, on average, some of the least likely websites to contain the quality indicators.

As I was hoping to learn more about just what the website “quality indicators” were, I was fortunate enough to have a chance to sit down and chat briefly with study’s lead author, Brian Reichow. He shared some of the important ones with me, and I think most readers would agree with the importance of their presence on trusted websites – things like: clear authorship (who’s written the website’s content), the use of references (citing sources), website currency (out of date could be a problem), clear disclaimers with respect to expertise and advice, reading level, and presence of a clear feedback mechanism.

Yep, I do wonder if Left Brain/Right Brain was picked up in those top 100 searches conducted by these researchers, and yep, I wonder how LB/RB fared by their actual criteria.

Other interesting press conference items.

There were, of course, more abstracts presented than the two that interested me the most which I’ve described here. I’ll have to simply point them out with some very brief notes and abstract pages noted.

Kids learn better from their peers Page 17

104.004 Social Inclusion of Children with ASD at School: Effects of a Randomized Controlled Treatment Study. C. Kasari*, University of California, Los Angeles

Dr. Kasari shared some interesting results, that will probably seem like a no-brainer to many. It’s good to have some supporting science though. Autistic kids targeted along with peers for what looks to me like “inclusion intervention” (such as specific paired-friend playground activities during recess), did better on some specific social measurements than kids targeted for intervention, but not along with peers.

Sleep fMRI as a diagnostic tool? Page 125

107.002 Abnormal Brain Response to Language Stimuli in Sleeping Infants and Toddlers with ASD. L. T. Eyler*1, K. Pierce2 and E. Courchesne2, (1)University of California San Diego, (2)University of California, San Diego

Admittedly, I find this fascinating. There is emerging brain imaging and a tool that may lead to the ability to diagnosis of autism very early – like infant early. This particular research group has identified a potential abnormality in the laterality of language in autistic children, as identified by the use of a newly developed sleep fMRI. Of course this raises a million potential ethical quesitons, but it seems possible that understanding potential language acquisition issues could lead to the development of new adaptive and perhaps helpful early teaching/parenting/family strategies.

Tomorrow’s program

In case anyone wants to follow along in the program (see around page 12 of the PDF), I’ll be trying to attend the following tomorrow:

8:15-9:30 Keynote (Mouse Models…)

10:00-12:00 Oral Session Epidemiology 1

1:30-3:30 The Ethics of Communicating Scientific Risk

4:00 Tom Insel – IACC Upate

(Disclosure: my attendance at IMFAR was funded in part, by a travel grant from the Autism Science Foundation.)

U. Rochester researchers discuss diet-autism trial

20 May

We’ve already blogged this story a couple of times on LeftBrainRightBrain. The GFCF diet is not effective as an autism treatment. When I found these videos on the University of Rochester website, I thought they would be interesting to many readers.

Obviously, the Rochester team knew this study would be getting publicity

They discuss the methodology and show pictures of some of the snacks. They discuss how the GFCF diet is non trivial to implement. They recommend (strongly) working with a good nutritionist.

Clinical Trial of the GFCF diet in children with GI disorders

19 May

The gluten free, casein free diet is not beneficial to all autistics. Not even most. But the question remains, how about a small subset? What about autistics with gastrointestinal (GI) conditions?

A Study to Assess the Role of a Gluten Free-dairy Free (GFCF) Diet in the Dietary Management of Autism Associated Gastrointestinal Disorders

I find the phrasing “Autism Associated Gastrointestinal Disorders” a bit odd. Are they trying to say that the GI disorders are linked to the autism? Since there is no group as yet shown to have GI disorders linked to autism, this would seem a tricky criteria to implement. How will they, for example, chose those who have GI disorders “associated” with autism vs. those who have autism and GI disorders which are not associated?

Ah well, best not to get tied up in those details.

Here are the inclusion criteria:

Inclusion Criteria:

* Informed consent / Assent, as applicable must be signed prior to executing any study related procedure
* Children, male or female, 2 to 17 years old (inclusive)

Confirmed diagnosis of ASD according to the diagnostic measures:
o DSM-IV Symptom Checklist
o Autism Diagnostic Observation Schedule(ADOS)&/or Autism Diagnostic Interview Revised(ADI-R)within 18 months prior to entry into the study
* Able to consume at least 2 cartons of the study drink daily

Subjects must present with a current history of at least two of the following persistent GI symptoms as confirmed by the study physician:
o Diarrhea, as characterised by three or more loose stools a day for at least 8 out of 14 days
o Constipation as characterised by less than 3 bowel movements per week, for at least a 2-week period
o Esophageal reflux, as characterised by 3 or more episodes of regurgitation per day on 10 out of 14 days
o Abdominal pain manifested as pain after eating or self injurious behavior on at least 8 out of 14 days
o Suspected food allergy which is confirmed by a physician, as characterized as a recurrent reaction or association with specific foods

I think that last one is key–suspected food allergy with recurrent reactions to specific foods. Of course such conditions should be treated, and would likely respond to changes in diet.

I also question “Abdominal pain manifested as pain after eating or self injurious behavior on at least 8 out of 14 days”. How is self-injurious behavior a manifistation of abdominal pain? Yes, I can see how a child with abdominal pain could be self injurious, but I can also see that many children with self injurious behaviors could have them as a result of other conditions.

Here are the exclusion criteria:

Exclusion Criteria:

* Children with a history of anaphylaxis to dietary milk and wheat proteins
* Children with severe concurrent illness
* Children who are prescribed systemic steroids
* Children currently receiving chelation therapy, hyperbaric or antifungal treatment within 1 month of entry into the study and during the study period.
* Children with a confirmed diagnosis of celiac disease
* Subjects who have previously tried dietary elimination of casein and gluten for at least 1 month period and failed to demonstrate a response by parent perception
* Children who are unable to consume at least 2 cartons of the study drink daily

It strikes me a bit odd that children who have been on “The Diet” in the past but didn’t respond would be excluded while those whose parents who tried “The Diet” and perceive benefit would be included. But, I guess this is a treatment study, not a “demonstrate that GI complaints exist in autistic children” so that selection bias may be OK. It will be interesting to see to what level parents’ perceptions are accurate in these cases.

The real question I have is, why? Why do this study? Why focus on autistics? If a person, child or adult, autistic or not, has a food allergy and reacts to those foods, of course take them out of the diet.

But, not all of the children in this study will have suspected food allergies. Any two of the criteria above are required for inclusion in the study. But, I’m still stuck with “why autistics”. Why not study children, any children, who have GI complaints and see if they respond to the GFCF diet? Or, why not study both autistics and non-autistics and shed some light on the assertion that GI disorders are associated with autism?

The study is being conducted at Massachusetts General Hospital with Dr. Tim Buie as the investigator. Anyone interested in participating can find the contact information on the Clinical Trials announcement.

Blogging IMFAR: Opening Press Conference and GFCF Diet Trial Results

19 May

After air traffic/weather delays, I arrived in Philadelphia late last night. By the time I made my way downtown to the hotel, and had a chance to catch up on some required work e-mail, I was was pretty well ready for bed. Having had a very busy past couple of weeks at work did not leave me much time to preview the IMFAR program materials, so before turning in, I’d figured I’d better look through it thoroughly.

And that’s when the pure size of IMFAR finally sunk into my brain. To cover this, from one blogger’s perspective, is going to be a huge challenge. There is absolutely no way for one human to assign attention to all that is here in the field of autism research – a great deal of the presentations occur simultaneously in separate meeting rooms.

For me, IMFAR started with this afternoon’s press conference. Organized by INSAR, and following a brief introduction by Dr. David Amaral (INSAR’s president), Dr. David Mandell (the IMFAR Scientific Program Committee Chair) spoke briefly about just how large IMFAR has become – from couple of hundred abstracts and a few hundred attendees nine years ago, to closer to a thousand accepted abstracts and a couple thousand attendees this year.

Dr. Mandell shared what he thought were two imporant themes from this year’s scientific program, the first being the volume of good research that seems to be emerging. Although Dr. Mandell pointed to progress in animal models and gene research (and its subsequent relevance in gene-brain imaging/brain functioning research), he seemed to ascribe importance to pointing out a second theme, in that reasearch is also beginning to focus on more pragmatic things – or to paraphrase his words, research is beginning to look at things that can effect “real and positive change”.

For many in the autism community, this is bound to raise ethics questions about “treatment” for autism in general, but put aside debate over social vs. medical model of autism, if only for the moment. There’s another important aspect, and Dr. Mandell did not miss this. Studying treatments has the potential to effect real and positive change, because many treatments and “alternative medicine” in use by families on children are simply untested, and some even have the potential to be dangerous.

As an example of a treatment study that has the potential to encourage parents to take a closer look at the science, Dr. Susan Hyman from the University of Rochester presented her team’s findings from their GFCF study (this is the randomized, double-blind, placebo-controlled that began in 2003). I’ll spare the gory details, as they are well-documented in the previous post GFCF of no benefit. Suffice it to say that what started with anecdotal reports of specific benefits for autistic children from a GFCF diet, is not supported by scientific data when studied with good research methodology. While it’s important to note that this small study has more rigorous methodology than any previous study on the use of the GFCF diet with autistic children, it’s also important to note that these are pre-publication results shared with the press and at IMFAR. Additionally, when asked about any real scientific basis for the GFCF diet for autism, and after acknowledging the historical [but not necessarily scientifically founded] aspect of a “leaky gut and opioid excess hypothesis”, Dr. Hyman was careful to point out that there may be other complex areas in nutrition that are relevant for learning and behavior in autistic children.

Even with what are essentially negative results for this study, it appears that “nutrition and autism” research will continue at the University of Rochester. I suspect that this University of Rochester GFCF RCT will dominate autism news for the next couple of days, as it seems to have that appeal of a topic of popularity. It also wouldn’t surprise me if this story is a headline for some of the mainstream media tomorrow.

Next up: More on Autism and Divorce Debunked! Plus a little more about some of the other abstracts from the press conference. I’ll also share a little about the pieces of the program I plan to attend, so anyone wishing to, can follow along in the published program, as I attend and report back here.

(Disclosure: my attendance at IMFAR was funded in part, by a travel grant from the Autism Science Foundation.)

The Gluten Free and Casein Free (GFCF) Diet: A Double Blind, Placebo Controlled Challenge Study

19 May

This study has been a long time coming. I’ve been hearing about it for years: a study on the GFCF diet for autistics. The study, led by Dr. Susan Hyman of the University of Rochester, has been on clinicaltrials.gov since August 2004.

The concept was fairly simple: get children on a GFCF diet. Monitor their diet for proper nutrition. Once the child is on the diet, give the child small snacks, some with small amounts of gluten or casien or both and some without. Track behaviors. The parents and children and most of the researchers were “blind” to which snacks had the gluten and or casien.

The results, as Kev has already blogged, are finally in. The result: autistic children, in general, are not affected by gluten or casien. The “autism is just a leaky gut” theory was never very well supported.

Does this mean that no autistic children have sensitivities to gluten or casien? Hardly. Being autistic is not a shield against food sensitivities. What this does tell us is that autism is not caused by these nutrients.

The abstract is up on the IMFAR website:

S. Hyman , Strong Center for Developmental Disabilities, Pediatrics, University of Rochester, Rochester, NY
P. A. Stewart , General Clinical Research Center, University of Rochester, Rochester, NY
T. Smith , Strong Center for Developmental Disabilities, University of Rochester, Rochester, NY
J. Foley , Pediatrics, University of Rochester, Rochester, NY
U. Cain , General Clinical Research Center, University of Rochester, Rochester, NY
R. Peck , General Clinical Research Center, University of Rochester, Rochester, NY
D. D. Morris , Pediatrics, University of Rochester, Rochester, NY
H. Wang , Biostatistics and Computational Biology, University of Rochester, Rochester, NY
Background: Approximately 1/3 of children with ASD receive dietary interventions. While families report dramatic clinical effects, two prior trials do not confirm these positive outcomes. Neither examined nutritional sufficiency or controlled for other interventions. This study was undertaken to examine the behavioral and physiologic effects of the GFCF diet and assess its nutritional adequacy.
Objectives: To evaluate the nutritional adequacy, physiological effects, and efficacy of the GFCF diet on symptoms of ASD using randomized double blind placebo controlled challenges in preschool children with ASD. Methods: ADI-R/ADOS positive children ages 30-54 months receiving at least 10 hours/week of early intensive behavioral intervention (EIBI) were recruited. They were screened for milk/wheat allergies, celiac disease, and anemia/iron status by RAST, TTG and CBC/ferritin respectively. After a strict GFCF diet for at least 4 weeks, they received weekly, grouped, randomized double blind challenges containing either 20 g wheat flour, 20 g evaporated milk, both, or neither on three separate occasions over 12 weeks . The challenges appeared identical and were similar in taste and texture. Laboratory monitoring and BMI recording occurred at baseline, 6,18,and 30 weeks. Behavioral data was collected at these times plus the day before then 2 and 24 hours after each challenge, Measures included: Bristol Stool Scale, Sleep Diaries, Actigraphy, Conners Abbreviated Rating Scale, and Target Symptoms Scale. Ritvo Freeman Real Life Rating Scales (RFRLRS) were recorded at 2 and 24 hours post challenge. Challenges occurred only if measures were at baseline levels. Data were analyzed by group and for individual children comparing baseline with 4 weeks on diet and then pre/post challenges.
Results: Twenty one children were recruited. Two were excluded for positive TTG, one for anemia. Four additional children were unable to establish the diet or left EIBI. Group data on the 14 successful participants (43.5 months, range 35-54 ; 12 males) demonstrated no statistical change in frequency or quality of stools, sleep, actigraphy for activity, or parent/teacher/observer scores of attention/activity for baseline/ diet or in pre/post challenge ratings. The group RFRLRS data 2 hours post challenge were higher after placebo than after challenges of casein (p=.013), gluten (p=0.024) or gluten + casein (p= 0.021). These differences were not present 24 hours post challenge. Single case analysis will be presented. All children were maintained within acceptable ranges for micro/macronutrients with intense weekly dietary monitoring.
Conclusions: This is the first study to examine the behavioral effects of a nutritionally monitored GFCF diet on attention, sleep, stool pattern, and core symptoms of ASD. While no favorable effects of the GFCF diet on attention, sleep and stool patterns were identified in group analyses, such effects may occur for individuals or for subgroups of children (e.g. with significant GI disease), providing the basis for positive anecdotal reports. Future studies need to address the potential effects of nutrition on behavior in children with ASD and be powered to evaluate subtle changes in core symptoms.
Funded by STAART NIMH PO1HD35466 and National Center for Research Resources (NCRR) NIH UL1RR024160; Autism Treatment Network/Autism Speaks – AIRP Network(HRSA)

The study has been picked up by a number of news outlets, including the LA Times, USA Today and ABC News.

Families with autistic children do not divorce at a higher rate

19 May

Autism and divorce. There is a “statistic” that gets repeated that 80% of families with an autistic child end in divorce. Turns out, this isn’t true. Kev here at LeftBrainRightBrain has already discussed the recent press release on this.

As a blogger here, I have the opportunity to write long responses and post them separately. When I read that the study is going to be presented at IMFAR later this week, I looked up the abstract.

B. H. Freedman , Center for Autism and Related Disorders, Kennedy Krieger Institute, Baltimore, MD
L. Kalb , Center for Autism and Developmental Disabilities, Kennedy Krieger Institute, Baltimore, MD
B. Zablotsky , Mental Health, Johns Hopkins University, School of Public Health, Baltimore, MD
E. Stuart , Mental Health, Biostatistics, Johns Hopkins Univ. School of Public Health, Baltimore, MD
Background: A large body of research suggests that raising a child with an Autism Spectrum Disorder (ASD) is a uniquely stressful experience for parents (Fisman et al., 1989; Konstantareas & Homatidis, 1989). The demanding nature of parenting a child with ASD can be particularly deleterious to the parents’ relationship, causing a significant decrease in marital satisfaction (Bristol et al., 1988). However, it is presently unclear if having a child with an ASD increases the risk for separation among biological parents. While speculation abounds in the mainstream media about increases in separation and divorce for this population, very little empirical and no epidemiological research has addressed either this claim or the unique factors that may contribute to separation of these parents.

Objectives:

1. Examine the association between having a child with a current ASD diagnosis and the relationship status of their parents.

2. Identify factors that contribute to a greater likelihood of a child with ASD living with two biological or adoptive parents.

Methods: Data used for this study were taken from the 2007 National Survey for Child Health (Blumberg et al., 2009). Using children ages 3 to 17 years, our final sample size was 77,911. Survey weights allow the results to generalize to the noninstitutionalized US population of children. The outcome variable of family structure was dichotomized as being either traditional (two parent household, either biological or adoptive) or non-traditional (a two parent household with step-parents, a single mother or father, other relatives, or other family types). A four-stage sequence of survey weighted logistic regression models were developed to examine the association between having a child with a current ASD diagnosis and living in a traditional family, while controlling for potential confounders. Model 1 controlled for basic demographic confounders; Model 2 added maternal characteristics; Model 3 included additional socioeconomic indicators; and Model 4 included co-occurring psychiatric diagnoses in the child (Externalizing, Internalizing, and ADHD).

Results: No association between a child having a current ASD diagnosis and their family structure was identified in the first three logistic models (OR range .98 – 1.06, all p>.05). However, this association reached marginal significance when concurrent psychiatric diagnoses were included (OR 1.66, 95% CI (1.03-2.67), p=.04).

Conclusions: Results from the analysis found no consistent evidence of an association between a child having an ASD diagnosis and that child living in a traditional versus nontraditional family. Once we control for co-occurring psychiatric disorders, our results show that a child with an ASD is slightly more likely than those without ASD to live in a traditional household. This somewhat counter-intuitive result is likely due to particularly low probabilities of living in traditional households for children with those other disorders, regardless of whether or not they have ASD. In fact, exploratory analyses suggest that having ADHD, Externalizing, and Internalizing disorders are more strongly related to the probability of not living in a traditional household than is ASD. Findings from this study hold important implications to both research and intervention for families of children with ASDs.

Repeated for emphasis: “Once we control for co-occurring psychiatric disorders, our results show that a child with an ASD is slightly more likely than those without ASD to live in a traditional household”

Not only is the “80%” figure wrong, but families with an ASD child are more likely to be in a “traditional” household.

The fact that parenting an autistic child does not lead to more divorce is not all that surprising to me. As the abstract notes, they used the National Children’s Health Survey data in the study. You may recall that this study was a hot topic for a while last year, with various groups and bloggers claiming it as evidence for an autism epidemic (note, it isn’t evidence of an epidemic at all. Actually the contrary). Amid that flury of attention, we here at LeftBrainRightBrain looked at other information in the Survey, including family structure, in Interesting information in the National Children’s Health Survey

At that time I presented the results of the question “Are the kids living in a household where the parents are married?”

69.4% of families who identified their child as autistic
74.0% of all families who responded.

D’oC also discussed Autism And Divorce in a post following a survey released by Easter Seals and the Autism Society of America which showed lower divorce rates amongst families with autistic children.

Does this mean that parenting autistic children (or parenting at all for that matter) isn’t difficult? No. Does it mean that supports are in place for autistic children and their families? No.

But, we must keep one final question in mind–Does misinformation help anyone? No.

GFCF of no benefit

19 May

This post is from Eureka Alert

A popular belief that specific dietary changes can improve the symptoms of children with autism was not supported by a tightly controlled University of Rochester study, which found that eliminating gluten and casein from the diets of children with autism had no impact on their behavior, sleep or bowel patterns.

The study is the most controlled diet research in autism to date. The researchers took on the difficult yet crucial task of ensuring participants received needed nutrients, as children on gluten-free, casein-free diets may eat inadequate amounts of vitamin D, calcium, iron and high quality protein. Unlike previous studies, they also controlled for other interventions, such as what type of behavioral treatments children received, to ensure all observed changes were due to dietary alterations. Past studies did not control for such factors. And although no improvements were demonstrated, the researchers acknowledged that some subgroups of children, particularly those with significant gastrointestinal (GI) symptoms, might receive some benefit from dietary changes.

“It would have been wonderful for children with autism and their families if we found that the GFCF diet could really help, but this small study didn’t show significant benefits,” said Susan Hyman, M.D., associate professor of Pediatrics at Golisano Children’s Hospital at the University of Rochester Medical Center (URMC) and principal investigator of the study which will be presented Saturday (May 22) at the International Meeting for Autism Research in Philadelphia. “However, the study didn’t include children with significant gastrointestinal disease. It’s possible those children and other specific groups might see a benefit.”

In response to widespread parent-reported benefits, URMC initiated the trial in 2003 to scientifically evaluate the effects of the gluten-free and casein-free diet, which eliminates wheat, rye, barley and milk proteins. Parent observation has played an important role in earlier treatment discoveries in children with autism, such as melatonin’s benefits for sleep.

Hyman’s study enrolled 22 children between 2 ½- and 5 ½-years-old. Fourteen children completed the intervention, which was planned for 18 weeks for each family. The families had to strictly adhere to a gluten-free and casein-free diet and participate in early intensive behavioral intervention throughout the study. Children were screened for iron and vitamin D deficiency, milk and wheat allergies and celiac disease. One child was excluded because of a positive test for celiac disease and one was excluded for iron deficiency. Other volunteers who were excluded were unable to adhere to the study requirements. The children’s diets were carefully monitored throughout the study to make sure they were getting enough vitamin D, iron, calcium, protein and other nutrients.

After at least four weeks on the strict diet, the children were challenged with either gluten, casein, both or placebo in randomized order. They were given a snack once weekly with either 20 grams of wheat flour, 23 grams of non fat dried milk, both, or neither until every child received each snack three times. The type of snack was given in randomized order and presented so that no one observing – including the family, child, research staff and therapy team – knew what it contained. The snacks were carefully engineered to look, taste and feel the same, which was an exercise in innovative cooking. In addition, the nutrition staff worked closely with the families to make a snack that met their child’s preferences. Casein was disguised in pudding, yogurt or smoothies and gluten in banana bread, brownies, or cookies depending on the child’s food preferences.

Parents, teachers and a research assistant filled out standardized surveys about the child’s behavior the day before they received the snack, at two and 24 hours after the snack. (If the child’s behavior wasn’t usual at the scheduled snack time, the snack would be postponed until the child was back to baseline.) In addition, the parents kept a standard diary of food intake, sleep and bowel habits. Social interaction and language were evaluated through videotaped scoring of a standardized play session with a research assistant.

Following the gluten and casein snacks, study participants had no change in attention, activity, sleep or frequency or quality of bowel habits. Children demonstrated a small increase in social language and interest in interaction after the challenges with gluten or casein on the Ritvo Freeman Real Life Rating Scale; however, it did not reach statistical significance. That means because of the small difference and the small number of participants in the study, the finding may be due to chance alone.

The investigators note that this study was not designed to look at more restrictive diets or the effect of nutritional supplements on behavior. This study was designed to look at the effects of the removal of gluten and casein from the diet of children with autism (without celiac disease) and subsequent effect of challenges with these substances in a group of children getting early intensive behavioral intervention.

Hyman said, “This is really just the tip of the iceberg. There are many possible effects of diet including over- and under-nutrition, on behavior in children with ASD that need to be scientifically investigated so families can make informed decisions about the therapies they choose for their children.”

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