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AutismOne throws their support behind the Geiers in “Autism Science Digest”

16 Jun

When news came out about the legal troubles Mark and David Geier are facing, there was some hope expressed that maybe, just maybe, some of the groups that have supported the father/son team would take the chance to distance themselves. The Generation Rescue/Autism One conference was at that time still in the future, and the Geiers were scheduled to speak. Dr. Mark Geier had his license suspended for the “therapy” he was planning to tout at AutismOne, and that David Geier was facing the charge of practicing medicine without a license.

As we have seen, the optimism was ill founded. The Geiers presented their talk at AutismOne. And, as it turns out, AutismOne had already in-press their new magazine, the “Autism Science Digest”, which included an article by the Geiers. Someone forwarded it to me and it is frankly painful to read.

It is a nice glossy advertisement for the Geiers and their testosterone/autism theory. I don’t throw that out lightly. It is pseudo-science generated to promote an idea. and idea which really doesn’t stand up to real science.

For example, they present the article like a science study, complete with references. It makes it seem as though what they say is backed up by legitimate science. But citations do not make a study. Especially when they are misused.

It is difficult to describe the Geier hypothesis. This is for two reasons. First, it is hard to accept that they actually believe their own work, it is so bad. Second, it has morphed dramatically over the few years of its existence.

Let me explain. When they first proposed their idea that testosterone was somehow important, they claimed that testosterone was binding mercury in the brain, rendering it difficult to remove through chelation. If you listen to Lisa Sykes talk about the Geiers (the Rev. Sykes being a major spokesperson for the Geiers over the years), she tells how David Geier told her, “We figured something new out…..we think we can get rid of the mercury by lowering the testosterone”.

By the way, the Rev. Sykes mentions that she tested her child for testosterone. The range was 0 to 25 and her kid was “at the top of the range”. Not above it. At the top. As in, high but within normal.

If you listen to the Geiers speak now (and, again, I find this painful to do), they are still pushing the idea that mercury is the main causation factor in autism. But, here’s the shift with Lupron, they are downplaying the idea that is part of a chelation protocol. It’s all about reducing testosterone.

Is anyone surprised that if you change the testosterone levels in a person you will see changes in behavior? Does this have anything to do with autism? Does it have anything to do with mercury?

The Geier article relies heavily on the work of Dr. Simon Baron-Cohen’s group. They cite Dr. Baron-Cohen’s group 5 times in their article. It makes the article look legitimate. The first paragraph states, “In fact, ASD’s have even been described as the result of an “extreme male brain” by psychologist Dr. Simon Baron-Cohen”.

At this point, it is worth recalling what Dr. Baron-Cohen had to say about the work the Geiers are doing:

Simon Baron-Cohen, a professor of developmental psychopathology at the University of Cambridge in England and director of the Autism Research Center in Cambridge, said it is irresponsible to treat autistic children with Lupron.

“The idea of using it with vulnerable children with autism, who do not have a life-threatening disease and pose no danger to anyone, without a careful trial to determine the unwanted side effects or indeed any benefits, fills me with horror,” he said.

Some how “fills me with horror” was not included in the Geier article.

Dr. Baron-Cohen’s theories include the idea that fetal testosterone levels affect the development of the brain. This is a prenatal process. The Geier notion is that autistics have high testosterone levels (even though they have documented cases of children they treated who do not have high levels). It is intellectually (and otherwise) very dishonest to claim that the work of Dr. Baron-Cohen in any way supports the Geier’s application of the drug Lupron to autistic children.

It isn’t just Dr. Baron-Cohen’s work that is misused to sell this therapy. The Geier’s write, “”Also, some investigators have found that leuprolide acetate administration resulted in improvements in cognition” ( Bryan et al. , 2010)”

Here is the abstract for Bryan, et al.:

Down-regulation of serum gonadotropins is as effective as estrogen replacement at improving menopause-associated cognitive deficits.
Bryan KJ, Mudd JC, Richardson SL, Chang J, Lee HG, Zhu X, Smith MA, Casadesus G.
Source

Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA.
Abstract

Declining levels of estrogen in women result in increases in gonadotropins such as luteinizing hormone (LH) through loss of feedback inhibition. LH, like estrogen, is modulated by hormone replacement therapy. However, the role of post-menopausal gonadotropin increases on cognition has not been evaluated. Here, we demonstrate that the down-regulation of ovariectomy-driven LH elevations using the gonadotropin releasing hormone super-analogue, leuprolide acetate, improves cognitive function in the Morris water maze and Y-maze tests in the absence of E2. Furthermore, our data suggest that these effects are independent of the modulation of estrogen receptors alpha and beta, or activation of CYP19 and StAR, associated with the production of endogenous E2. Importantly, pathways associated with improved cognition such as CaMKII and GluR1-Ser831 are up-regulated by leuprolide treatment but not by chronic long-term E2 replacement suggesting independent cognition-modulating properties. Our findings suggest that down-regulation of gonadotropins is as effective as E2 in modulating cognition but likely acts through different molecular mechanisms. These findings provide a potential novel protective strategy to treat menopause/age-related cognitive decline and/or prevent the development of AD.

The short version: the authors removed the ovaries from mice, putting them into a menopause state. They found that these mice decline cognitively, but that they can treat this with a leuprolide acetate (a drug similar to lupron).

Yes, somehow the animal model for autism to the Geiers are post-menopausal mice.

This study has nothing to do with improving cognition in children, or autistic children in particular. Don’t take my word for it. I contacted one of the researchers who wrote the paper:

Well… The principle of gonadotropins working on cognition in menopausal women or patients with AD has nothing to do with autism nor with improving cognition via the depletion of gonadal steroids such as testosterone or estrogen. For example, we know that when women that are in reproductive age (and men to a lesser extend) are given leuprolide their cognition is impaired, indicating that gonadal steroids are important for cognition. However, we have shown that after menopause, gonadal steroids can be by-passed by downregulating gonadotropins to improve cognition.

If you want the message in a single sentence:

The beneficial effects of leuprolide on cognition in ovariectomized (menopausal) female mice has nothing to do with the treatment of autism in children.

Another study the Geiers cite: “Increased marble-burying behavior in ethanol-withdrawal state: Modulation by gonadotropin-releasing hormone agonist”

No, I am not kidding. It is a study about alcoholic mice burying marbles. Here’s the abstract:

A characteristic behavior in alcohol abstinence state indicates the possibility of obsessive–compulsive behavior in alcoholics. Ethanol is known to reduce hypothalamic synthesis, release, and mRNA expression of gonadotropin-releasing hormone (GnRH) that modulates serotonergic, dopaminergic, and glutamatergic systems, which experience adaptive changes on chronic exposure to ethanol. Such changes are also evident in obsessive–compulsive disorder. Therefore, it was proposed to investigate the effect of ethanol-withdrawal on marble-burying behavior in mice, particularly because it simulates some aspects of obsessive–compulsive behavior; further, the influence of GnRH agonist was studied on the same. Ethanol-withdrawal state was induced after its chronic administration, and marble-burying behavior was observed at 0, 6, 24, 48, and 96 h interval. Further, the influence of leuprolide—a GnRH agonist (50–600 ?g/kg, s.c.) or fluoxetine (5–30 mg/kg, i.p.) was investigated on ethanol-withdrawal-induced changes in marble-burying behavior. The results indicated that ethanol-withdrawal led to a gradual increase in marble-burying behavior upto 48 h with peak at 24 h interval. Administration of leuprolide (100–600 ?g/kg, s.c.), 30 min prior to 24 h interval, dose dependently reduced ethanol-withdrawal-induced increase in marble-burying behavior, and this effect was comparable to that of fluoxetine (15 and 30 mg/kg, i.p.). Further, twice daily administration of leuprolide (50 ?g/kg, s.c), concomitant with ethanol, prevented the gradual increase in marble-burying behavior after ethanol-withdrawal and this effect was comparable to fluoxetine (5 mg/kg, i.p.). In conclusion, ethanol-withdrawal on chronic administration increases marble-burying behavior in mice; its development and expression is attenuated by leuprolide.

The researchers gave mice alcohol over a long period. When they made the mice stop, cold turkey, they exhibited behaviors such as burying marbles. While the mice are going through the first stages of withdrawl, the researchers gave them a lupron like drug and found that the mice didn’t bury marbles as much.

Once again, who finds this to be a valid animal model for autism? Is your child an alcoholic, marble-burying mouse?

But you don’t see this if you just read the article. What you read is, “similarly, other investigators have used an anti-androgen medication called leuprolide acetate, which reduces the production of male hormones, in the treatment of anxiety, hyperexcitability, depression, impaired social interaction, and obsessive compulsive behaviors in laboratory animal species”.

The Geiers have obviously felt the need to respond to the criticism that they are using a drug used for chemical castration. They write

Finally, the administration of anti-androgen medications to individuals diagnosed with an ASD is not intended to deprive the individual of their sexuality nor to alter their normal developmental trajectory, but rather to regularize a process that was proceeding in an abnormal fashion and producing adverse effects and, thereby, improve the health of the patient and reduce the clinical symptoms associated with abnormally elevated androgen levels.

Here is an example patient from the patent application the Geiers submitted (US20070254314A1: Methods of treating autism and autism spectrum disorders):

Laboratory analyses did not reveal elevated levels of mercury or elevated levels of at least one androgen. Specifically, undetectable levels of mercury were present in Child D’s urine and minimal levels of mercury were in Child D’s blood (1.5 ?g/L, reference range=0.0-14.9 ?g/L). Additionally, analyses of Child D’s blood androgen metabolites revealed a serum testosterone=153 ng/dL (age- and sex-adjusted LabCorp reference range=0-350 ng/dL) and serum/plasma DHEA=291 ng/dL (age- and sex-adjusted LabCorp reference range=183-383 ng/dL) within their respective reference ranges.
After extensive discussions with his parents concerning the risks, benefits, and alternative treatments available, a decision was made to place Child D on a course of LUPRON® therapy.

Yes, Child D has testosterone well within the normal level. And, yet, the child was treated with Lupron. How, exactly, does this fit with improving “…the health of the patient and reduce the clinical symptoms associated with abnormally elevated androgen levels”?

Also, in the Autism Science Digest article itself, the authors note:

The child underwent antiandrogen therapy until the age of 13, when he entered puberty at an age typical of his sibling

Age 13 is within the normal range to start puberty. So is 9. Why did they delay this child 4 years? As of age 9, the child was not in central precocious puberty.

The Geiers make this comment in their recent article:

Two months prior to his 9th birthday, he was given a test dose of leuprolide acetate. After administration, he went outside and began to swing on a tire swing using his feet to push – a neurotypical behavior never seen before.

Dramatic, isn’t it? First shot, and the kid goes outside and uses the swing for the first time. This caught my eye, because they mention swinging in their patent. In the patent they note, “Within a few days of the second shot of LUPRON DEPOT®, Child X learned to swing by himself using leg timing for propulsion”

I’m betting that this is the same kid. If so, did the kid get his first shot and go outside and start swinging, or did he go a few days after his second shot?

One issue the Geiers (and others) have faced is inflation of credentials. David Geier, for example, listed himself as a “diagnostician” to get on the Maryland Autism Commission. The Autism Science Digest article is no different. Mr. Geier gives as his credentials that he “Has been a research scientist at the National Institutes of Health in the laboratory of Biochemical Genetics.”

Take a moment, if you will, and think what that statement means to you, ” research scientist at the National Institutes of Health in the laboratory of Biochemical Genetics”. I ask you to do this before we see what his job really was.

We can read Mr. Geier’s resume here, which lists his experience including:

I. T. R. A. Summer Fellow Appointment at The National Institutes of Mental Health (under Laboratory Chief [Redacted] of The Laboratory of Biochemical Genetics)
Projects:
(1) Protein Gel and Phage Research

That was in the summer of 1998. That’s the summer before he entered college, if I read the rest of his resume correctly. At this point I have to do something I rarely do, point out my own credentials. I’ve been a summer intern. I’ve been a research scientist. I’ve been a research scientist supervising summer interns. While I find the work of my summer interns has been valuable and of high quality, they weren’t “research scientists” in the way that is clearly implied in the article. Sure, it would have taken more space to write, “He was an intern the summer of his freshman year at the NIH”, but it would have made his position much more clear.

Dr. Mark Geier lists as part of his credentials, “His extensive research has resulted in him being invited to address the Institute of Medicine at the U.S. National Academy of Sciences on six occasions.” I find it remarkable that he uses this to build credibility, given the fact that the IOM clearly was not impressed by his work.

Let’s look at what the Institutes of Medicine had to say about the Geiers’ research:

The first was an ecological study (Geier and Geier, 2004a) that reported a potential positive correlation between the number of doses of measles-containing vaccine and the cases of autism reported to the special education system in the 1980s. The second was a study of passive reporting data by the same authors (Geier and Geier, 2003c) that reported a positive correlation between autism reports in the Vaccine Adverse Events Reporting System (VAERS) and estimated administered doses of MMR. However, these two studies are characterized by serious methodological flaws and their analytic methods were nontransparent, making their results uninterpretable, and therefore noncontributory with respect to causality (see text for full discussion).

It isn’t news that the Geiers are poor scientists. It isn’t news that the Geiers have been called out for their ethical lapses multiple times over the years. It is fairly recent news that the Geiers have actually faced charges. And, yet, AutismOne and Generation Rescue continue to support this team by inviting them to speak at conferences and giving them space in their magazines to promote the same bad medicine that has cost Dr. Geier his license.

Dr. Geier has lost his license to practice medicine. To which I can only say, what took so long? What do they have to do to lose the support of the alternative medical community?

Online Release of 2009 IACC Portfolio Analysis Report

16 Jun

Below is the latest email announcement from the Interagency Autism Coordinating Committee (IACC). This is the committee which sets out the strategic plan for autism research funding in the United States. The IACC has published the latest portfolio analysis of autism research. Also, members of the IACC participated in the IMFAR (International Meeting for Autism Research) conference. This includes Tom Insel, director of the National Institute of Mental Health (NIMH) and the chair of the IACC.

On behalf of the Interagency Autism Coordinating Committee (IACC), The Office of Autism Research Coordination (OARC) is pleased to announce that the 2009 IACC Autism Spectrum Disorder Portfolio Analysis Report is now posted online on the IACC website. This report provides a comprehensive analysis of the 2009 autism spectrum disorder (ASD) research portfolios of U.S. Federal agencies and private organizations as well as an overview of progress being made in implementation of the IACC Strategic Plan for Autism Spectrum Disorder Research. In the near future, the IACC/OARC will be releasing a comprehensive listing of the individual projects related to each question and objective of the Strategic Plan containing detailed descriptive and funding information.

In addition to the 2009 Portfolio Analysis Report, please see the two latest articles about recent activities of the IACC:

· 2011 International Meeting For Autism Research Features Opening Address from IACC Chairman Insel and Contributions from IACC Members

– Click here for Dr. Insel’s slides from IMFAR, which contain information about NIH’s implementation of the IACC Strategic Plan

· IACC Members Participate in White House Autism Awareness Month Conference

– Links to video footage from the meeting, Secretary Sebelius’ speech and President Obama’s April proclamation can be found at the end of the article

The IACC and OARC greatly appreciate the contributions of each agency and organization that participated in the development of the 2009 IACC ASD Portfolio Analysis Report. Thank you!

Sincerely,

The Office of Autism Research Coordination

NIH Research Matters: Study Undermines XMRV Connection to Human Disease

15 Jun

Study Undermines XMRV Connection to Human Disease is an article up on the U.S. National Institutes of Health “Research Matters” site. xenotropic murine leukemia virus-related virus (XMRV) has recently been hypothesized to be involved in chronic fatigue syndrome, prostate cancer and, as you guess from the discussion here at Left Brain/Right Brain, autism.

The discussion below (copied in whole from the NIH website) does not touch on autism, but does give some insight into how the false-positive link to prostate cancer came about, and how the link to chronic fatigue syndrome is not standing up to scrutiny.

The retrovirus previously tied to prostate cancer and chronic fatigue syndrome (CFS) is unlikely to be responsible for either, according to new research. The virus appears to have arisen in the laboratory. The association with human disease was probably due to contamination of samples.


Transmission electron micrograph of round virus particles.
XMRV particles, as visualized by transmission electron microscopy. Photo by Dr. Ila R. Singh, University of Utah

The xenotropic murine leukemia virus-related virus (XMRV) was first found in samples from a human prostate tumor in 2006. It was reported to be present in 6% to 27% of human prostate cancers. A study in 2009 also found XMRV in the blood of 67% of people with CFS. However, these results were challenged by several studies that failed to detect XMRV in samples from people with prostate cancer or CFS.

A research team led by Dr. Vinay Pathak of NIH’s National Cancer Institute (NCI) set out to investigate whether XMRV could have originated in the laboratory. When studying cancer, researchers often graft human tumors onto mice to create what are called xenografts. The scientists examined the process used to create the xenografts as well as the subsequent procedures that led to the identification of XMRV.

In the online edition of Science on June 2, 2011, the researchers reported that the initial prostate tumor xenografts didn’t contain XMRV, but that later tumors derived from them did. The virus appears to have infected the human tumor cells while they were in mice.

Closely related murine leukemia viruses are known to cause cancers and other diseases in mice. In the laboratory, these viruses can infect cells from other species, including humans. The team did a genetic search in the strains of mice previously used for xenografting the prostate tumor cells. They detected 2 previously undescribed viruses, which they dubbed PreXMRV-1 and PreXMRV-2. Genetic comparison of the PreXMRV-1 and PreXMRV-2 sequences revealed that each has a long stretch of DNA that’s nearly identical to XMRV.

The scientists postulate that genetic recombination between these 2 viruses generated XMRV while human prostate tumor cells were being grown in a mouse. The recombination—a common outcome when cells are infected by 2 or more viruses—likely occurred sometime between 1993 and 1996. The recombined virus then infected the human tumor cells.

Another report in the same issue of Science failed to find an association between XMRV and CFS, even in the same patients from the 2009 study. The research team found evidence of sequences from the 2 mouse viruses in commercial laboratory reagents. They concluded that the previous results likely stemmed from laboratory contamination.

“After the reports of XMRV in human prostate cancer, and later of XMRV in people with CFS, retrovirologists all over the world were excited to explore its role in human infection and disease,” Pathak says. “The results published today are not what we would have expected, but due to the time and resources dedicated to the understanding of this virus by researchers at NCI and NIH as well as others, scientists can now concentrate on identifying the real causes of these diseases.”

“Taken together, these results essentially close the door on XMRV as a cause of human disease,” says coauthor Dr. John Coffin, special advisor to the NCI director and a professor at Tufts University School of Medicine. Some evidence still suggests that these diseases may stem from viruses, but not from XMRV.

Dads and Grads

15 Jun

June is the season of graduations. It is also the time for Father’s Day (at least in the U.S.), which occurs this Sunday. Around this time we see a lot of ads for “Dads and Grads”, mostly by people selling greeting cards and presents.

I’d like to send out congratulations to the grads out there. I’d like to send out a good word to fellow Dads out there. I hope Sunday is a great day for you.

I’d really like to take the opportunity to single out: autistic grads and autistic dads. Autistic grads: congratulations. I was reminded of the “dads and grads” season by the story of an autistic graduate who is absolutely one of my heroes. I’ve never met the person, but that person inspires me in ways I never knew possible. Autistic dads: I’ve “met” some of you online, here and elsewhere. I’ve spoken to some of you on the phone and in person. I wish you all an especially good father’s day.

Autistic moms: sorry I missed a message for Mother’s Day. Completely an oversight on my part as you are also a great inspiration to me.

Use of school recess time in the education and treatment of children with autism spectrum disorders: A systematic review

14 Jun

Use of school recess time in the education and treatment of children with autism spectrum disorders: A systematic review is, as you will see, a small study on what is a relatively unstudied area: recess as part of the educational day for autistic students. This caught my eye for a simple reason: I think a lot about recess. I think about special education kids, kids who are working really hard, who need the break that recess provides as much or more than anyone.

Here is the abstract:

School recess is an opportunity to include students with autism spectrum disorders (ASD) with their typically developing peers and is a setting in which instruction can occur. However, the educational opportunities for children with ASD within recess are often overlooked and recess time is being reduced or eliminated in the United States. This review involved a systematic search and analysis of 15 studies that utilized recess to implement academic, social, or behavioral interventions for students with ASD. Each identified study that met pre-determined inclusion criteria was analyzed and summarized in terms of: (a) participant characteristics, (b) intervention procedures, (c) dependent variables, and (d) intervention outcomes. This review has three main aims: (a) to evaluate and synthesize the evidence-base, (b) to inform and guide teachers interested in utilizing recess time for educational purposes, and (c) to stimulate and guide future research in this area. Results demonstrate that recess time can indeed be used to teach target behaviors to students with ASD.

Here is the first part of the conclusion

Systematic search procedures identified 15 studies that used recess time to deliver intervention to preschool and elementary school students with ASD. Summaries of the studies revealed that a variety of different interventions have targeted a range of behaviors including challenging behavior, social skills, play, and communication. The most common dependent variables were social skills, and the most common intervention component involved typically developing peers serving as models of target behavior or as therapists with an active role in prompting and reinforcing target behaviors (e.g., McGee et al., 1992). Overall, the existing literature base is perhaps best described as limited given the paucity of studies and the relatively low number of participants (N = 46). However, despite these limitations several important points do emerge.

Baseline levels of dependent variables across the included studies demonstrate that, prior to intervention, students with ASD engaged in high levels of stereotypy and challenging behavior and low levels of appropriate play and social interaction. Therefore, unlike typically developing students who benefit simply by being given access to recess (e.g., Pellegrini & Smith, 1993), students with ASD may need additional supports in order to benefit form educational and social opportunities on the playground ([Lang et al., 2009a], [Lang et al., 2009b] and [Lang et al., 2009c]). Consequently, if a student lacks the skills necessary to meaningfully participate in recess, goals and objectives related to recess should be included in their individualized education plans.

OK, even as a review, where they pool data from multiple other studies, this is small: 46 participants.

The authors note that (a) recess is important for kids, especially younger children and (b) recess time seems to be declining in general (possibly due to the no child left behind laws in the U.S.).

I really have to pose the question: how much is recess valuable precisely because it is self-directed time? How do you define if “a student lacks the skills necessary to meaningfully participate in recess”? If a typical child spends recess in a corner of the playground reading a book or doing homework, is that a meaningful participation in recess? If an autistic kid needs that time to blow off steam in some other way, is that “meaningful”? Who defines “appropriate play”? If a child, say, spends recess screaming–is that “inappropriate play” or is that a sign that the classroom environment may be overstressing the child? Sure, if a student has the desire, but not the skills, to use recess for social interaction, let’s see about supporting that. If a child enjoys working on play skills, again. But I have a bit of a reservation about making recess into more time for work.

Disabled Children: A Legal Handbook

13 Jun

This for UK parents only but if you are such – its free for PDF download from here

Recording IEP meetings, part 2

13 Jun

Last December I wrote about my search for a good recorder for IEP meetings. I’ve had a little experience since, and I thought I would offer that.

I have now used 2 solutions. First, an iPod touch. Second, a Tascam DR-05.

The iPod touch was much more useful than I expected. It was handy. I had to put it in the corner of a fairly large room (in order to be near a power outlet) and I still got reasonable clarity. There are no settings on the iPod touch, just start and stop. What bugs me is that once the screen turns off, there is no feedback that the recording is going on. Also, I tend to fidget with the iPod during meetings (looking at pictures of my kid primarily). Not ideal if it is the recorder.

I’d like to say that the second solution, the DR-05, came after much comparison of features and quality. Instead, it came from a brief visit to the local Guitar Center. The staff were friendly, but unable to tell me anything that wasn’t obvious (like price, size, number of microphones, memory…).

Here are some features that work well for me with the DR-05:

A lot of space using the least compressed mp3 format (about 12 hours). I am paranoid of running out of storage. I also dread the fatigue of listening to over compressed sound for hours while transcribing. If I could feel comfortable about capacity, I’d use .wav format files.

Easy controls. Once the basic settings are in place (such as mp3 vs. wav, audio levels, etc.), the DR-05 is very easy to use. Push the on button and it boots in about 5 seconds. Hit record once to see levels. Hit again to start. Hit stop to finish. The only thing that worries me is the possibility of leaving the recording in the initial pause state where you check the levels. This brings up the next feature I like:

A little red light that shows it is recording. This is what bothered me about the iPod. I worry about getting to the end of a meeting and finding that the recording stopped for some reason and I didn’t know. With the DR-05, this isn’t a problem.

The DR-05 is a not the smallest recorder, and not the cheapest (at about US$100). The buttons are easy to use for me, and that beats a smaller size. Without the batteries it feels like a cheap plastic shell. Yes, much of the heft of the device is 2 AA batteries.

I put fresh batteries in before a meeting, so I can’t speak to the battery life other than it is more than sufficient.

Recordings can be transferred by a USB cable. Also, you can listen directly to the DR-05 with headphones (or with the built in, tiny and quiet speaker. I’d not recommend that for transcription, though). There is a feature to loop or to go back a set period of time (between 5 and 30 seconds, user settable) which makes transcriptions easier.

The sound quality was reasonable. I have to see if there are any important statements missed in the noise.

I considered using a netbook, with or without an external mic. This has the advantage that I already own them. But it seemed cumbersome and, well, a bit odd. The Tascam is big enough without being obtrusive. The iPod was OK, and I expect most smart-phones would do the job. I just find the worries I listed above to be enough to warrant spending the $100 on the dedicated recorder.

ACTION ALERT: What Does Community Mean To You? Let Medicaid Know!

11 Jun

Here is an action alert from the Autistic Self Advocacy Network (ASAN)

What does community mean to you? For some people, this question doesn’t mean much but for the hundreds of thousands of Americans receiving Medicaid Home and Community Based Services (HCBS), the meaning of community has huge implications. Last year, the State of Missouri attempted to use Medicaid dollars allocated to serving individuals with disabilities in the community for the construction of group homes on the grounds of an institution. The Center for Medicare and Medicaid Services (CMS) quite rightly refused to allow Missouri to use Medicaid HCBS funding for this plan, as the purpose of the HCBS program is to help people avoid institutionalization, not to support settings that further segregate people from their communities.

Now our friends at CMS are trying to put in place strong minimum standards for HCBS settings, to prevent what almost happened in Missouri from occurring in the future. CMS has proposed regulations which would prevent HCBS dollars going to institutional facilities, settings which are on the grounds of an institution, settings which are segregated on the basis of disability and settings which have the characteristics of an institution, such as lack of privacy or rules about when people can eat and sleep. This is an unprecedented opportunity for the disability community to support a real minimum standard for community living.

We need your help to make these standards a reality. CMS’ proposed rulemaking (available here) is only open for comments for four more days (it closes this Tuesday, June 14th at 5 PM) and we know that the usual suspects in the institution and nursing home industry have already written in opposing any standards for how HCBS dollars are used. We need people to write in to tell CMS that community living does not occur on the grounds of an institution and doesn’t include arbitrary restrictions on the rights of people with disabilities.

Here’s what you can do:

1. Write in to CMS and tell them that you SUPPORT the proposed rulemaking by going to: http://www.regulations.gov/#!submitComment;D=CMS-2009-0071-0302

2. Don’t hesitate to add in your thoughts about what Community should mean and make suggestions about things that CMS could add to their proposed rulemaking. If you’re looking for ideas, don’t hesitate to use ASAN’s comments as an example. You can feel free to use our language if it makes it easier. Our comments are available here: http://www.autisticadvocacy.org/modules/smartsection/item.php?itemid=153

3. Send a copy of this advocacy alert to your friends and colleagues encouraging them to write in too – the more people who write in – be they people with disabilities, parents, professionals or just supportive allies – the stronger our position will be. Help us get the word out!

Remember to write in by THIS TUESDAY June 14th at 5 PM. This is a critical opportunity to have our voices heard and we shouldn’t let it pass us by. Remember, Nothing About Us, Without Us!

Regards,
The Autistic Self Advocacy Network

Speech impairment and autism, inseparable?

11 Jun

In a recent paper purporting to link autism and vaccines, the author, Gayle DeLong, chose to lump autism and speech or language impairments together to create an autism “prevalence” from special education data:

To determine autism prevalence by U.S. state, the number of 8-year old students classified with either (1) autism or (2) speech or language impairments (speech disorders) was divided by the total number of 8-year-olds in the state.

The author has defended the choice over at the Respectful Insolence blog:

Orac,
I won’t respond to the personal attacks, but I will correct one error. The Herbert reference in the paper is incorrect. The correct citation is: Herbert and Kenet (2007) Brain abnormalities in language disorders and in autism. Pediatr. Clin. North Am. 54:563-583 (abstract: http://www.ncbi.nlm.nih.gov/pubmed/17543910). The paper shows that brain injury of people with autism is similar to brain injury of people with speech and language disorders. Another paper that makes much the same point is Herbert et al. (2002) Abnormal asymmetry in language association cortex in autism. Ann. Neurol. 52:588-596 (abstract: http://www.ncbi.nlm.nih.gov/pubmed/12402256).

Speech impairment is such a fundamental symptom of autism that the two conditions cannot be separated, especially when the child has a speech/language impairment that is strong enough to be classified as a learning disability.

First, kudos to Ms. DeLong for taking her statement to Orac’s blog. The participants are clearly not supportive of her statements–such as:

“Speech impairment is such a fundamental symptom of autism that the two conditions cannot be separated, especially when the child has a speech/language impairment that is strong enough to be classified as a learning disability.”

All I can say is that I disagree. Strongly.

Here is the definition that California uses for Autism as a special education category:

56846.2. (a) For purposes of this chapter, a “pupil with autism” is a pupil who exhibits autistic-like behaviors, including, but not
limited to, any of the following behaviors, or any combination thereof:
(1) An inability to use oral language for appropriate communication.
(2) A history of extreme withdrawal or of relating to people inappropriately, and continued impairment in social interaction from
infancy through early childhood.
(3) An obsession to maintain sameness.
(4) Extreme preoccupation with objects, inappropriate use of objects, or both.
(5) Extreme resistance to controls.
(6) A display of peculiar motoric mannerisms and motility patterns.
(7) Self-stimulating, ritualistic behavior.
(b) The definition of “pupil with autism” in subdivision (a) shall not apply for purposes of the determination of eligibility for
services pursuant to the Lanterman Developmental Disabilities Services Act (Division 4.5 (commencing with Section 4500) of the
Welfare and Institutions Code).

One can not say that SLI and autism are directly linked.

The data don’t support it either. Her own paper gives administrative prevalence numbers for autism+SLI which are as high as 10%, about a factor of 4-10 than reported for autism.

Also, consider this: if you look at the administrative prevalence of SLI with age in a given year, it is sharply peaked at around age 6 or seven. Here are the data for SLI and autism from the most recent year data are available in California. (click to enlarge)

(note–when this was first published, the graph was not in color).

No, that isn’t a “tidal wave” of SLI. This is what SLI looks like every year. It is a category mostly for younger children. I’ve often wondered if many of these children end up in the specific learning disability category in later years as this category is largely made up of older kids. Either way, it is clear that children tend to leave the SLI category, and they certainly aren’t being reclassified as autistic. Clearly, SLI is not something which can not be separated from autism.

I don’t know why Ms. DeLong chose to lump autism and SLI together for her study. I do feel quite strongly that the idea that they are basically the same is incorrect.

Vulnerable parents

10 Jun

I read this phrase often on the web: vulnerable parents. Usually in some discussion of families involved in alternative medicine or vaccine causation. It’s a phrase that bothers me.

I have to say that I find the phrase very odd. Odd as in it is redundant. To be a parent by definition is to be vulnerable. Every time we make connections to others, be they children, spouses, friends, heck even pets, we make ourselves vulnerable. Of course we feel pain when a loved one suffers or is in pain.

If you’ve ever spent the night in the ER with a kid with a broken arm, you know what I mean. Worse in many ways is to be the one at home while your kid is in the hospital, waiting for messages.

We are all vulnerable. Parent or no. Need I say it: autistic or no.

Vulnerable parent. That phrase has no meaning for me.

It is how we deal with our vulnerabilities that defines us. And I believe that’s what people really mean when they say “vulnerable parents”: parents who make choices they probably wouldn’t if they weren’t influenced by their love of their children.

There’s a whole spectrum of ways people respond to their vulnerability. And, yes, for some parents of autistic kids that involves being susceptible to some very questionable and poorly supported ideas. But it’s too simplistic to attribute this to “vulnerable” parents. We all are vulnerable.

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