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Autism Science Foundation’s Recipe4Hope campaign

9 Dec

The Autism Science Foundation is a charity which focuses on funding autism research. They have a very clear mission statement:

The Autism Science Foundation’s mission is to support autism research by providing funding and other assistance to scientists and organizations conducting, facilitating, publicizing, and disseminating autism research. The foundation also provides information about autism to the general public and serves to increase awareness of autism spectrum disorders and the needs of individuals and families affected by autism. Read about our achievements in 2010 on our Ingredients page.

Our organization adheres to rigorous scientific standards and values. We believe that outstanding research is the greatest gift we can offer our families. Every research dollar needs to count toward that goal, and we make sure that it does.

The Autism Science Foundation is a nonprofit corporation organized for charitable and educational purposes and exempt from taxation under Section 501(c)(3) of the IRS code. All donations are tax deductable to the full extent allowed by law.

Learn more about our foundation at http://www.autismsciencefoundation.org.

One focus of the ASF has been to fund graduate level researchers. I find this an especially good goal in that in addition to promoting research, this brings more people into the autism research community.

The Recipe4Hope campaign will raise money for autism research. According to the ASF: “Every dollar donated by December 31 through this special year-end campaign will go directly to autism research.”

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Upcoming IACC Full Committee Meeting – December 14, 2010 – Bethesda, MD

8 Dec

The Interagency Autism Coordinating Committee will have a full committee meeting on December 14th. This meeting is to work on the update for the Strategic Plan.

Now is a good time to send the IACC your input. What would you like them to know as they make the Plan? What research should they focus upon? What should they not focus upon?

Want a quick way to send your thoughts? Click here to send an email with the subject “IACC public comment”.

Here are some links to send emails with various subject lines:

Please do more research involving issues concerning autistic adults

Please do more research on services

the current science doesn’t support spending money on the vaccine hypothesis

Here is the announcement. If you have the time, even for part of the day, it is worthwhile to listen in and hear how these decisions are made.

Interagency Autism Coordinating Committee (IACC) Full Committee Meeting

Please join us for an IACC Full Committee meeting that will take place on Tuesday, December 14, 2010 from 10:00 a.m. to 5:00 p.m. ET in Bethesda, MD. Onsite registration will begin at 9:00a.m.

Agenda: The IACC will discuss plans for the annual update of the IACC Strategic Plan for Autism Spectrum Disorder Research.

Meeting location:
The Bethesda Marriott – Google map imageMap and Directions
5151 Pooks Hill Road
Bethesda, MD 20814

The meeting will be open to the public and pre-registration is recommended. Seating will be limited to the room capacity and seats will be on a first come, first served basis, with expedited check-in for those who are pre-registered.

The meeting will be remotely accessible by videocast (http://videocast.nih.gov/) and conference call. Members of the public who participate using the conference call phone number will be able to listen to the meeting, but will not be heard.

Conference Call Access
USA/Canada Phone Number: 888-577-8995
Access code: 1991506

Individuals who participate using this service and who need special assistance, such as captioning of the conference call or other reasonable accommodations, should submit a request to the contact person listed above at least seven days prior to the meeting. If you experience any technical problems with the webcast or conference call, please e-mail IACCTechSupport@acclaroresearch.com.

Please visit the IACC Events page for the latest information about the meeting, including registration, remote access information, the agenda and information about other upcoming IACC events.

Contact Person for this meeting is:

Ms. Lina Perez
Office of Autism Research Coordination
National Institute of Mental Health, NIH
6001 Executive Boulevard, NSC
Room 8185a
Rockville, MD 20852
Phone: 301-443-6040
E-mail: IACCpublicinquiries@mail.nih.gov

SafeMinds retaliates against skeptic blogger

7 Dec

SafeMinds is an organization with the stated purpose to “…to restore health and protect future generations by eradicating the devastation of autism and associated health disorders induced by mercury and other man made toxicants. ” SafeMinds has stayed with this purpose even as the years have gone by and the evidence has mounted that the SafeMinds hypothesis was incorrect (autism is not a form of mercury poisoning). Recently, SafeMinds produced an advertisement, framed as a public service announcement, focusing on mercury in the flu vaccine and tried to get these shown in movie theaters. As we discussed here recently, Elyse over at Skepchick started an effort to inform the movie theaters about SafeMinds. Her effort snowballed into a large petition and resulted in the movie theaters deciding to not show the SafeMinds advertisement.

Recently, SafeMinds has chosen to leave the discussion of ideas and take on Elyse in a personal attack, through their media effort at the Age of Autism. SafeMinds is not only a key sponsor of Age of Autism, but Mark Blaxill (SafeMinds board member) is one of the three principle editors of the Age of Autism blog.

Again, rather than discuss the issues, they pulled Elyse’s facebook photo


and posted this message

This is the woman who fought to pull the SafeMinds PSA’s from the theatres. It’s her FB profile page photo. She is anti-choice and wants to tell you that mercury is safe and that Thimeosal is good – according to her blog. She trolls AofA regularly. As do all the pro-vaccine-injury bloggers.

It was a call to mock and insult Elyse. A perfect example of cyber bullying. Amongst the comments to that FaceBook page was one extreme enough that one of the Age of Autism editors noted it and promised to remove it. “While I agree that the broken thermometer comment was out of order (the blog does not condone violent speech, so that comments is going.”

It took a while for them to make good on the promise. As in many hours later, after Elyse reported the abuse to the police. That comment does appear to be gone now. Many other abusive comments (but not all) also appear to be removed.

Rather than apologize for inciting the bullying effort, SafeMinds/AgeofAutism are defending themselves by claiming that Elyse was standing in the way of choice.

Stopping Americans unable to understand? What is she St. Skepchick? She interefered with medical choice and commerce. That’s her right to make the attempt. We dis not use her name. We pulled her public photo that she used here on FB. We ran it on FB, not the main site – our readers deserved to know who was behind (at the outer level anyway) the AMC campaign to stop the ads. We provide news. This was news.

No. It wasn’t news. And, no, Elyse was not interfering with medical choice or commerce. She was quite simply providing the theaters with information–allowing them to make informed consent about the SafeMinds advertisement.

The idea of SafeMinds being pro-choice on vaccines is rather ironic. Again a story from their outlet blog, the Age of Autism makes this clear. Two years ago, a theater in New Mexico was going to show the movie “Horton Hears a Who” combined with a free vaccination clinic. At that time, they had a connection to Horton star, Jim Carrey. Instead of allowing choice, providing information, they got Jim Carrey to force the cancellation of the event:

Following a long discussion with his representatives at Fox Entertainment – Who-ville – once again through Horton – was heard. The New Mexico test market of drive thru vaccines while at the movies with your children was stopped. Halted by Horton himself because he heard “we are here, we are here, we are here!” once again.

The bullying attack on Elyse wasn’t about choice, it was just a childish attempt at some sort of petty vengeance. Unfortunately it got out of control. I thank SafeMinds and the Age of Autism for editing the comments, but even what is left is unacceptable. It’s time for apologies, not excuses.

Girls less likely to be diagnosed with autism than boys

6 Dec

A recent study out in the Disability and Health Journal shows that girls are more likely than boys to remain undiagnosed. The study, by David Mandell‘s group at the University of Pennsylvania, evaluated data from the Autism and Developmental Monitoring Network (ADDM). This is the same group that collects and analyzes data for the CDC’s autism prevalence studies.

Each ADDM study concentrates on children from a specific birth year. In this case, children born in 1994. They review records (medical, educational or both as available) to determine which children meet the criteria for autism. Some children already have a diagnosis of autism in their records. Other children are determined to be autistic via the ADDM review.

Prof. Mandell’s group found that for those with existing diagnoses at the time of review, girls and boys were similar in terms of average age of diagnosis and first age of evaluation. However girls were more likely to be undiagnosed (medical or educational) at the time of the ADDM review.

Here is the abstract.

Sex differences in the evaluation and diagnosis of autism spectrum disorders among children.

Giarelli E, Wiggins LD, Rice CE, Levy SE, Kirby RS, Pinto-Martin J, Mandell D.

Division of Biobehavioral Health Systems, University of Pennsylvania School of Nursing, Philadelphia, PA 19104, USA.
Abstract

BACKGROUND: One of the most consistent features of the autism spectrum disorders (ASDs) is the predominance among males, with approximately four males to every female. We sought to examine sex differences among children who met case definition for ASD in a large, population-based cohort with respect to age at first developmental evaluation, age of diagnosis, influence of cognitive impairment on these outcomes, and sex-specific behavioral characteristics.

METHODS: We conducted a secondary analysis of data collected for a population-based study of the prevalence of ASD. The sample comprised 2,568 children born in 1994 who met the case definition of ASD as established by the Autism and Developmental Disabilities Monitoring (ADDM) Network for ASD surveillance. Children who had a history of developmental disability and behavioral features consistent with the DSM-IV-TR criteria for autistic disorder, Asperger’s disorder, and Pervasive Developmental Disorder-Not Otherwise Specified in existing evaluation records were classified as ASD cases via two paths: streamlined and nonstreamlined. Streamlined reviews were conducted if there was an ASD diagnosis documented in the records. Data were collected in 13 sites across the United States through the ADDM Network, funded by the Centers for Disease Control and Prevention.

RESULTS: Males constituted 81% of the sample. There were no differences by sex in average age at first evaluation or average age of diagnosis among those with an existing documented chart diagnosis of an ASD. Girls were less likely than boys to have a documented diagnosis (odds ratio [OR] = 0.76, p = .004). This analysis was adjusted for cognitive impairment status. In the logistic model, with the interaction term for sex and cognitive impairment, girls with IQ of 70 or less were less likely than boys with IQ of 70 or less to have a documented diagnosis (OR = 0.70, 95% confidence interval [CI] = 0.50-0.97, p = .035). Boys with IQ greater than 70 were less likely than boys with IQ of 70 or less to have a documented diagnosis (OR = 0.60, 95% CI = 0.49-0.74, p < .001). This finding (less likely to have a documented diagnosis) was also true for girls with IQ greater than 70 (OR = 0.45, 95% CI = 0.32-0.66, p < .001). Girls were more likely to have notations of seizure-like behavior (p < .001). Boys were more likely to have notations of hyperactivity or a short attention span and aggressive behavior (p < .01).

CONCLUSIONS: Girls, especially those without cognitive impairment, may be formally identified at a later age than boys. This may delay referral for early intervention. Community education efforts should alert clinicians and parents to the potential of ASDs in boys and girls.

IACC Subcommittee for Planning the Annual Strategic Plan Updating Process tomorrow (Dec. 3rd)

3 Dec

Tomorrow there will be a subcommittee meeting for the IACC to work on the Strategic Plan. You can listen in or watch via webinar. It is likely past time for any public comments to be accepted for this meeting, but if you have anything to suggest, they will keep it and distribute it after the meeting (possibly in a future meeting).

Reminder: Interagency Autism Coordinating Committee (IACC) Subcommittee for Planning the Annual Strategic Plan Updating Process

Please join us for an IACC Subcommittee for Planning the Annual Strategic Plan Updating Process meeting that will take place on Friday, December 3, 2010 from 10:00 a.m. to 4:00 p.m. ET in Bethesda, MD. Onsite registration will begin at 9:00a.m.

Agenda: The subcommittee will discuss the updating of the IACC Strategic Plan for ASD Research.

Meeting location:
The Bethesda Marriott
5151 Pooks Hill Road
Bethesda, MD 20814

The meeting will be open to the public and pre-registration is recommended. Seating will be limited to the room capacity and seats will be on a first come, first served basis, with expedited check-in for those who are pre-registered.

The meeting will be remotely accessible through a webinar and conference call. Members of the public who participate using the conference call phone number will be able to listen to the meeting, but will not be heard.

Conference Call Access
USA/Canada Phone Number: 888-577-8995
Access code: 1991506

Individuals who participate using this service and who need special assistance, such as captioning of the conference call or other reasonable accommodations, should submit a request to the contact person listed above at least seven days prior to the meeting. If you experience any technical problems with the conference call, please e-mail IACCTechSupport@acclaroresearch.com.

Webinar Access: https://www2.gotomeeting.com/register/687738010

If you experience any technical problems with the web presentation tool, please contact GoToWebinar at (800) 263-6317.

Please visit the IACC Events page for the latest information about the meeting, including registration, remote access information, the agenda, materials and information about other upcoming IACC events.

Contact Person for this meeting is:

Ms. Lina Perez
Office of Autism Research Coordination
National Institute of Mental Health, NIH
6001 Executive Boulevard, NSC
Room 8185a
Rockville, MD 20852
Phone: 301-443-6040
E-mail: IACCpublicinquiries@mail.nih.gov

Advancing paternal age and risk of autism

2 Dec

This isn’t the first study to look at paternal age as a possible risk factor for autism but it is, I believe, the first meta-analysis of the subject. The conclusions of the study were:

Based on data from a birth cohort, a family-based study and a meta-analysis, we provide the strongest and most consistent evidence available that advancing paternal age at the time of birth of offspring increases the risk of autism. De novo germline mutations, epigenetic alterations and life course toxic exposure may partly explain the observed association. The evidence is substantial enough to justify a search for the underlying mechanisms in both human and animal models

An interesting conclusion for a few reasons. First and foremost the idea of paternal age being a definite risk factor for autism. Secondly the authors don’t shy away from the idea that ‘life course toxic exposure’ may explain the association. Its not exactly a new observation amongst science (despite what some observers think) but its good to see it placed so clearly amongst the other clear risk factors.

There will be those, I predict, who will have a go at this study for somehow ‘blaming’ fathers/parents. It has happened in the past and will no doubt have the same effect on those who’ll attack this study for their own reasons.

Hope and False Hope

25 Nov

Hope. It’s a wonderful thing, and something that parents of children with autism deserve to have in their lives. Fortunately, science shows that there is very good reason for hope. It shows that children with autism continue to learn and develop throughout their lives. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2765385/
http://www.ncbi.nlm.nih.gov/pubmed/15666341

But false hope is another matter. As we saw in my guest blog Truth and Consequences – The Anti-Vaccination Movement Exacts a Price from last year, “biomedical support groups” for autism, so prevalent and so active on the internet, provide a sense of hope and community for parents of children with ASD. But, that hope is not real. The case of “Mary” and her son “Saul” illustrates this – Mary joined a multitude of groups, and tried dozens of “treatments” only to be left poorer. And her child, at age 8, had not “recovered”, but still exhibited many of the challenging behaviors which he had at age 2.

Mary is a bit unusual because she has persisted with “biomedical autism treatments” for 6 years. The typical cycle of membership on such “biomedical support groups” is much shorter. A new parent joins, and attempts to follow the protocol or the advice of the other parents, but if this approach does not help their child, the parent simply abandons the group, usually without comment. However, there are always newly diagnosed children, so one sees a continuous influx of new parent members, asking the “newby” questions. Typically, there is a core of self-proclaimed “go-to” people in the group who have devoted themselves to advising these parents.

The purpose of this blog post is to introduce you to one such “go-to” person, a woman called Dana, a resident of California, and the owner of a website http://www.danasview.net.

Here’s how Dana describes herself:

Hello, my name is Dana and I am 41 years old. I am an attorney, I am married, and I have four children. I homeschool all four of my children, and I do legal work part time from home.
When my second child was diagnosed with autism at age 3, I began searching the internet to learn more about him and who he is, and I was surprised to discover that I also qualified as AS, which I will use here to refer to Autistic Syndrome although I am aware it is used for other uses as well. My third child would probably qualify as PDD, but I have not pursued an official diagnosis for him. My first and fourth child are NT.

Notice that Dana makes it clear that she has no medical background, and she is always careful never to present herself as a medical professional. Nevertheless, she has a lot of credibility on the “autism biomedical support groups”. The reason for this credibility is that she is supposed to have “recovered” her second child, or rather both her second and third children. Here is how she describes her second child in 2001 when he was 5 or 6:

My son’s pedneuro told me that he was very low functioning, never developed at all, classic genetic Kanner’s autism, that my best hope for him would be assisted living in a group home some day. Now my son no longer qualifies as autistic, he will be productive and independent some day, and all of it is because of information I read in books and on the internet. Keep going, you are doing the right thing, as you now know!

Wow! a child who no longer qualifies as autistic! That was pretty impressive in 2001, and it made Dana into an authority on biomedical treatments. However, the story has changed quite a bit over the years:
2003, age 7-1/2

My son was not as old as yours when I started biomedical, altho he was older than most kids I read about. He was age 4 when I started, now is age 7-1/2. When I started biomedical, he basically did not tolerate anything.

He is nearly recovered, his last issue is language delay, all his other issues are gone. Chelation was the intervention that provided the final measure of recovery. I did a few other things along the way, but with chelation he can eat all foods now with no problems, he never has a yeast issue any more, stims only very occasionally and voluntarily stops almost immediately. He is now working on catching up with his language delay.

2006, age 10

My son has a Kanner dx, autistic from birth. In reality, he was injured from my dental amalgams plus HepB vax at birth. I chelated him with ALA, and he is almost biomedically recovered now [chelation being one part of that recovery]. Still developmentally delayed, but catching up.

2008, age 12

Well, when he was 3, the pedneuro told me he would never talk or even acknowledge my existence. Today he is 12 and just completed a first grade program. He talks, he reads, he does simple math, he loves giving me hugs, he calls us “mommy” and “daddy” and says “I love you” and lots of other things. He plays well with his siblings, defends them when we gang up on them to tickle them, is concerned when they get hurt, and he is the only child I have who will do his chores without prompting or complaining.

Because he is so far behind and is already 12, I don’t know if he will be age appropriate. But so far I am pleased with his progress. He has gone from “classic Kanner’s autism, severe, low functioning”, to not qualifying as autistic, but definitely developmentally delayed.

2010, age 14

My son has a dx of “classic Kanner’s autism, severe, low functioning”. The pedneuro who dx him, told me he would never talk or even acknowledge my existence. He said his first word at age 6, after I added digestive enzymes.

The things he needed the most for speech, were enzymes, ALA chelation, anti-virals, B vitamins especially B1 and B12, and anti-fungals. There were several other supps that were also helpful.

Today he is 14 and not yet age-appropriate, but sometimes I do need to tell him to be quiet because he is talking too much.

To me it’s clear that her second son is not actually “recovered” from ASD.

Dana is an amazingly prolific poster. When using the handle “danaatty”, between 2001-2003, she made a total of 9882 posts to just four yahoo groups, abmd, Autism-Mercury, EnzymesandAutism and GFCFKids. In 2003, she adopted the handle “danasview”, and since has made a mind-blowing 48,187 posts to just three groups, with the largest number, 23,705 posts to GFCFKids. That’s an average of 17 posts per day, every day, for 9 years!

Dana blames vaccines for her childrens’ ASD, even though she recognizes that she herself is also on the spectrum. And like most parents who blame autism on vaccines, she has an obsession with eliminating both viruses (presumably the residual measles virus from vaccination) and mercury (from thimerosal containing vaccines). There is absolutely no clinical evidence for any of her recommended protocols. Everything is based on her reputation as a parent who has “recovered” her children.

When viewed in isolation, a single piece of her advice may seem reasonable. However, a small sampling of her posts taken together shows a different story. Here are some symptoms that Dana has blamed on viruses or on viruses leaving the body:

plantar warts
molloscum contagium
yeast, which causes constipation
goopy green eye discharge
major red rash
dry patches of skin
bad case of the “chewies”
visual stims
pushing finger joints and cracking knuckles
OCD
low white blood cell count
loud talking
mouth sores
language difficulty
high fever
sore throat
runny nose
aching bones
fine bumps on chest

In Dana’s view, some symptoms of mercury poisoning are:

dilated pupils
headaches
neck pain
sinusitis
asthma
ear infections
tingling down arms/legs
urinary incontinence
jitters
restlessness
can’t sleep very well
heart palpitations or weird feelings around heart
fungus on feet
pain in jaw
ears popping
pressure in ears
pain in intestines/bowels when exercising
food intolerances
lazy eye

Conventional “autism biomedical” wisdom is that “yeast infections” are common in autism. And that “yeast infections” can result from either anti-viral “protocols” or chelation. According to Dana, some of the symptoms of “yeast” are:

symptoms of Tourette
OCD
anxiety
dark circles under eyes
squinting eyes
needing to chew things
eating plastic and rubber
persistent nail biting
redness/bumps around the mouth
sinus infection
hitting oneself
hitting one’s ears
head banging
making pig noises and snorting a lot
standing on the head
hands always in mouth
severe dandruff
biting a parent
yellow bowel movements
yellow finger nails
pee accidents
tics
crying uncontrollably for 20 minutes or more
cystic acne
constant high pitched vocal stims
non-stop talking
low grade fever
loose sounding cough
ringing in the ears
dizziness
constipation
humming
licking things
hyper and giggling
laughing hysterically
flying into a rage
sleep problems
problems falling asleep
sleep walking
teeth grinding
stinking armpits in a five year old
spinning around in circles
balance issues
chapped lips
extra bad handwriting
visual stims
sexual behavior
red ring around the anus
“spaciness”
anger and aggression,
headache
head banging
sound sensitivity [holding the hands over the ears]
climbing on furniture and jumping off
vestibular sensory issues
and
multiple personalities

It strains credulity that such a diversity of symptoms could possibly be attributed with such precision to only three causes. In fact, there are very few things Dana will NOT attribute to these three causes. For example:

Q: What can cause low white blood cell + low red blood cell count? A hematologist has performed blood tests and ruled out antibodies (lupus, rheumatoid arthritis, etc) and now wants to proceed with a bone marrow biopsy. He appears to think he has ruled out everything else and is now looking for Leukemia or Lymphoma.
Could mercury/metal exposure cause these symptoms? Anything else?

A: It is very possibly a mercury toxicity issue. May also be related to a latent virus issue.
Dana

Dana on viruses:

He had a wart that did not go away with high dose vitamin C [which eliminated a lot of cold/flu viruses in his brain], so I tried lysine, which caused more gains.

I watched a cold virus migrate into my son’s brain once. And after starting
anti-virals, I watched the viruses come out one by one.

The above four supplements (Vitamin A, vitamin C, vitamin D, and lysine) eliminated my son’s viruses, they no longer lie dormant.

Dana on food intolerance:

At my house, controlling yeast and bacteria was required to stop raging. Also, most of the SCD-legal foods my son did not tolerate. He tolerated nothing orange or green, and he did not tolerate fats until mito cocktail. That would have caused major problems for him.

Dana on short stature:

One of my kids had this problem. He needed carnitine and thyroid support.

Dana shows her knowledge of chemistry:

Arginine and lysine are “opposites”, sort of like zinc and copper. If
you suspect a herpes virus issue, definitely do NOT give arginine, it will increase the virus.

Dana on yeast:

The yeast is in his head/brain, not in his GI tract. This happened with my son for a few years. Just because you don’t see signs of yeast in the bm/GI tract, does not mean yeast is not present in other areas of the body.

With her prolific posts and her continuous flow of “biomedical autism treatment” advice for parents, Dana has established herself as a guru. She is one of the key people personally responsible for encouraging parents to subject their children to unproven and potentially dangerous experimentation. According to the Office of Dietary Supplements, consumers in the USA spent $20.3 billion on dietary supplements in 2004. Someone is getting rich on her advice.

Addendum:
In researching this story, I encountered something astonishing. Remember “Mary” and her son “Saul”? Saul is very clearly NOT recovered despite all the experimentation performed on him. The ultimate irony was to see “Saul” featured on Dana’s website, touted as an example of a chelation recovery!

Study finds evidence of gender bias toward diagnosing boys with autism

17 Nov

As dad to a daughter and ‘step-dad’ to a ‘step-daughter’ who are both autistic, I always find stories and studies like this interesting:

With the severity of autistic traits held constant, boys were more likely to receive an ASD diagnosis than girls.

And

“We wanted to find out what distinguishes those children without diagnosis but with autistic traits from those who have received a formal ASD diagnosis in the clinic,” explained lead researcher Ginny Russell, from Egenis at the University of Exeter. “We thought that there may be social and demographic factors that explain why some children are diagnosed and others are not. Understanding social factors that act as access barriers may provide useful insights for clinicians in practice.”

And one of those things that they found was that boys were more likely to be diagnosed than girls. Also found was the results that ethnic origin, maternal class and mother’s marital status played no part in receiving a diagnosis whereas the average age of mothers with an ASD diagnosis was 3 years higher than in the population generally.

Financial hardship, partner cruelty and affection, home ownership status, maternal mental health, substance abuse, maternal psychopathology, and being in trouble with the police showed no significant associations with a child receiving an ASD diagnosis.

All this backs up the idea that diagnoses – or the art of diagnosing – autism depend on social factors as well as behavioural and biological factors.

Age of diagnosis for autism: individual and community factors across 10 birth cohorts

6 Nov

Prof. Peter Bearman’s group at Columbia has a new paper out: Age of diagnosis for autism: individual and community factors across 10 birth cohorts.

The study looks at children receiving services from the California Department of Developmental Services (CDDS). The CDDS dataset is not a “census” of autistics in California, but is a registry of those who have sought services, have been identified as autistic and and who have been granted services. Factors which can affect who seeks services for their children, who seeks and how easy it is to identify an autistic child (e.g. access to people who can do the diagosis) will have an effect on who is identified and when that person is identified.

As an aside, I focus on autistic children here because the study does. The authors focused on those identified who were under age 8. They did this to make the comparisons consistent across birth cohorts. For example, one can’t look at 15 year olds born in the year 2000.

Age of diagnosis was taken as age of autism into the entry for the child into the CDDS registry. This can occur either when the child undergoes an intake or a change in the child’s status occurs (say, a diagnosis of autism is given to a child already in the CDDS system)

California statutorily requires that regional centres confirm eligibility for services, including verifying or conferring a diagnosis, within 120 days of intake, so the date at which DDS clinicians either provided or confirmed a first diagnosis of autism is within a few months of caregivers’ initial request for assistance. Combined with the child’s date of birth, we then used the date of entry from the first available CDER to calculate the age of diagnosis. Diagnoses earlier than age 3 years are empirically rare, as infants and toddlers below 36 months with suspected developmental delays and those considered at risk are served by the early start programme.

I don’t have the data, but my very anecdotal and likely biased experience is that currently diagnoses earlier than 36 months are not rare at all.

Prof. Bearman’s group shows that the age of diagnosis steadily dropped during the 1990’s, from 4.4 years of age in 1992 to below 3.4 years of age in 2002. Here’s the figure from the paper (click to enlarge):

Non-White and Hispanic children were diagnosed later. Children of highly educated parents were diagnosed earlier. Both of these effects remained throughout the time span considered (1992-2002). Children of mothers born outside the US and first born children were diagnosed later, but this effect disappeared over time. Children with better communication skills were diagnosed later.

They also found that the age of diagnosis depends on the parents socio-economic status (ses). As one might predict, better off families got diagnoses for their children earlier. Here is the figure showing the trend of age-of-diagnosis vs. birth year for low and high ses:

It is good to see the gap decreasing with time, but it shouldn’t be there at all.

One obvious question that comes up from this study–a question that it can not answer–is how many people are never correctly diagnosed, and what gap might there be in that number based on ses?

The full paper can be found on Prof. Bearman’s team website. Here is the abstract:

Background The incidence of autism rose dramatically between 1992 and 2001, while the age at which children were first diagnosed declined. During this period the size and composition of the autism caseload has changed, but little is known about whether the factors associated with the timing of diagnosis may also have shifted. Using a multilevel analysis strategy, the individual and community-level factors associated with age of diagnosis were modelled across 10 birth cohorts of California children.

Methods Linked birth and administrative records on 17?185 children with diagnoses of autistic disorder born in California between 1992 and 2001 and enrolled with the California Department of Developmental Services (DDS) were analysed. Information on cases, their parents and their residential location were extracted from birth and DDS records. Zip codes of residence were matched to census data to create community-level measures. Multilevel linear models were estimated for each birth cohort, with individual-level effects for sex, race, parental characteristics, poverty status, birth order and symptom expression. At the community level measures of educational and economic composition, local autism prevalence and the presence of a child psychiatrist were included.

Results Children with highly educated parents are diagnosed earlier, and this effect has strengthened over time. There is a persistent gap in the age of diagnosis between high and low socioeconomic status (SES) children that has shrunk but not disappeared over time.

Conclusion Routine screening for autism in early childhood for all children, particularly those of low SES, is necessary to eliminate disparities in early intervention.

Here is the press release for the study.

Autism is diagnosed later for children with less educated parents
A Columbia study, appearing this week in the Journal of Epidemiology and Community Health, has found a gap in age of diagnosis for autism between children of high and low socioeconomic status in California. This gap has become smaller over time, falling from about fourteen months to about six months in a decade, but it remains significant. The strongest factor in this gap was parental education. Children of highly educated parents tend to be diagnosed at earlier ages, and this effect has not diminished over time.

The findings suggest that although the median age of diagnosis for autism has dropped from about four and a half years in the early 1990s to about three and a half in the 2000 birth cohort, there are some groups of children who are still diagnosed late. Diagnosis is the crucial first step to treatment, widely believed to be most effective at younger ages, and even six months may be important at an age when children are developing rapidly. “Our findings point strongly to the idea that some children may be at a great disadvantage when it comes to access to diagnosis and treatment for autism,” said Peter Bearman, the Jonathan Cole Professor of the Social Sciences and principal investigator of the paper. “These delays may have important consequences for later behavioral and cognitive outcomes.”

Autism impairs social interaction and predisposes children to restrictive and repetitive behaviors. Over the past two decades California has witnessed a particularly large spike in autism cases. Between 1992 and 2006, the state’s caseload increased 598 percent. At the same time, the typical age of diagnosis has dropped from school-age to the early pre-school years.

This study was based on 17,185 children with autism born in California from 1992-2001. In addition to looking at characteristics of the children and their parents, from the birth records, the researchers used the zip code at birth and diagnosis to examine the characteristics of the communities in which the children lived.

The researchers found that children born to less-educated mothers, and those whose births were paid for by Medi-Cal (California’s Medicare program) were diagnosed later. In addition, non-White and Hispanic children, and those with mothers born outside the US, showed delayed diagnosis. In the early part of the decade, firstborn children were also diagnosed later, suggesting that parental familiarity with typical child development may have been a factor, however this effect disappeared over time as autism awareness spread.

The kinds of neighborhoods where children lived also mattered, particularly in the early years of the study. In these years, children living in areas that had many children with autism were diagnosed early, which indicates that familiarity with the symptoms of autism may have been important. Children born in neighborhoods with higher property values were also diagnosed earlier. In general though, over time the importance of neighborhood characteristics seems to have diminished, perhaps because autism became more visible and recognized.

“The findings suggest that for many children, increasing awareness of autism and regular screening has succeeded in indentifying cases of autism at earlier ages,” said Christine Fountain, postdoctoral researcher and lead author of the paper. “However we need a better understanding of how information about autism spreads between parents, teachers, and physicians, and how parents marshal their resources to obtain diagnoses and services for their children in a timely way. This will help us to make sure that some children aren’t left undiagnosed and without the help that they need.”

The study was supported by a National Institutes of Health Pioneer Grant, given to scientists pursuing new strategies to improve health, and was conducted through Columbia’s Paul F. Lazarsfeld Center for Social Sciences. More information on this study can be found at http://understandingautism.columbia.edu.

How an autistic brain is re-wired by genes

4 Nov

UCLA’s David Geffen School of Medicine and Semel Institute for Neuroscience and Human Behavior have released a paper that

demonstrate[s] a relationship between frontal lobar connectivity and common genetic variants in CNTNAP2. These data provide a mechanistic link between specific genetic risk for neurodevelopmental disorders and empirical data implicating dysfunction of long-range connections within the frontal lobe in autism. The convergence between genetic findings and cognitive-behavioral models of autism provides evidence that genetic variation at CNTNAP2 predisposes to diseases such as autism in part through modulation of frontal lobe connectivity.

“This is a key piece of the puzzle we’ve been searching for,” said co-principal investigator Dr. Daniel Geschwind, a professor of neurology and psychiatry who holds UCLA’s Gordon and Virginia MacDonald Distinguished Chair in Human Genetics. “Now we can begin to unravel the mystery of how genes rearrange the brain’s circuitry, not only in autism but in many related neurological disorders.”

For anyone genuinely interested in the science behind autism this is fascinating and exciting news. For the very first time science illustrates how a gene variant tied to autism rewires the brain. For those merely interested in continuing to support the idea of an epidemic to uphold their own unscientific but heavily personally invested causation ideas this news will hopefully be a wake up call.

Over at autism.about.com, Lisa Jo asks

For many parents, of course, the $64,000 question is not “what do autistic symptoms look like,” but rather “what causes these symptoms in the first place?” If the problems are a result of spontaneous genetic mutations, what causes those mutations to occur?

I would respectfully say to Lisa Jo that answering the question of what causes specific genetic mutations was beyond the scope of this particular paper but that _without_ this paper it would’ve been impossible to say with any accuracy how exactly the gene in question affected development. Without that knowledge, looking for answers to causation would be very difficult.

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