Autist's Corner

Signal Transduction in Autism

2011-11-11T17:52:00.000-06:00

EXECUTIVE SUMMARY: A study published this past summer analyzed tissue extracts from 20 donated brains, half (10) of which came from autistic donors. Half (5) of those people had histories of regression --- that is, they started out developing normally, speaking and everything, but then they lost some of the skills they had gained.

The brain tissue extracts were analyzed using a technique I describe in the main body of this post, that tests for the presence of a certain enzyme (protein kinase A, here) by giving it an opportunity to react with a sort of dummy peptide that can't really do anything except sit there and let the enzyme (and only that enzyme) act on it, and then introducing antibodies that will "tag" the altered peptides with an enzyme that will change a solution's color under certain conditions. This allowed the researchers to measure the relative activity of the enzyme across subjects or across brain regions; a similar measure, but using antibodies to the enzyme itself, rather than to its product, was used to measure the amount of enzyme present in each extract.

Using this method, the researchers found differences in protein kinase A activity and expression only in the frontal lobes, and only between the autism-with-regression subgroup of the autism group and both the controls and the rest of the autism group.

Protein kinase A is involved in intracellular signaling; it's one of the signal-boosting enzymes that helps the cell react quickly to changes in its environment. It modifies other proteins, affecting their activity. Some of its targets are proteins involved in neurotransmission (signaling between brain and nerve cells) and long-term potentiation (reinforcing those connections between neurons that are frequently used). It's this latter process that the study authors think may be disrupted in regressive autism.
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SFARI News posted some time ago on a study published on August 31 in PLoS ONE, comparing the amount of a certain enzyme present in tissue extracts from different regions of the brain between deceased subjects with and without autism who had donated their brains to the National Institute of Child Heath and Development Brain and Tissue Bank for Developmental Disorders.

The enzyme in question is protein kinase A, which plays a hugely important role in the cell, helping mediate a process called signal transduction, through which the cell is able to react to its changing environment, or to signals from other cells. In signal transduction, a molecule from outside the cell (usually a hormone) attaches to a receptor outside the cell and causes the receptor to change shape, thus altering the part of the receptor that's inside the cell and triggering a chain reaction of changes in enzymatic activity within the cell.

Protein kinase A participates in one particular signaling pathway: the one involving a class of receptors called G proteins, which are actually clusters of several smaller proteins that split apart whenever something attaches to its extracellular binding site. The now-mobile subunits then go on to do other things in the cell, most importantly to activate* an enzyme responsible for turning adenosine monophosphate (AMP) into cyclic AMP, which works as a signaling molecule inside the cell.

(Here is a cartoon from Nature Publishing Group's Scitable website illustrating that splitting apart of the G protein after a signaling molecule binds to its associated receptor; I adapted the image somewhat to make it less busy)

(Cyclic AMP)

Cyclic AMP is part of a class of molecules called "second messengers," which are small molecules that can bind to, and either activate or inhibit, a wide range of enzymes. Also, the enzymes responsible for making these molecules are regulated by receptors on the surface of the cell, so that when a signaling molecule binds to the receptor, the enzyme gets switched on (in the case of adenylyl cyclase, which is what turns regular AMP into cAMP) and starts churning out second-messenger molecules, which then go on to tinker with their target enzymes. In this way --- by coupling receptor binding with synthesis of these second-messenger molecules --- the cell can amplify the signal it receives, allowing it to react more quickly to changes in its environment.(Cartoon showing signal transduction using cyclic AMP as a second messenger, taken from this community college's Anatomy & Physiology II webpage. You can see how a hormone binding to its receptor frees up the receptor-coupled G protein to exchange its GDP for GTP and then go off and --- depending on the hormone --- either activate or inhibit adenylyl cyclase, which either starts or stops churning out cAMP, which goes on to do lots of different things, like activating enzymes, telling the cell to secrete various things, opening ion channels, etc. The only thing I don't like about this cartoon is that it only shows one cAMP molecule as the output of all the running around happening in the cell membrane, when really cAMP is being continuously produced by every active adenylyl cyclase. So, what that looks like, relative to the amount of hormone coming to the cell from outside, is more like this other cartoon, down below) (See, look at the arrows coming out of that yellowish triangle. One arrow splits into five, then 25, then more than you can clearly see. This table from the Memorial University of Newfoundland's cell biology webpage lists the number of molecules affected by each step in a cAMP-dependent signaling pathway, from the one molecule changed when a single molecule of hormone binds to its receptor, to the 10,000 molecules changed by the time adenylyl cyclase starts producing cAMP).

Anyway, protein kinase A is one of the enzymes activated by cAMP binding to it, and it is also mostly a regulatory enzyme --- that is, it activates or deactivates other enzymes. Protein kinase A does that by transferring a phosphate group from ATP (a small molecule made up of a sugar, a nucleotide base and three phosphate groups) to certain amino acid residues on any of its target proteins.

What kinds of proteins does protein kinase A regulate? Well, that depends on what kind of cell all this is taking place in. Every cell in the body contains a complete human genome; the differences between cell types are differences in which genes are expressed --- i.e., which proteins are present. So each cell type is going to have a different mix of proteins whose activity needs to be coordinated.

Some of its targets are proteins expressed in almost every cell type: these include a histone, one of a large family of proteins whose function is to condense chromosomal DNA that is not actively being transcribed or replicated; transcription factors (most notably, from the CREB family); a metabolic enzyme involved in storing energy for later use; ion channels; and other kinases (enzymes that alter the activity of other proteins by transferring phosphate groups onto them from ATP).

Although protein kinase A performs specialized functions in just about every cell type, I'm only going to talk about what it does in the brain, since that is the cell type relevant to this post. There, in addition to the stuff mentioned above, protein kinase A 1) helps regulate the synthesis of a common precursor to a variety of neurotransmitters, 2) helps form synapses by guiding the specialized proteins that allow the membranous sacs that deliver neurotransmitters from one neuron to the next toward the tip of the developing axon, and 3) with another protein kinase, regulates the ion-channel activity of the NMDA receptor, which is involved in strengthening the more frequently-used conntections between neurons. There may be more, but this is what I've been able to find.

For all that background information, the experiment I'm going to describe is actually pretty simple: like I said above, the researchers took tissue samples from five different regions of donated brains from autistic and non-autistic subjects, homogenized them (basically, ran them through a blender) and tested each sample for protein kinase A activity. The test they used is called the ELISA (for Enzyme-Linked ImmunoSorbent Assay --- see why people would rather call it Eliza?), which is a plastic plate covered with small circular wells (0.7 cm across by 1 cm deep) with, in this case, short peptides containing either serine or threonine (the two amino acids to which protein kinase A can attach a phosphate group), anchored to the bottom. (ELISA is most often used to test for the presence of antibodies --- that's how HIV testing is done --- so for that, the thing stuck to the bottom of the well would be the antigen to which whatever antibody you're testing for responds). They added their brain tissue extracts one by one to each well, along with a small amount of ATP dissolved in water (for the protein kinase to "borrow" phosphate groups from), then waited an hour and a half before emptying out the wells (the substrates, which were permanently affixed to the bottoms of the wells, would stay, along with, presumably, any phosphate groups that had been attached to them during the previous 90 minutes) and introducing an antibody specifically designed to bond with the phosphorylated form of the substrate peptide. Next, they washed the wells out thoroughly (to weed out everything that was not chemically bonded to the fixed substrates) and added a second antibody, chosen for its ability to bind to the first antibody, and which was also attached to an enzyme known for producing dramatic color changes as a side effect of its interaction with certain organic molecules. (A solution containing the molecule in question was also added, so that the wells in which the greatest proportion of the well-bottom peptides had been phosphorylated, and thus had the whole antibody rigmarole sticking off of them, would have the deepest color. There is even a way to measure color --- a device that can measure the degree to which something absorbs light at a given wavelength --- so that you don't have to rely on just your eyes to tell you whether this well or that one is a darker shade of yellow).

They used a somewhat similar technique, called Western blotting, to compare the amount of active protein kinase A between groups for each brain region. They injected their tissue samples from each of the different brain regions into a polyacrylamide gel, and ran an electric current through the gel to get the proteins to move through it. Since the gel resists having things move through it, different size proteins will travel through it at different rates. After a while, most of the proteins will separate themselves into bands along the gel, by size. Once this happened, the researchers transferred the proteins to a nitrocellulose membrane, and added antibodies specific to the catalytic (active) subunit of protein kinase A. Just like with the ELISA, there was also a secondary antibody coupled to a color-producing enzyme.

One thing that's a bit unusual in this study is that the researchers divided their brains from autistic donors into two groups, based on the developmental history of the donors. They had a "regressive autism" group, whose members started out developing typically but then lost some of the skills they'd acquired: speech was the most common skill that was lost, but some of the donors in this category also lost social skills and interest in social interaction. There was also a "non-regressive autism" group, whose members were delayed in language and social development from birth.

Subtyping autism is an increasingly popular thing for researchers to do, since "autism" is such a broad, flexible category that encompasses people with a very wide range of developmental and medical histories. It makes sense that researchers would want to subdivide this large, diverse group further to make sure they're comparing apples to apples when they look at different studies of "the autistic brain" or "the autistic immune system" or whatever.

The thing that's strange about subtyping in this study is that the number of brains being looked at is already so small. Each big group (autism, both regressive and not, and controls) had samples from ten people in it, and the researchers couldn't always get a sample from every point of interest on every brain, so sometimes the number of samples in a given category (brain region + donor neurotype) was less than ten; the smallest n for any category was 7. But that means that, with subtyping, the biggest n possible for either autism subgroup is 5, which looks more like a case study than a comparison across populations. But then, histological studies of donated brains always have to deal with smaller sample sizes, since there isn't exactly a superabundance of donated brains, and I guess if you have big differences among your subjects, you might as well sort them into subcategories, even if your subcategories are tiny.

At some point in this post I should probably mention the results of this study I've gone to such lengths to describe. The authors only found differences in protein kinase A activity in one region --- the frontal cortex --- and this difference was largest between one subgroup of the autistic group --- the autism-with-regression subgroup --- and both the non-regressive autism subgroup and the control group. The regressive autism subgroup had maybe a little less than half the PKA activity of the controls and the non-regressive autism subgroup (those two groups did not differ). Taken as a whole, the autism group had about 35% less PKA activity in the frontal-lobe samples than the control group.

The results were similar for the Western blot; the only region that showed any differences in PKA expression was the frontal lobe, and again, it was only the regressive autism subgroup that differed. Tissue extracts from that group had siginificantly less PKA in them than extracts from either the control group or the non-regressive autism subgroup; the unified autism group did not differ from the control group.

The researchers also looked for a correlation between their measure of PKA activity and various possible confounding factors, like how long each donor had been dead, the age of the donors when they died, whether they had any history of seizures, and what medications they were taking; they didn't find any relationship between any of these things and either outcome variable. Their measure of PKA expression also involved measuring how much of another protein was present in each tissue extract, both because that protein is about the same size as PKA, and thus cannot be separated from it using electrophoresis, and also to have a protein whose expression is not expected to vary across groups with which to compare relative amounts of the protein that is expected to vary.

Here is a picture of the Western blot showing both PKA (top row) and the other protein, a structural protein called beta-actin (bottom row), from all tissue samples:(Figure 2A, in Ji et al., 2011 - samples from autistic donors are on the left, and subdivided into non-regressive and regressive subtypes. Controls are on the right. You can see that, in the bottom row, the blobs are all approximately the same size, indicating expression of beta-actin is more or less the same across groups. You can also see that the blobs in the top row are a lot thinner - one space has nothing at all in it - in the regressive autism group than they are in either the non-regressive autism group or the control group. It looks like PKA expression is a bit more variable within the control group than beta-actin is, though.)

So, for a couple of reasons --- the extreme smallness of sample size, and also the degree of variation in PKA expression within the control group --- I am a bit skeptical as to whether this finding will hold up. It definitely needs to be tested a few more times, with bigger donor pools.

Leaving that aside, though --- what are the implications of this finding, should it be substantiated? The study authors refer to earlier literature that describes a role for cAMP signaling pathways in both brain development (obviously germane to a study about developmental disability) and long-term memory formation and learning (relevant to the question of how people can lose skills they once had). But it's not clear yet exactly what that role is; if you search for "protein kinase a brain" on BioNOT (a database of negative experimental results), you find an article claiming to find no difference in PKA activity between tissue samples taken from donors with Alzheimer's disease and those taken from healthy donors. So that complicates things a bit, as Alzheimer's is, even more than regressive autism, characterized by a loss of learned skills and memories.

Sources:
Ji, L., Chauhan, V., Flory, M., & Chauhan, A. (2011). Brain Region–Specific Decrease in the Activity and Expression of Protein Kinase A in the Frontal Cortex of Regressive Autism PLoS ONE, 6 (8) DOI: 10.1371/journal.pone.0023751

*What does it mean to activate an enzyme? Well, an enzyme is a kind of protein, and like all proteins, it has a range of three-dimensional configurations** it can assume, and only some of these possible shapes leave the binding site for the molecule the enzyme acts upon freely accessible. So when an enzyme is in one of those arrangements, and molecules of its particular substrate can just drift along and come into contact with the binding site(s), that's when the enzyme can be considered active. Binding of a phosphate group or some other small molecule at a different binding site will usually trigger a shape change; that is how enzymes can be activated or deactivated by other enzymes.

**I have this idea that proteins are called proteins just because of this shape-changing ability they have, in which they resemble the mythical Proteus.

Link Roundup: What I've Been Reading

2011-11-10T16:15:00.001-06:00

I'm working on a post that has surprised me with how long it's taken to write; it's a researchy post, but it's only dealing with one article, and the experiment that article describes is a fairly simple one. I thought I'd be able to knock it off in a day or two, but instead I find I keep having to provide more and more background information about the methods the researchers used, and the enzyme they're studying, and the physiological processes that enzyme participates in.

(This experience has led me to reflect on the particular nature of the language used in the "Methods" sections of biomedical research articles; it's clear as day if you know what they're talking about, but it's a sort of shorthand, with as much precise meaning as possible crammed into the smallest possible space, which makes it all but impenetrable to someone not versed in those techniques. I think I might have to post about that, too ...)

Anyway, while I've been working on that I've also been reading blogs, and this is what's impressed me recently:

s. e. smith has written an indispensable post at Tiger Beatdown about Hillary Adams, the brave and resourceful young woman with cerebral palsy who filmed her abusive father (who is, horrifyingly, a family court judge) beating her back when she lived with him, and has just recently posted the footage on YouTube. s. e.'s post focuses on the elevated rates of abuse children with disabilities face, and cultural factors that allow that abuse to go on, even when people know it's going on.

Kassiane guest-posted at The Thinking Person's Guide to Autism about how important it is for caregivers to take "no" seriously and respect their charges' boundaries, physical and otherwise.

This blog post by the Dean of Health Sciences at Queen's University in Ontario mentions a paper given at a conference by recent sociology Ph.D. Elise Paradis about the use of the word "epidemic" to describe chronic, non-infectious diseases and conditions, particularly obesity. Paradis considers ways in which this terminology is misleading and stigmatizes obese people. The paper doesn't seem to be in print anywhere, but it looks like it will be soon.

Emily at The Biology Files has a list of things that have been proposed as causes or risk factors for autism. It's droll, and seeing them all side by side (even just the ones that are actively under consideration today, leaving out the ones that have been debunked) makes you marvel that there are still some people who are not autistic.

For My New Reader

2011-10-12T17:47:00.001-05:00

I just had someone contact me on Etsy to tell me they loved the blog, and to ask for suggestions on further reading.

I rattled off a few of my favorite bloggers, but also suggested to the person that they check out various aggregator sites (and, I'd like to add, blog carnivals) to look around and see what most appeals to them there.

So, here you go, Olin.

Blog Aggregator Sites
Autism Blogs Directory (mostly personal blogs by autistic people or parents of autistic children)
AutismBlog.org
Autismo
The Autism Hub (not as big as it used to be, but still going)
wrtAUTISM (has a lot of research-oriented blogs)

Blog Carnivals
Autistics Speaking Day
Blog Against Disablism Day (2011, 2010, 2009, 2008, 2007, 2006)

Also, if any of you have any ideas for blogs, websites etc. that you consider Essential Reading, feel free to mention it in comments!

Autistic Artist: Justin Canha

2011-10-09T14:58:00.003-05:00

An article in the New York Times from a few weeks ago profiled a young man named Justin Canha, who is a very interesting person. He loves to draw, and would like to be an animator or illustrator one day.

The article was about his struggles to find a job and live independently, and the "transition to adulthood" program* that is helping him to do that, but it also mentioned his art, and included a link to his website, where you can see a whole lot of his work, which includes charcoal and pastel drawings, comic strips and Flash animations.

I really like his "Carnivorous Plants" series; they look eerie and alien, but are beautifully colored. The drawings look representational and abstract at the same time, which is an effect I find mesmerizing.

Here are a few of my favorites:

*One thing that stood out to me, reading the article, was how intensively micromanaged his life seems to be! I notice this a lot about the lives of autistic people younger than I am, who have had behavioral therapy throughout their childhoods. I don't doubt that it's helping him learn to navigate the world, and I'm sure graduates of such programs end up better equipped for it than I am (maybe - one blogger has described behavioral therapy as taking away her ability to make decisions on her own, without "rules" to go by), but damn, if that were my life, with someone telling me how to spend every minute of every day, and getting on my case if I wanted to engage in "activities not directly related to finding a job"? I'd be a walking powder keg of fury. I don't respond well to control. I suspect that a large part of the reason I don't have a huge anger problem today is that I am used to having my boundaries respected; I don't feel like I have to explode and destroy things in order to be heard.

Did You Know ...

2011-09-22T17:09:00.000-05:00

(T. S. Eliot, wearing a white rose)

One of my favorite poets, T. S. Eliot, apparently wore a white rose in his lapel to show loyalty to Richard III (whom he is supposed to have called the last legitimate English king, per this article in The New Yorker about him) and the house of York, on the anniversary of the Battle of Bosworth Field (when Richard was killed).

From this, and from the fact that the Song of Ice and Fire is (very loosely) based on the events of the Wars of the Roses, I conclude that, if he were alive today and would condescend to read science fiction or fantasy (which is probably a greater leap than bringing him back from the dead --- the man was a humongous literary snob), he would probably be a Stark fan. :)

Winter is coming!

Simon Baron-Cohen Responds to Criticism from an Autistic Blogger - Part II

2011-09-17T17:17:00.000-05:00

Now, I'd like to focus on the first two points in Simon Baron-Cohen's response to Rachel Cohen-Rottenburg, where he addresses her argument that autistic people's generally heightened perceptual sensitivity, and our lack of any sort of filtering mechanism, tends to make us more empathic, not less.

She says:

Many of us experience such a high degree of empathy that we are constantly putting ourselves in other people's shoes and trying to see all sides in any controversy or conflict. Many of our problems with sensory and emotional overload derive from an excess of this ability, not a deficit.

He replies:

1. Rachel challenges whether people with autism have 'theory of mind' difficulties and instead argues that people with autism have high degrees of empathy.

This is however hard to reconcile with the scientific evidence. Literally dozens of studies from around the world have documented the theory of mind difficulties in autism. And the empathy difficulties are also well documented and widely replicated, both on performance tests (e.g., emotion-recognition tests from the face and voice) and on self-report measures (such as the Empathy Quotient or EQ).

Consider the latter, where 81% of people with autism score less than 30/80 on the EQ, by their own self-report, whilst only 12% of people without autism score at this low level. These results are mirrored when parents complete the EQ about their children, in many independent samples. So, whilst some people believe that theory of mind and empathy difficulties in autism are mythical, the results of many independent scientific studies suggest otherwise.
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2. Rachel challenges whether people with autism have difficulty knowing when they have hurt others, and wishes I had not stated that children with Asperger syndrome (AS) are delayed in being able to figure out what might hurt another person. Indeed, she finds my statement hurtful.

As a working scientist, all I can do is summarize the empirical evidence. An example is the Faux Pas Test, where children are asked to identify if anyone said anything they shouldn't have said, whilst listening to short audio recorded stories. Children with AS as a group on average scored significantly lower than children without AS, despite being older than the comparison group. Indeed, the design of this experiment allowed us to estimate the size of the developmental delay in AS, since the 12 year old children with AS performed more like typical 9 year olds. So, although Rachel may not like hearing these results, this is what the science finds.

I am not Rachel, but it seems to me like she wasn't denying the existence of those results at all; just saying that those results don't tell us much of anything about what the autistic people in the various studies were actually thinking that led them to do the test "wrong." We know that autistic people don't interpret social situations the same way non-autistic people do; what we don't know is how autistic people do interpret them.

(I am basing the above paragraph on what Rachel has written in this post on the Sally-Anne test for Theory of Mind, as well as her three-part series critiquing the EQ. Her post on the Sally-Anne test, in particular, is interesting because it describes an alternate thought process for a hypothetical autistic child taking the test, and coming up with reasons why Sally might look in other places than where the researcher wants her to look. What's important is that it's not that the kid in this example can't imagine Sally's point of view, it's that ze is drawing on different thought processes and experiences to arrive at different predictions for what Sally will do. The problem with the test is that it treats all wrong answers as failures to imagine Sally's mental state.)

Because I understand Prof. Baron-Cohen's need for empirical validation of these possibilities, I've even come up with an experimental design he (or anyone) could use to evaluate the two-way-street hypothesis that I've been promulgating here.

You'd have a bunch of people, half of them autistic and half of them not, and you would group them into pairs, with each pair including one autistic and one non-autistic member, both the same sex, same age and roughly similar verbal abilities, and just have them interact together for a short while, like 5-10 minutes. You would record their interaction on video, and then you would ask each person, separately, some questions about what happened between them. What they thought felt at certain points (decided on by the researchers sometime between the actual exchange and the individual Q&A sessions), what they thought the other person was thinking or feeling at certain points. You would then compare the two participants' answers to see how well they overlapped. You would also do this with autistic/autistic and NT/NT pairings, and then compare the average degree of similarity of the paired accounts across all three permutations.

This would allow you to see whether autistic people seem to understand each other better than they do NTs, or whether NTs are equally baffled by autistics.

It would also end the stalemate between Baron-Cohen's "well, the evidence says autistic people just don't understand social situations" and autistic people's self-reported experiences of both understanding other autistic people, and of having non-autistic people spectacularly fail to understand, or empathize with, them.

Simon Baron-Cohen Responds to Criticism from an Autistic Blogger - Part I

2011-09-14T22:38:00.000-05:00

EXECUTIVE SUMMARY: Many autistic and feminist bloggers have criticized Simon Baron-Cohen's theories about autism and gender differences, but not very many have had him respond to their criticisms personally. Rachel Cohen-Rottenburg is one of those lucky people; she posted a critique of his E-S theory on her blog a couple years ago, and he has just now written a ten-point response to it. In this part of the post, I talk about Rachel's objection that the characterization of autistic people as poor empathizers ignores the differences between cognitive and affective empathy, and that even autistic people who lack cognitive empathy often have great capacity for affective empathy. I also talk about Baron-Cohen's response to this objection, and how his thought on empathy and autism has undergone a further evolution in the two years since Rachel wrote her post.
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Sandrine (a French woman living in Turkey, who has an autistic son) at The Paris Ankara Express pointed me to this guest post by the famous autism researcher Simon Baron-Cohen at the Autism Blogs Directory.

In his guest post, Prof. Baron-Cohen responds to criticism of his Empathizing-Systemizing (E-S) theory of autism from Rachel Cohen-Rottenburg, who writes the blog Journeys with Autism and also curates a web-anthology on Autism and Empathy.

He identifies ten points that Rachel makes in her essay, and writes a paragraph (or two or three) addressing each one. They seem to be split about half and half between questioning Baron-Cohen's conception of empathy (as in, autistic people actually tend to be quite sensitive to other people's emotions, particularly distress) and questioning whether his model is actually any more descriptive, or helpful, than older "deficit" models.

(You could argue --- and many people do --- that the E-S/Extreme Male Brain theory is still a deficit model since it considers a deficit in empathizing skills to be a defining characteristic of autism; it offsets this by also including normal or superior systemizing skills as part of the definition, but if you look at most of the psychological, educational, or behavioral literature on autism, you find all sorts of articles on remediating, or sounding the depths of, autistic deficits and not very much on nurturing or characterizing autistic strengths. So the offset deficit model isn't actually offset all that much, in practice.)

Rachel's post is a response to this paper from 2009 (Rachel's post is also from 2009) spelling out what the E-S theory says about autism. The article describes the E-S theory, particularly its evolution from Baron-Cohen's earlier "mindblindness" theory of autism. He lists five things the earlier model failed to explain that he thinks the newer one does adequately explain: 1) nonsocial aspects of autism, like attention to detail, love of patterns or routines, stimming etc., 2) empathy isn't just "mind-reading", it's also feeling something for the other person, and the "mindblindness" model only deals with mind-reading, 3) autism isn't the only condition that can produce mind-blindness, 4) some studies have failed to find any differences in Theory of Mind between autistic and non-autistic subjects, and 5) autistic strengths.

Rachel responds that, no, actually the E-S theory doesn't do any better at explaining these things. She thinks he totally misreads stimming, for one thing: to her, it's not about "systemizing" at all, it's about self-calming. It's a way to handle emotions, not a form of empirical investigation.

She also takes issue with his contention that we lack both cognitive and affective empathy:

The everyday experience of many autistic people, all across the spectrum, contradicts the professor's theory. Many of us experience such a high degree of empathy that we are constantly putting ourselves in other people's shoes and trying to see all sides in any controversy or conflict. Many of our problems with sensory and emotional overload derive from an excess of this ability, not a deficit.
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From my contact with autistic people, it's clear to me that our empathy leads many of us to constantly question the impact of our words. While I am far from perfect, choosing my words carefully may very well rank as one of my Aspie obsessions. However, the professor believes that "the typical 9-year-old can figure out what might hurt another's feelings and what might therefore be better left unspoken. Children with Asperger syndrome are delayed by around 3 years in this skill." (Baron-Cohen, 69)
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Baron-Cohen goes on to say that, in addition to not empathizing well, we don't know how to respond to someone even after the person tells us what's wrong.

News flash: Once someone tells me how he or she feels, I don't usually have a problem with an empathetic response. Sometimes, I'll make sure that my response is welcome, out of respect for the other person's boundaries. For instance, if a person is crying, I might ask whether the person would like a hug, or whether the person would like to talk. Some people want hugs, and some people want to be left alone. I consider it courteous to ask. Once I know people fairly well, however, and I know what works for them, I simply respond. Just ask my husband, my daughter, my daughter's friends, my friends, my former co-workers, my neighbors, and all the animals I've ever helped care for in various stages of illness.

I feel like I have to back up now, because Prof. Baron-Cohen says explicitly in his response to her (he even draws a picture!) that he thinks autistic people are only impaired in cognitive empathy, and that we are just as capable of affective empathy as anybody, which is pretty close to what Rachel was saying, too.

His thinking has shifted somewhat since he wrote the paper Rachel was responding to; in that paper, he not only doesn't say that autistic people have affective empathy, but he also implies that we are deficient in both kinds of empathy --- he mentions the EQ as a measure of both affective and cognitive empathy, and also mentions that autistic people tend to score lower on the EQ than non-autistic people:

Most people regard [Theory of Mind] as just the cognitive component of empathy in that it simply involves identifying someone else's (or your own) mental states. ... [M]issing from ToM is the second component of empathy, the response element: having an appropriate emotional reaction to another person's thoughts and feelings. This is referred to as affective empathy (Davis 1994). On the Empathy Quotient (EQ), a questionnaire is filled out either by an adult about themselves or by a parent about their child, both cognitive and affective empathy are assessed. On this scale, people with autism spectrum conditions score lower than comparison groups.

So, while Rachel's objection --- yes, we do have affective empathy --- might seem redundant to someone who has read Baron-Cohen's more recent writing on the subject of empathy (his most recent book, Zero Degrees of Empathy, contrasts autistic people with psychopaths: the former group has poor cognitive empathy but normal affective empathy, while the latter has normal cognitive empathy but poor affective empathy), she is actually bringing up something that is not addressed in the text she's working with.

(I also think there is still a problem in Baron-Cohen's work with measuring empathy --- measuring it at all, much less measuring each component separately --- in that most of the tests he uses that directly measure some aspect of empathy, like the Sally-Anne test, the Faux Pas test, or the Reading the Mind in the Eyes test, are measures of cognitive empathy only. The indirect measures, which are usually questionnaires, have their own problems. With any self-reported measures, there's a risk of stereotype threat, where the test takers' awareness of stereotypes about some group to which they belong biases their answers toward whatever the stereotype predicts: women/girls and members of some ethnic minorities, like African-Americans, Latin@s, or Native Americans, tend to do worse on math tests when they are reminded of their group membership, even by something as innocuous as a check-box at the top of the page for race and gender. Since autistic people are often taught from early childhood that their way of speaking, acting, feeling, or relating to other people is weird and wrong, I would not be surprised if they tended to rate themselves low on things like fitting in, participating in conversations or getting along with other people. Also, a lot of the questions on things like the EQ measure some mixture of cognitive and affective empathy; they ask about intuitively knowing what a person feels and then reacting to it, like knowing to comfort someone who is upset. There is one measure that has subscales geared just toward having intense feelings on other people's behalf, and that is the Interpersonal Reactivity Index, which one study found autistic people scored either very close to, or even better than, non-autistic people on all but one subscale.)

So his position on affective vs. cognitive empathy in autism has shifted somewhat since he wrote the paper Rachel was responding to, and he doesn't explicitly acknowledge that in his response to her; instead, he makes it sound like that's what he was saying all along:

Rachel says "once someone tells me how he or she feels, I don't usually have a problem with an empathic response." This is exactly the point. For most people, they don't need to be told by the other person, "I am upset." They can just read this information in the other person's facial expression, vocal intonation, or 'body language', and they can make inferences about what the other person might be thinking, in the absence of being directly told. For many people with autism these non-verbal cues may be hard to read and instead they may only know how someone feels if they are told explicitly. The evidence for this again comes from many scientific studies documenting difficulties by people with autism in reading the mind in the eyes, the face, the voice, or in action (e.g., film). Rachel's own self-description seems consistent with this: "Now, I will readily admit that I cannot infer a person's mental state by reading nonverbal cues."

But I completely agree that once it is explicitly pointed out, people with autism are very capable of an empathic response. Rachel may be surprised to hear that I agree with her on this one, but it hinges on the distinction between 'cognitive' and 'affective' empathy. Cognitive empathy is the ability to identify another person's state of mind (not just through language) and affective empathy is the drive to respond with an appropriate emotion to another person's state of mind. A growing number of studies suggest that the empathy difficulties in autism are largely restricted to the cognitive component, whilst the affective component is often intact. For this reason, people with autism are often highly motivated not to upset others or hurt others, and are themselves upset to hear that they may have done this if it is pointed out. And once they know that someone else is upset or suffering, they are very often motivated to want to help or offer comfort.

(This seems like a really patronizing response to me. She has addressed theory of mind in other parts of her post; with the passage he's quoting, she is explicitly addressing the "emotional response" aspect of empathy. To make the point that her capacity to form an empathic emotional response is working just fine, thank you, she's describing that faculty in isolation. He ignores that context so that he can go, "Ah-ha, see, she has to be TOLD what someone is feeling!" Well, no, she doesn't always. She's just describing a particular scenario where her cognitive empathy cannot be called into question --- because she doesn't have to use it --- in order to focus on her affective empathy.)

No, I am glad he understands that we care about other people, too. I still disagree somewhat with his assessment of our difficulties with cognitive empathy; that, I think, stems as much from our being profoundly different from other people in terms of our sensory and emotional responses as it does from any objective inability to "read" other people. I think he ignores just how badly non-autistic people fail to notice the signs of our distress, or misinterpret our body language or tone of voice. I think they are just as bad at reading us as we are at reading them; it's just that because they're the majority, their failure to understand us is not as disabling as our failure to understand them.

I had more things I wanted to point out about his response to Rachel, but I've ended up spending so much time untangling this one little snag where they seem to be talking past each other that I think I will split this into multiple posts.

Cat Pic of the [variable time period]

2011-09-13T19:43:00.000-05:00

Boots, on a wicker chair on the deck. Ben is behind the chair, visible through the space under the arm.

Boots is very assertive; if something new appears, he has to get on it, play with it, bite it, or otherwise make it his own right away. Ben and Magic are more conservative; they have to wait awhile to make sure the new thing isn't a threat before they will approach it.

Two New(ish) Necklaces

2011-09-13T19:37:00.000-05:00

One of them really is new; I made it a few days ago, and only took pictures of it today.

Here I am, modeling it: (In that light, I have to hold the camera above my head and tilt it downward somewhat to avoid triggering the flash --- it doesn't always work. But it gives a warped impression of how big my head is compared with my neck and shoulders; here's another photo taken from a more straight-on angle: you can see that my neck is actually about the same width as my face at its broadest point. But the top photo is the only one in which I'm not making some kind of "Eek! Flash! Too bright!" face.)
I took advantage of having the camera out and wearing a purple shirt to model another necklace, one I made a while ago.
I don't think any of the pictures I took of this one really do it justice; I really like the way it turned out, with the mix of colors and the little beaded panels, but if I want to get my face in the picture, too, I can't zoom in to show the details that I think are the best thing about this necklace.

With some of my jewelry, the overall shape of it is interesting enough, or big enough, that a photo of me wearing it shows something a photo of just the necklace can't show; I guess the necklaces like the second one shown here aren't in that category.

This Is Awesome

2011-09-10T15:20:00.002-05:00

Amanda Forest Vivian has an idea that I think really rocks, and one that I definitely want to be part of.

It's a website for people with disabilities to post pictures/videos of their art, with each person getting their own site where they can showcase their art however they want:

Crazy House is the name of a book by Henry Darger, an outsider artist. Outsider art is a hard-to-define category, but many people labeled as outsider artists have psychiatric or developmental disabilities.

Crazy House the website is an imaginary house where you can have your own room. Which is to say you can apply to be hosted on the domain which I have yet to buy, and then you could make a site for your art. All of these sites would be linked to from the main page, and would make up the Crazy House.

It's perfectly worth asking why this is necessary when there are so many places on the Internet where you can upload and share art. I'm not really sure why I want to make the Crazy House, except that I like the idea of sharing an imaginary house with other people instead of just having a lot of usernames on different huge websites. I also like the idea of an art space that is somewhat centered on disabled identity.

I would like to buy the Crazy House domain with other people for two reasons. First, it would be cheaper, and second, I would like the Crazy House to be something that isn't dependent on one person, but on several people. If anyone is interested in buying the Crazy House domain with me, please email me at awf.vivian at gmail (I'm hoping to figure this out by November or December).

If anyone can't or doesn't want to be part of buying the Crazy House, but would like to room in the Crazy House, sit tight. Hopefully I will be back in November or December telling you how to do so. And please signal boost.

I don't know if I have any readers who aren't also readers of Amanda's blog, but I thought I'd try and signal-boost anyway.

I also think the idea of a smaller, self-selected group of artists having a website to showcase their art together is a cool one, and I also like the idea of each person having total control over what their own site looks like. With Flickr or other image-sharing websites, you're restricted to showing your images one at a time in a slideshow, which can take away from the effect if you've got a series of related pieces. This also gives people room to have things together on one page that are in different formats, like art, video, music, animation, whatever else.

(I am a little intimidated by the prospect of having to build my own webpage from scratch, since I don't know anything about programming, but I figure I can probably learn what I need to. My dad has built a webpage for me before, to showcase my jewelry, and I learned a bit about how to do it by watching him. It doesn't look super hard; just something I've never done before.)

Another Writer Uses "Autism" Where He Means "Selfishness" or "Amorality"

2011-09-09T21:14:00.001-05:00

I'm getting quite a collection of examples of this sort of rhetoric, in which the writer/speaker tries to discredit someone else's political philosophy by calling it, or them, "autistic."

So far, I have a literary critic contrasting Jean-Paul Sartre's nihilism and profound alienation from other people (which he calls "autistic") with Albert Camus's more humanistic philosophy; a liberal editorial writer asking "Are Republicans Autistic?"; a liberal talk-radio host comparing Republican reliance on "talking points" to autistic verbal stims; and a liberal podcast blaming President Barack Obama's inability to overcome opposition by a vocal Republican minority on his inability to understand them, coupled with his overly scrupulous adherence to rules.

The latest addition to this group, which I saw on Emily's blog, A Life Less Ordinary?, is the author, neuroscientist and outspoken atheist Sam Harris talking about why he thinks Ayn Rand's philosophy of rational selfishness is unrealistic, morally obtuse and incompatible with actual human nature.

Here is the relevant part of that post (I'm including a bit more context for the offending one-liner than Emily did, because I'm interested in exactly what "autism" is supposed to imply here):

Many readers were enraged that I could support taxation in any form [in an earlier post on taxes and income inequality in the US]. It was as if I had proposed this mad scheme of confiscation for the first time in history. Several cited my framing of the question --- "how much wealth can one person be allowed to keep?" --- as especially sinister, as though I had asked, "How many of his internal organs can one person be allowed to keep?"

For what it's worth --- and it won't be worth much to many of you --- I understand the ethical and economic concerns about taxation. I agree that everyone should be entitled to the fruits of his or her labors and that taxation, in the State of Nature, is a form of theft. But it appears to be a form of theft that we require, given how selfish and shortsighted most of us are.

Many of my critics imagine that they have no stake in the well-being of others. How could they possibly benefit from other people getting first-rate educations? How could they be harmed if the next generation is hurled into poverty and despair? Why should anyone care about other people's children? It amazes me that such questions require answers.

...

As someone who has written and spoken at length about how we might develop a truly "objective" morality, I am often told by followers of Rand that their beloved guru accomplished this task long ago. The result was Objectivism --- a view that makes a religious fetish of selfishness and disposes of altruism and compassion as character flaws. If nothing else, this approach to ethics was a triumph of marketing, as Objectivism is basically autism rebranded. ...

And I say this as someone who considers himself, in large part, a "libertarian" --- and who has, therefore, embraced everything that was more or less serviceable in Rand's politics. The problem with pure libertarianism, however, has long been obvious: We are not ready for it. Judging from my recent correspondence, I feel this more strongly than ever. There is simply no question that an obsession with limited government produces impressive failures of wisdom and compassion in otherwise intelligent people.

This passage rests on the same assumption I noticed in the editorial "Are Republicans Autistic?", which is that autism is the same thing as selfishness. There is also the implication that to be autistic is to be profoundly ignorant of how the world works, how people are (Randians try to live by a philosophy that might work for some alien species that is 100% rational and naturally solitary, but which does not map very well onto human lives), or even the circumstances of their own lives (later in the article he mentions how much luck is involved in even the most "self-made" person's success, and alludes to people erroneously attributing to their efforts things that practically fell into their laps by virtue of their being in the right place at the right time, knowing the right people, and being the right "kind" of person).

It seems to me that it's no accident that all these rhetorical uses of "autism" to characterize a deeply selfish person or worldview are cropping up at the same time the popular conception of autism is shifting to "someone without empathy." It seems to me that those two things are actually mirror images of each other; as long as people talk about autistic people as being without empathy, autism will be the metaphorical diagnosis of choice whenever someone wants to talk about an actual lack of empathy.

So the stereotype gets reinforced from both ends.

City Mouse, Country Mouse, Autistic Mouse

2011-09-08T22:34:00.001-05:00

There's one more thing from Unstrange Minds that stuck in my head, that I didn't think to include in this post and which probably deserves its own post anyway, given how much stuff was already in the other post.

Anyway, in the chapter on autism in South Korea, Roy Richard Grinker alludes to something I've seen mentioned before, and am curious about.

While describing differences between rural South Korean villages and the capital city of Seoul in how these communities treat their autistic members, Grinker mentions some research conducted by the World Health Organization comparing how well people with mental illnesses fare in developed vs. developing countries:

An agricultural area often belittled by Koreans and long neglected by the government, Cholla-do remains the most underdeveloped region in one of the richest countries in the world. Cholla residents are familiar with discrimination and adversity and find it hard to improve their class and social status. They consider it a great success to make one's career in Seoul, where more than 25 percent of South Korea's 44 million people now live.
...
Still, after asking a few questions here and there (Are there any children who don't speak well? Are there children here with brain disorders?), I found a sixteen-year-old boy and a nine-year-old girl in a mountainous county. Everyone seemed to know about them. And when I talked to the barber and the local grocery-store owner about them, there was no hint of discomfort or pity. Peter, as his mother wanted him to be called, was good with bicycles and served as a messenger for two villages, delivering letters and packages with a broad smile. He saw a doctor once every two months and was medicated with a small dose of an antipsychotic drug that calmed his anxiety and some of his repetitive movements. The girl, Soo-Rin, was in the village with her single mother only on weekends because she attended a special school for children with Down syndrome, cerebral palsy, and mental retardation. But everyone knew her too. Her room at home was lovely, pink with lace curtains, stuffed animals, and Disney characters. Her mother said she takes a medication at school to help her pay attention, but she didn't know what it was called. In these villages, you can find proof of something the World Health Organization has been arguing for years: People with mental disorders do better over time in remote, nonindustrial societies than in urban, industrial ones.

I'd read about that research before, in Robert Whitaker's book Anatomy of an Epidemic; in that book, he argues that the reason the people in developing countries are more likely to recover from acute mental illnesses, and don't become chronically mentally ill as often as people in developed countries, is because people in developing countries often don't have access to psychiatric medication, which Whitaker argues actually worsen a person's condition over time.

Grinker lists an earlier book by Whitaker --- Mad in America --- in his bibliography, along with a book-length follow-up to this study (full text here), but he is not making Whitaker's argument here. Instead, he thinks the people in the rural villages are more accepting than the people in the cities:

This is not to say that life for the disabled is easy in the villages --- even someone with a mild speech impediment, who is otherwise normal, will have just as much trouble finding a spouse as an urban dweller with the same problem. And parents can be just as devastated. One man confessed to me that in his despair he once took his young autistic son high up in the mountains, intending to slit his throat, but couldn't bring himself to do it. But for most parents of disabled children, life in the rich city of Seoul is more stressful than in the more humble village. One of the paradoxes of rural life is that people in the villages tend to be relatively accepting of diversity. Little remains secret, and there seems to be a place for everyone. In the rural areas, people assume that things would be much better for their children in the city. But in the city, in the sprawling, indistinguishable apartment complexes of Seoul, most people do not know their neighbors, even though they watch them as closely as they can. The pressures to measure up can seem overwhelming, and families try to keep anything that might reflect badly on their status hidden from view. The moment you bring your disabled child outside in this densely populated city is the moment you are confronted by strangers, people who will watch and judge you.

Later on, he says something that would seem to rule out Whitaker's non-drug hypothesis: the children he met in the rural villages were taking psychiatric medications, while very few of the children he met in Seoul were taking any.

He sees this as symptomatic of the prevailing viewpoint in Seoul that autism is basically a death sentence; if nothing can make an autistic child non-autistic, what's the point of drugs or therapies? It all just costs money, and with drugs there's also the matter of side effects to consider.

(I actually thought his interviewees' concern about the side effects of psychotropic drugs was sensible; I thought Grinker in this passage was being way too uncritical of US psychiatrists' willingness to prescribe these drugs to children when so little is known about their long-term or developmental effects. I think his point about the all-or-nothing mentality is a valid one --- and that mentality is certainly not restricted to South Korea! --- but I don't share his faith that drugs always lead to better quality of life. Indeed, often their use is a symptom of the same societal rigidity that he blames for making urban life so much harder for autistic people to participate in than rural life.)

Anyway, his mention of those WHO studies reminded me that I had wanted to read them (and there are still more follow-ups, meta-analyses and similar studies from more recent years, too), and post about them.

Strangers in an "Unstrange" Land

2011-08-25T13:38:00.008-05:00

I just finished Roy Richard Grinker's book Unstrange Minds: Remapping the World of Autism, and I very much recommend it to just about anyone with an interest in autism.

It's written from a parent's point of view, and mostly (it seemed to me) for an audience of other parents, but there's a lot in it to interest people outside that core audience, too. There's a lot of historical stuff about the first descriptions of autism, and about how psychologists have tried to understand it over the past six decades or so; Grinker's father, grandfather and great-grandfather were all psychoanalysts (psychiatrists, too --- his grandfather founded the Archives of General Psychiatry), so he has a very strong grounding in the history of psychology and psychoanalysis.

He also addresses the question of whether there is or is not an autism epidemic, going into some detail about how diagnostic categories have changed, how the availability of special-education services varies by diagnosis, and how the ways of measuring the prevalence of autism have changed.

The first edition of the DSM to have "autism" as a category was the DSM-III, published in 1980. The criteria for "Infantile Autism" were fairly specific:

A. Onset before 30 months of age
B. Pervasive lack of responsiveness to other people (autism)
C. Gross deficits in language development
D. If speech is present, peculiar speech patterns such as immediate and delayed echolalia, metaphorical language, and pronominal reversal.

(There was also a category for people meeting all of these criteria, but with the condition not appearing until after 30 months of age; there were also "residual state" diagnoses for people whose speech problems or unresponsiveness had lessened to the point that they no longer met the above criteria).

The DSM-III-R criteria were somewhat looser, getting rid of the age-of-onset criterion and collapsing the "residual states" into Autistic Disorder itself --- you could have an autism diagnosis even if you did not currently meet all the criteria, as long as you had met them before.

The loosest criteria of all were those of the DSM-IV, which I had already known, but what I didn't know was that their flexibility wasn't all by design:

[T]here was an error in the final manuscript. It is not well known, even among experts, but in 1993, when the authors of the child psychiatry section of the DSM were editing the proofs of the new DSM-IV, which would be published in 1994, they missed a critical mistake. For PDD-NOS, the largest group of autism spectrum disorders, they had intended to write as the criteria, "impairment of reciprocal social interaction and in verbal or nonverbal communication skills." A different text was accidentally published. It said, "impairment of reciprocal social interaction or verbal and nonverbal communication skills, or when stereotyped behavior, interests, and activities are present." The authors had wanted someone to qualify as autistic only if they had impairment in more than one area, but the criteria, as published, required impairment in only one area for a diagnosis of PDD-NOS.

Another interesting aspect of his discussion of autism diagnoses hinges on the different priorities of clinicians and researchers, and his idea (well-buttressed with quotations from prominent psychiatrists) that autism diagnoses are often made not because "autism" accurately describes the child being evaluated, but because they think the special-education services targeted at autistic children will do the most good for that child. That would go a long way toward explaining the "diagnostic substitution" that's occurred over the years, with more children being classified as "autistic" at the same time as fewer children are being classified as having plain old intellectual disability. (Grinker also includes a parallel instance of a diagnostic category that no one would argue is actually becoming more common --- traumatic brain injury --- becoming more widely used over the same period of time, due to changes in the U.S. Department of Education's disability coding system).

The part of the book that was most interesting to me was the series of chapters on cultural attitudes toward autism in three other countries: India, South Korea and South Africa. For each country, Grinker profiles one or two families with autistic children, usually starting with the mother, and letting her tell the story of how she came to suspect that there was something different about her child, and how she overcame varying degrees of stigma, disbelief and lack of services to get her child therapy, special education and a place to live when she could no longer take care of him/her.

We meet Golden and Suzanna Khumalo, and their son, Big Boy, who moved from Soweto to Cape Town in South Africa to get their son to a psychiatrist, and away from Golden's parents and ex-wife, who blamed Big Boy's autism on, respectively, displeased ancestors and witchcraft. We meet a woman named Merry Barua, in Delhi, India, who founded a school for autistic children called Open Door, which she began for her own son, in the absence of any other school that met his needs. We also meet two families from South Korea: a woman named Seung-Mee, with an autistic daughter named Soo-Yong, who joined a Christian church because the church members were the only people she ever met who really seemed to accept her or her daughter, and another family with three children, one of whom is autistic and kept hidden from the world. Autism is a highly stigmatized condition in South Korea, and one that reflects poorly on an entire family, so often doctors will diagnose a child with an attachment disorder instead. Grinker does think it's getting better for autistic people there, though: a recent film about an autistic marathon runner is lessening the taboo somewhat, and giving people the idea that autistic people can do more, and have fuller lives, than they had previously thought.

There was one aspect of autism that I thought this book didn't go into very much, though: he doesn't include very many quotes from autistic people themselves. (I can only remember one, actually --- at the very end, talking about a college class on autism he taught where one of the students had Asperger's syndrome). This didn't bother me as much as it might have, since he wrote about his autistic daughter Isabel in such an empathic way; rather than simply describe her behavior as if she were some kind of space alien, he gives context for everything she does, and tries to convey something of her feelings. He lets us see her grow up, learn things, acquire skills, and pursue her special interests. He writes from a caregiver's point of view, and everyone he interviews is also a caregiver, but he writes about his daughter with such love, respect and understanding that I never got the feeling that he thought of her as a burden, as an extension of himself or as anything but her own person.

Born This Way

2011-08-22T22:40:00.001-05:00

Some book I read a long time ago --- it may have been Steven Pinker's The Blank Slate --- maintained that, in the US, conventional wisdom has swung back and forth on whether differences between people that show up in adulthood have been present since birth, or whether they are acquired during childhood and adolescence.

It's usually intelligence that gets discussed in this way, almost always in the context of racist, sexist, or otherwise inequality-justifying theories about some groups being naturally smarter than others, but there's been a similar periodicity in thinking about other things, like personality traits. (Gender differences in cognitive style, interests, and personality are some of the things that are now widely believed to be present at birth; see Cordelia Fine's book Delusions of Gender for a lot more about these ideas' ubiquity and the still-ambiguous nature of the evidence they're supposed to be grounded in).

Right now, I want to talk about how this idea has gotten established in two different subcultures to which I belong: the autism community* and the gay community.

Autism and homosexuality have somewhat similar recent histories in US culture: both either are, or have been, considered mental disorders, both were thought in the 1950s and early '60s to be caused by some warping of the normal bond between mother and child (either, as with autism, too much distance between them, or with male homosexuality, not enough), and papers from the 1960s, '70s and '80s document various attempts to "treat," with aversion therapies that would now be considered abusive, children showing signs of either one. (One researcher even worked on both projects: O. Ivar Lovaas, who has done famous, if controversial, work adapting Applied Behavior Analysis (ABA) for use with autistic children, has also co-written several articles about "feminine boys," and using ABA to normalize their behavior).

Homosexuality was removed from the DSM in 1973, but there are still people who consider it (or anything deviating from straight, married monogamy, really) a pathological condition, and therapists who specialize in trying to turn gay people straight.

In contrast to that idea --- that gay people can change, and therefore should change --- the gay-rights movement has embraced the idea that sexual orientation is inborn. (And most mental-health professionals, including groups like the American Psychological Association, the American Psychiatric Association, the American Counseling Association, the National Association of Social Workers, and the American Medical Association, pretty much agree with them that no sexual orientation is inherently pathological, and that you can't change a person's sexual orientation through therapy).

The picture is somewhat different for autistic people. Not only is autism still considered a disease, and a pretty serious one, by almost everybody, but the idea of innateness, when it comes to autism, doesn't have the same implied corollary of "... and therefore you should accept us the way we are" that it has in reference to sexuality.

No, the shift from "psychogenic" to "biogenic" theories of autism happened for two reasons: first, and probably most important, the evidence (what little there was in the early '60s) didn't fit well with the psychogenic model**, and fit better with the biogenic one; another factor was activism by parents, who were fed up with being blamed for their children's condition, and who called for more research into potential biological causes.

Here, Boston University law professor Daniela Caruso, who has written an article on the history and legal impact of autism advocacy in the US, describes the relationship between the nascent field of biomedical research into autism and the beginnings of the US's major autism-advocacy groups:

It was only in 1964 that Bernard Rimland put forth an alternative explanation of the syndrome, based not on psychodynamics but rather on neurobiology. In 1965, Rimland founded the American Society for Autism (ASA) which is, to this day, a major center of advocacy.

Following Rimland's work, activism in the name of autism began to flourish thanks to both grassroots efforts and power houses. Some groups - most visibly Cure Autism Now (CAN) and the National Alliance for Autism Research (NAAR) - coalesced around genetic research and investigation of toxic substances potentially related to the surge of autism. It is no coincidence that such movements emerged in a context of burgeoning environmental activism. Many other capillary initiatives focused instead on the reality of living with autism by developing information centers for parents of newly diagnosed children, and starting awareness campaigns aimed at educating the public about this poorly-understood phenomenon.

(See also: this post, which discusses another article on the history of autism advocacy in the US. I also found another recent article about the role of parent activism throughout the history of autism, but I can't get at the full text of it).

I also found this snippet in Rimland's book itself (that part of it I could see on the Internet, anyway; I don't own the book), discussing why he thought so many researchers were reluctant to consider the possibility that autism had a biological basis:

In discussing the obvious prejudice against the hereditary viewpoint, Nolan Lewis (1954) points out, "It would seem that most of the prejudice against genetic inheritance stems from a feeling in the realm of wish fulfillment, based on the idea that acceptance of genetic factors would create an attitude of therapeutic hopelessness." Williams (1956) cites this point among others in his attempt to penetrate the prejudice against heredity. He notes that hopelessness is by no means justified by the evidence, and cites the ready correction of diabetes, phenylketonuria and hypothyroidism as examples.

So, that's kind of interesting --- that, at the outset, there was reluctance to adopt a conception of autism as innate and biologically based because of worries that that might mean it was impossible to eradicate through treatment --- but the answer to that wasn't, "so let's not try to make them non-autistic, let's just try to integrate them into society to the best of our, and their, ability", it was "don't be silly, of course we can make them non-autistic!"

I'd also want to point out that the two competing narratives of autism came from the same source: medical professionals, whether psychoanalysts or biomedical researchers. This is in contrast to the two competing narratives of homosexuality, one of which came from medical professionals and the other of which came straight (heh) from the people they were trying to describe. It wasn't until much later that autistic people's own viewpoints were even known to exist, much less taken into account by medical professionals and policymakers.

So, while as far as I know most autistic people do think they were born autistic, that idea doesn't have the same liberatory subtext for autism that it has for sexual orientation. (Indeed, the switch over to a mainstream view of autism as innate and biologically based had already happened when research into "extinguishing" autistic behaviors was at its peak.) The biggest thing it did was to free parents from guilt at having caused the autism, which is important and was definitely needed, but it left the position of the autistic people themselves unchanged.

*I'm using that phrase --- instead of "the autistic community" --- because I am mostly talking about parents. I've made this distinction before: the autism community, which includes parents/caregivers, healthcare workers, autism researchers, and educators; and the autistic community, which is the autistic people themselves. Sometimes the latter group is included in the former, but mostly it is not, and sometimes the two groups are at odds with each other.

**See Chapter 3 of Rimland's 1964 book, Infantile Autism, for a discussion of what those findings were and how they conflicted with the psychogenic model of autism.

More Autistic Strengths: Symmetry-Spotting

2011-08-16T23:43:00.002-05:00

EXECUTIVE SUMMARY: A recent study has added to the list of cognitive strengths peculiar to autism: in this study, a group of autistic teens/young adults and a group of age-, IQ-, sex- and eyesight-matched control subjects were shown a series of paired images, all of them different arrangements of lots and lots of tiny black-and-white dots, and determine which of the two images has some of the dots arranged in a symmetric pattern. Consistently, the autistic young people were able to pick out the symmetrical images at lower signal-to-noise ratios (i.e., with smaller proportions of the dots possessing mirror images) than their non-autistic peers.
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Michelle Dawson and Laurent Mottron have done lots of research on perception and cognition in autism --- particularly visual processing. (Morton Ann Gernsbacher is another frequent collaborator, but she didn't participate in the research I'm about to describe).

Their research has identified several cognitive strengths* specific to autism: enhanced sensitivity to pitch; enhanced sensitivity to, and recall of, details (without any corresponding loss of ability to see the big picture); ability to switch between different strategies (big-picture vs. small details) as needed; . Autistic people also do a lot better on one particular IQ test, Raven's Progressive Matrices, than you would predict based on their scores on other IQ tests (e.g., various Wechsler tests).

A new skill has just been added to this constellation: the ability to quickly determine whether a complex pattern is symmetrical or not.

In a study published this past spring in PLoS ONE, a group of Canadian researchers --- Mottron and Dawson, along with three others: Audrey Perreault, Rick Gurnsey and Armando Bertone --- had participants look at very complicated, visually "busy" patterns of small dots arranged on a video screen and determine, in the very short time the pattern remained onscreen (250 milliseconds), whether it was symmetrical or not. (They were shown two different patterns, one symmetrical and one not, and they had to identify the symmetrical one.)

Here's an example of the kind of image they would have to categorize:
(If it looks obvious to you, remember they only got a fraction of a second to look at it!)

The images were all just black and white, except for the one colored dot in the center, where the participants were told to focus their attention. In the above image, which is 100% symmetrical, each dot has a twin, the same size and color, placed so that they would lie one on top of the other if you printed the image out and folded it along its axis of symmetry. In that image, you can see that the vertical axis is the axis of symmetry; some images are symmetrical along the horizontal axis, and others are symmetrical along an oblique axis, the line y = x in a Cartesian coordinate plane with the colored dot at the origin.

These shapes are symmetrical about the horizontal (x) axis:
These shapes are symmetrical about the vertical (y) axis:

The pink and green curves are symmetrical to each other about the line y = x (blue)

Some of the images were also only partially made up of symmetrically-paired dots; the study participants were supposed to identify which of the two images shown to them had any degree of symmetry at all. (It was always just one; I guess you could design an experiment where both of the images had some degree of symmetry and the participants had to determine in which the degree of symmetry was greater, but that would be harder than just picking out which one had any degree of symmetry at all.)

The two groups whose performance was compared in this study were a group of 14** autistic young people (ages 14 to 35) and 15 typically-developing young men matched with the autistic subjects for age, IQ and visual acuity.

The criterion used to compare the two groups was "symmetry detection threshold", or the proportion of dots in a symmetrical design that had to have mirror images before a given person could identify the symmetrical design 75% of the time. Average detection thresholds were compared across groups, and also across what type of symmetry the image displayed. Both groups did best at spotting symmetry along a vertical axis, and both groups did the worst at spotting it across the line y = x.

But for all of these conditions, the autistic people had lower detection thresholds --- they correctly found symmetry more often in patterns that had less of it, relative to background noise --- than their non-autistic peers.

The study authors see this as indicative of our (autistic people's) ability to look at things more than one way simultaneously. (Another recent study, not referenced in this one, also found something suggestive of that: autistic people were better able to reproduce "ambiguous figures," or line drawings that look like they could be one of two things, depending on how you look at them). They also see their results as incompatible with the "weak central coherence" theory of autism, which explains our relatively keen collective eye for detail as a deficit in big-picture thinking. But this symmetry-spotting task requires both processes at once --- local-level, small detail perception for checking individual dot pairs to see if they really are exactly symmetrical, and also larger-scale, "gestalt" perception of whole shapes created by all the dots together.

Perreault, A., Gurnsey, R., Dawson, M., Mottron, L., & Bertone, A. (2011). Increased Sensitivity to Mirror Symmetry in Autism PLoS ONE, 6 (4) DOI: 10.1371/journal.pone.0019519

*Other, earlier research has also identified autistic strengths: as early as 1983, Amitta Shah and Uta Frith discovered that autistic children did especially well at disembedding figures; those two researchers were also the ones who identified the other really well-known "islet of ability", in the Block Designsection on various IQ tests.

**There were originally 17 people in that group, but three of them couldn't do the experimental task, so they did not contribute any data.

A Fun Fact About Leo Kanner

2011-08-15T14:26:00.001-05:00

I just started reading Roy Richard Grinker's book Unstrange Minds: Remapping the World of Autism, and in a chapter on the early history of autism (covering Kanner and Asperger, plus Eugen Bleuler's and Sigmund Freud's use of the term "autistic" to describe aspects of other conditions, and also stories of feral children, whom Grinker believes were probably autistic), I came across this anecdote:

In 1943, a New York psychoanalyst named Abram Blau wrote a paper in which he argued that whereas there were numerous words, proper and slang, for the penis, there were few words, and virtually no slang words, for the analogous organ in women, the clitoris. Based on this assumption, Blau made grand arguments about the universal symbolic importance of the penis to humanity. Kanner, as evidence-based as anyone in psychiatry at that time, was furious about Blau's assumption, based on no data collection at all, and quickly wrote a paper with the dry title "A Philological Note on Sex Organ Nomenclature," which he published in a psychoanalytic journal. In it, Kanner listed dozens of words for the clitoris, from languages all over the world, and all of them, he claimed, from memory. He destroyed Blau's argument.

Grinker included it to illustrate Kanner's prodigious memory, which Grinker believes was one of the "subclinical," autistic-like traits Kanner possessed that may have given him insight into the inner lives of the children he studied.

I'm posting it here because I think it's funny. Male psychoanalysts and their penis fixations never cease to amuse me.

(Unfortunately, the only copy of the article I can find online is here, with the full text only accessible to subscribers to that website. So I can't find any of the words Kanner listed, which is annoying.)

Cat Pic of the [variable time period]

2011-08-13T14:22:00.003-05:00

(Can you spot Ben, the gray tabby, in this picture?)

I just finished this necklace, and was photographing it for listing on Etsy this morning. Ben was very interested in those proceedings, and decided he had to take part in them, too.

British Neuroscientist Thinks the Internet Is Rewiring Our Brains

2011-08-09T15:47:00.011-05:00

A famous British neuroscientist and popular-science writer, the Baroness Susan Greenfield, who is a Professor of Synaptic Pharmacology at Lincoln College, Oxford, a member of the House of Lords, and until recently was the Director of the Royal Institution of Great Britain, has suggested that widespread Internet use might have something to do with the increasing prevalence of autism.

Here she is, quoted in an article in the Guardian:

"It could be the case that this different environment is changing the brain in an unprecedented way. It's such an important issue and I'm just putting it before people to discuss." Greenfield said there was a need for work to be done, but measuring subtle changes in the brain was extremely difficult. She cited an article in Scientific American that showed US teenagers may be losing their ability to feel empathy. "When you are social networking online and not learning how to connect face to face or how to hug, not out there rehearsing those things, then could that mean a child goes on to exhibit autistic-like behaviour?"

"I point to the increase in autism and I point to internet use. That's all. Establishing a causal relationship is very hard but there are trends out there that we must think about. I have not said that internet use causes autism and I would apologise to any family who is upset by anything I have said."

She added: "I have never, ever said that the internet is bad for the brain. But if the environment is changing, then the brain will change to adapt. All I have ever said is, let's talk about this. The internet has become the central, iconic feature of young people's lives and to say our brains will not be affected by that is to deny our evolutionary heritage."

Asked in this interview with New Scientist for any evidence supporting this hypothesis, she cites two studies: this one describing differences in brain anatomy between healthy and Internet-addicted Chinese university students, and this review (full text here) of the psychological and neurological literature on the effects of various electronic media.

She also cited this article, mentioned in this Scientific American podcast, which is a meta-analysis of 72 studies of empathy in American college students, all conducted between 1979 and 2009, and all using the same measure of empathy: the Interpersonal Reactivity Index. I will talk about that study in another post; for now, I'd like to focus on the Internet-addiction study.)

The Chinese study used diffusion tensor imaging (a type of magnetic resonance imaging that measures the movement of water molecules along a tract of fibrous tissue and uses the three-dimensional vectors, or tensors, describing the water molecule's motion to build a three-dimensional computer model of the tissue) to look for differences in gray-matter volume and white-matter structure between two groups of eighteen young people (twelve young men and six young women in each group), one consisting of people meeting diagnostic criteria for Internet addiction (using the Young Diagnostic Questionnaire for Internet addiction), and the other consisting of healthy, age- and sex-matched control subjects who said they used the Internet for less than two hours per day.
(Figure 1A, in Yuan et al., 2011 - orange blotches represent brain regions where the 18 Internet-addicted young people in this study had less gray matter than non-addicted people of the same age and sex)

They found that the Internet-addicted people had less gray matter, on average, than the non-Internet-addicted people in a few areas: the dorsolateral prefrontal cortex (i.e., the part of the prefrontal cortex that's on top and to the sides), the rostral anterior cingulate cortex (on the left side only), the orbitofrontal cortex, the cerebellum and the supplementary motor area straddling the boundary between the frontal and parietal lobes. For a few of these areas (the left anterior cingulate, the right dorsolateral prefrontal cortex, and the right supplementary motor area), the degree of atrophy correlated with how long the person had been addicted --- i.e., the longer they'd been addicted, the smaller those brain areas would be.

They also found differences in white-matter distribution between the two groups in two regions: the left posterior limb of the internal capsule and the right parahippocampal gyrus.
(Figure 2, in Yuan et al., 2011 - top series of images show major white-matter tracts in study participants' brains; image (b) gives a side view of the brain and shows an area in blue where Internet-addicted subjects are thought to have less white matter than control subjects; image (c) shows an area in orange where the Internet-addicted subjects are thought to have more white matter than controls. Bottom graph shows the relationship between their measure of white-matter density, taken at the blue area, and the duration of individual study participants' Internet addictions.)

The measure they used, fractional anisotropy, reflects the degree to which the diffusion of water is constrained by the presence of linear fibers. If there were nothing there, water molecules would diffuse outward in a sphere; the degree to which the diffusion pattern deviates from a perfect sphere, and the direction in which the most diffusion occurs, give you an idea of where the fibers are and how many of them there are.

This short, but very technical, article describes how this measure is typically used in neuroimaging studies*:

Much progress has been made in modeling more complex diffusion geometries that a single tensor fails to model, but most clinical studies still rely on simple [diffusion tensor imaging]-derived scalar measures. Some of these, such as the trace of the covariance matrix or mean diffusivity (MD) can adequately describe isotropic water diffusion, but this only occurs in the cerebrospinal fluid spaces of the brain. In the white matter, myelinated fibers resist water diffusion orthogonal to the local dominant fiber orientation, and diffusion occurs preferentially along local fiber tracts. In clinical research, white matter fiber integrity is commonly assessed by determining how strongly diffusion is directionally constrained. One common scalar measure of directional diffusion, the fractional anisotropy (FA), is computed from the diffusion tensor's eigenvalues, and quantifies the magnitude of this directional preference. Clinical studies now routinely use FA as an index of white matter integrity, sensitive to white matter deterioration in aging and neurodegenerative diseases.

Using this explanation of what fractional anisotropy values are understood to mean --- higher numbers mean more diffusion occurring in the same direction, which is taken to mean that fibers running in that direction are numerous and thick; lower numbers imply fewer and/or thinner fibers --- you can see that the researchers are saying they think their Internet-addicted subjects have less white matter (lower FA value) than their non-addicted subjects in the parahippocampal gyrus, and also more white matter (higher FA value) in the left posterior limb of the internal capsule.

The researchers believe that these changes are a result of the Internet addiction, although they can't totally rule out the possibility that they existed before the onset of addiction, and may actually have been part of the reason those young people were susceptible to addiction in the first place. In favor of their brain-changes-as-effect-of-Internet-addiction model, they cite the positive correlations they found between several of the changes they found (decreased gray matter in the left anterior cingulate, right dorsolateral prefrontal cortex, and right supplementary motor area, along with increased white matter in the left posterior limb of the internal capsule) and duration of Internet addiction. But not all of the changes showed such a correlation --- less than half, to be exact.

When you take into account brain lateralization, you come up with eleven areas that differed between groups: four of the five regions showing loss of gray matter were affected on both sides, for a total of eight affected areas, plus one more (the left anterior cingulate) and the two regions showing white-matter changes (both confined to one side of the brain). That gives you only four out of eleven affected regions where the change showed any relationship to how long the person had been addicted; if the relation to time was meaningful, you'd expect it to show up more consistently. As is, it leaves open the possibility that whatever correlations were observed are just statistical noise.

Does extensive Internet use physically change the brain? It's certainly possible, given what we know about neuroplasticity, but this study doesn't shed a whole lot of light on it. Its design makes it impossible to know whether the brain differences observed between Internet-addicted and non-addicted students were effects or potential causes of Internet addiction.

Even granting that possibility (that extensive Internet use can, over time, remodel an Internet user's brain), though, it's still very, very unlikely that there's any connection between widespread Internet use and increasing prevalence of autism. The timing is wrong, for one thing --- most autism diagnoses are given in early childhood, and a lot of parents begin to ask questions and look into it when their child is an infant or toddler. Given the text-based nature of the Internet, it is highly unlikely that pre-literate children are doing a lot of web surfing on their own.

For more about this weirdness, see Neuroskeptic, Jon Brock, Dorothy Bishop, Neuroskeptic again, and this hilarious website riffing on Greenfield's gnomic comment "I point to the increase in autism and I point to the Internet. That's all."

*The article also criticizes the measure as being too vague, and not a very good predictor of actual fiber density and location. It describes an alternative measure that the authors consider more accurate.

Yuan, K., Qin, W., Wang, G., Zeng, F., Zhao, L., Yang, X., Liu, P., Liu, J., Sun, J., von Deneen, K., Gong, Q., Liu, Y., & Tian, J. (2011). Microstructure Abnormalities in Adolescents with Internet Addiction Disorder PLoS ONE, 6 (6) DOI: 10.1371/journal.pone.0020708

Readers, Help Me Name Things!

2011-08-04T23:19:00.004-05:00

Etsy has just added a new way to describe the things you've made to make it easier for people to find them; you choose a "style" that describes the general look of whatever it is you've made.

I like this idea, in theory: anything that will maximize my item's chances of showing up in a search is fine with me!

The only problem is, I have no idea what most of the labels mean. (Sometimes I might have a general idea, or know what it means in one area --- like, say, Art Deco architecture --- but have no idea how that same style translates into another area, like, say, jewelry.)
(One of my favorite bracelets of this type: 5-7 strands of one color of seed beads strung through a series of vertical spacer bars woven out of another, contrasting color of seed beads, with a large focal bead set off by a rectangular frame. This one is indigo/blue-green, with the focal bead made of dichroic glass.)(This bracelet is made from the same general pattern; it's grass-green/golden-yellow for its color scheme, though. I also have this in purple).
(Necklace made along the same lines --- multiple strands of dark red beads threaded through a whole bunch of round beads in square frames woven from beads in contrasting colors. This is one of my favorite necklaces!)

So I'm going to ask you, the readers of this blog --- or those of you who, unlike me, have a working knowledge of art history --- to comment and tell me what art-history/fashion terms they think might pertain to the things I have pictured in this post.
(One of those weird things I am not sure what to call. I love these, but the two names I've seen for them --- "handflower" and "slave bracelet" --- strike me as, respectively, dorky and creepy.)

(Another one!)
(One more!)
(Another recurring pattern: bracelets/necklaces with ribbed panels woven of alternating, vertical columns of seed beads and bugle beads, in different shades of the same color. I have necklaces in blue, blue/black, and green, and bracelets in purple, green and blue/black)
(I've also got a couple necklaces where the focal elements are arranged asymmetrically --- all clustered to one side)

(For the curious, here's the list of labels they suggest you choose from: Abstract, African (yeah ... European art gets all these very specific terms denoting style and historical period; all African art just gets lumped together indiscriminately), Art Deco, Art Nouveau, Asian (d'oh!), Athletic, Avant Garde, Boho, Burlesque, Country and Western, Edwardian, Fantasy, Folk, Goth, High Fashion, Hip Hop, Hippie, Hipster, Historical, Hollywood Regency, Industrial, Kawaii, Kitsch, Mediterranean, Mid-Century, Military, Minimalist, Mod, Modern, Nautical, Neoclassical, Preppy, Primitive, Regency, Renaissance, Resort, Retro, Rocker, Rustic, Sci-Fi, Shabby Chic, Southwestern, Spooky, Steampunk, Techie, Traditional, Tribal, Victorian, Waldorf, Woodland, Zen. You can also add others, but I'm too confused by all of this to try that. Besides, all the words I know that denote a certain style or subculture are obviously inapplicable to my work).

Women in Comics

2011-07-31T15:44:00.004-05:00

Comics fan Elliott Brown recently posted a short article on Change.org criticizing DC Comics for putting its "New 52" universe-wide reboot almost exclusively in the hands of male writers and artists:

The number of women working for DC has been hovering around 10% for years -- similar to their adversary company, Marvel. But this September, DC will be rebooting its universe and giving its characters (and creative teams) an overhaul. Many of the characters that will be erased are female, which in and of itself is a tragedy, but in addition to that, what few female creators DC has employed will also be cut from the team. Only 2 out of 100-odd people DC employs as ongoing creators will be women: Gail Simone, who will be writing Batgirl, and Amy Reeder, who will be doing pencils on Batwoman.

That tally immediately made me wonder exactly how many women were currently writing or drawing for Marvel, and on which titles.

(I don't shun DC or anything --- I love, or am interested in, quite a few things they've done, especially under their "mature" label, Vertigo. And they've given us that classic of modern comics, Watchmen! But most of the comics I own are Marvel --- I'm an X-Men fan, and the X-Men have been around a lot longer, and racked up a lot more back issues, than most of what else I read.)

Anyway, Marvel isn't having any similar across-the-board relaunch, so it's going to be a bit harder to track down all of their series that are still going concerns.

Here's a list of recently- and soon-to-be-released titles featuring women writers and/or artists:

Emma (a serialized adaptation of the Jane Austen novel of the same name) - written by Nancy Butler and drawn by Janet K. Lee

X-23 - written by Marjorie M. Liu; #'s 3, 7, 10, 11 and 12 drawn by Sana Takeda

Ultimate Fallout - #'s 2, 4 and 5 drawn by a team of artists including Sara Pichelli

The Iron Age - # 2 co-written by Jen Van Meter; #3 co-written by Louise Simonson, cover art by Jelena Kevic Djurdjevic

Hulk - #'s 37 and 38 drawn by Elena Casagrande

Fear Itself: The Worthy - cover art on #1 by Jelena Kevic Djurdjevic

Amazing Spider-Man - variant cover for #667 drawn by Stephanie Hans

Mystic - cover art on #1 by Amanda Conner

X-Factor - #'s 209, 214, 215, 216, 217, 218, 219, 221, 223 and 224 drawn by Emanuela Lupacchino

Spider-Girl - cover art on #8 by Jelena Kevic Djurdjevic

Spider-Island: Cloak & Dagger - drawn by Emma Rios

Anita Blake: Circus of the Damned (an adaptation of Laurell K. Hamilton's novel Circus of the Damned) - written by Laurell K. Hamilton and Jessica Ruffner

Journey Into Mystery - #626 drawn by Stephanie Hans

That's thirteen titles out of 250 putting out new issues in July and August; what's more, only about half of them appear to have women artists involved in whole projects rather than just coming in to do a cover, or to pencil one or two issues in the regular artist's absence.

(Just doing covers, or hopping from series to series doing single issues here and there, isn't a bad thing --- some artists might even prefer it. For instance, Jelena Kevic Djurdjevic seems to specialize in covers. I just bemoan the fact that so few women are involved long-term because that means their creative visions are less likely to make a lasting impact on a series, or to shape the way characters and events develop.)

Terrorist Attacks in Norway

2011-07-23T14:54:00.003-05:00

There's just been a terrible eruption of political violence in Norway: in the capital, Oslo, a car bomb exploded outside the office building that housed the prime minster's office, and also near other Norwegian government buildings, including its finance ministry, oil minostry and Supreme Court. Shortly after the bomb exploded, a man dressed as a police officer and armed with automatic weapons appeared on the island of Utoya, in a lake near Oslo, where an offshoot of the Norwegian Labor Party holds a summer camp for teenagers and young adults interested in politics, coaxed the campers to come toward him, and shot them as they came. He killed at least 84 people on the island, and is believed also to have planted the bomb in Oslo, which killed seven people and injured about ten.

A suspect, Anders Behring Breivik, has surrendered to the police and is being investigated. He was a fundamentalist Christian, interested in right-wing politics and hated Muslims, and he was also a member of Norway's far-right, anti-immigrant Progress Party, at one point being chairman of his local party. He had bought six tons of synthetic fertilizer ten weeks prior to these events, ostensibly for use on his farm.

A survivor of the attack on the island, Prableen Kaur, who is the head of the Worker's Youth League of her district in Oslo, has written a blog post describing her ordeal. The post has been translated into English and republished several places around the Web, including the UK's Daily Telegraph website.

I don't know if I have any Norwegian readers, but if I do, I hope you're all safe, and that everyone you know is safe. My deepest sympathies are with you; we in the U.S. are no strangers to terrorism, foreign or domestic, and we wouldn't wish it on anyone.

Autism-Related Gene Spotlight: MECP2

2011-07-17T22:10:00.002-05:00

Where is it?
Near the very end of the X chromosome, at Xq28.
Here is a picture of its position relative to some other genes at that part of the X chromosome:
You can see that it's not the last gene on there, and there are quite a few known and potential genes following it, but it's really, really close to the end. That picture I just posted? With MECP2 appearing at the far left? That's the very end of a 24-page image. So, based on that I feel comfortable calling MECP2 one of the last genes on the X chromosome.

What does it do?
It encodes a protein, MeCP2, that can bind to methylated DNA (and also to a variety of other transcription-repressing proteins) and whose function is to repress transcription of its target genes. (More recent research has also found that it can also serve as a transcriptional activator). It has a lot of target genes, and their functions vary widely; many of them are other transcription factors, and many are involved in cell-cell signaling, or in signal transduction within the cell. Overall, transcription and neurotransmission seem to be the physiological processes that the majority of MeCP2 target genes are involved with, though it is also important for nerve and muscle cell growth (and thus, needs to be expressed in different amounts at different times during development). It is highly expressed in nerve cells. It's also been found to have other functions, like RNA splicing, chromatin remodeling and DNA methylation.

What mutant versions of this gene have been discovered?
(Here's a very rough impression of where some of the more common mutations (and some less-common ones that I talk about in the next section) associated with Rett syndrome fall on a map of MECP2 coding regions. Mutations that only change an amino acid are outlined in different shades of red-orange; mutations that produce a truncated version of the MeCP2 protein are outlined in black, and indicated on the map with little stop signs. Image not drawn to scale)

This 1999 article in Nature Genetics (full text here) describes a genetic analysis of 29 girls with Rett syndrome* (8 of whom had a family history of the condition), which found seven point mutations (changes in a single nucleotide) and one case where an extra nucleotide (thymine) was inserted into the gene, which threw off the "reading" of everything that came after, since protein synthesis depends on grouping the nucleotides into threes, and stringing together the amino acids corresponding to each sequence of three nucleotides, or "codons". Changing one nucleotide to another will therefore change one amino acid in the resulting protein, while adding or subtracting a nucleotide will change every amino acid that follows. (Such "frameshift" mutations are much more likely than point mutations to result in a nonfunctional protein).

They were: a substitution of cytosine for thymine at nucleotide #538; substitutions of thymine for cytosine at nucleotides #390, #471, #547, #656, #837, and #1307; and the aforementioned insertion of (an extra) thymine between nucleotides #694 and #695.

Another genetic analysis described in a 2000 article in Human Molecular Genetics found 17 different mutations in 46 girls with Rett syndrome; these mutations included substitutions of thymine for cytosine at nucleotides #473, #502, #763, #808, #880, and #916; substitutions of guanine for cytosine at nucleotides #905 and #1038; a substitution of thymine for adenine at nucleotide #592; a substitution of cytosine for adenine at nucleotide #1461; a substitution of adenine for guanine at nucleotide #317; and a ten-nucleotide deletion starting at nucleotide #1158. Most of these mutations were in exon 3, though there were a few in exons 2 and 4 as well.

A 2004 analysis of DNA samples from 56 French women and girls with Rett syndrome found five frameshift mutations: a deletion of nucleotide #345, in exon 3; a deletion 202 nucleotides long, starting at position #895; another deletion 53 nucleotides long starting at position #1124; a deletion of 8 nucleotides and an insertion of 18 nucleotides starting at position #989; and an insertion of an AG dinucleotide after nucleotide #996. All of these last four were in exon 4.

An article from this year describes a 41-base deletion in a Korean girl with Rett syndrome; the deleted region started at nucleotide #1152, in exon 4.

Another article from this year found a substitution of thymine for cytosine at nucleotide #535 in a Tunisian girl with Rett syndrome.

This article (full text here) describes 17 mutations: a substitution of thymine for guanine at nucleotide #298; a substitution of adenine for guanine at nucleotide #398; a substitution of guanine for adenine at nucleotide #914; a substitution of thymine for cytosine at nucleotide #730; an insertion of (an extra) guanine after nucleotide #704; an insertion of cytosine after nucleotide #747; and multiple deletions, most of which had starting points between nucleotides 1,000 and 1,200, and all but one of which were deletions of multiple nucleotides. There was also a sequence of 137 nucleotides, starting at position #1169, that was repeated.

This 2009 genomic analysis of 74 people with Rett syndrome in New Zealand turned up four new mutations, including a fairly large deletion (1,596 nucleotides) that encompassed both exons 3 and 4.

There are a lot more --- the International Rett Syndrome Foundation's database of mutations associated with Rett syndrome (RettBASE) lists 4,225 different mutations. Not all of them are in MECP2, but a large majority of them are.

Mutations in MECP2 can also be associated with conditions other than Rett syndrome: this article describes mutations found in five children with Angelman syndrome. Two of them had deletions in exon 4, one had a two-nucleotide deletion in exon 3, and the others had single-base substitutions.

How do these mutations affect protein function?
The MeCP2 protein has two regions (called domains) that are crucial to its function in the cell: the methyl-DNA binding domain (MBD), which allows it to bind to methylated cytosines, and the transcription repression domain (TRD), which binds to other enzymes that condense chromosomal DNA and make it impossible for the enzymes reponsible for transcription to bind to it. MeCP2's role in transcription repression seems to be to bring the enzymes that do the actual repressing to its target sequences of DNA, rather than to block transcription itself.
(Image of the structure of the MeCP2 methylDNA-binding domain, showing the amino acids affected by some of the more common mutations)

The MECP2 gene has four exons, of which three contain sequences encoding these domains: Exon 2 encodes most of the DNA-binding domain, with some of it spilling over into exon 3, and parts of exons 3 and 4 encode the transcription repressor domain. So, depending on where it occurs in the gene, a mutation might disrupt either the MeCP2 protein's DNA-binding capacity, or its ability to bind to those other, transcription-repressing enzymes.

Most of the mutations associated with Rett syndrome (or other conditions mentioned in the above section) change the structure of one of those domains in such a way as to weaken, or completely destroy, its ability to bind to whatever it needs to bind to. This article describes the effect on DNA binding ability of several known mutations (including a few of the most common ones) that alter the amino-acid sequence of the MBD. The mutation with the greatest effect on MeCP2's DNA-binding ability, p.R111G, swaps out a positively-charged amino acid on the long, flexible loop within the MBD for a nonpolar one; since that loop normally lies close to the sugar-and-phosphate "backbone" of the DNA (the part of the DNA to which the A's, T's, G's and C's all attach, and which forms the two outer ridges of the double helix), and since that backbone carries a negative charge (from all the phosphate groups), knocking out positively-charged amino acids in this region will disrupt the attraction between the DNA and the methylDNA-binding region of MeCP2.

Another mutation that can cause a sharp decline in DNA-binding ability, which also happens to be one of the most commonly-occurring mutations in people with Rett syndrome, is p.R133C, which also replaces a positively-charged amino acid with a nonpolar one. This one occurs in a different part of the MBD than p.R111G does, a "beta sheet" made up of long, flat strings of amino acids laid side by side. One of the short loops connecting two of the component strands has a sequence of five amino acids with hydrophobic side chains that create a "pocket" sequestering the methyl groups attached to the DNA. It may not always lead to loss of function, though; this group of mostly Japanese researchers conducted a similar analysis (full text here) of protein function, comparing some of the most common mutant versions of MeCP2 with its normal, "wild-type" form, and they found that the R133C variant bound to DNA almost as readily as the wild-type MeCP2 did.

Other mutations associated with a near-total loss of DNA-binding ability are p.G114P, which replaces an amino acid in the middle of the long, flexible loop described above with one whose rigidly-structured, bulkier sidechain would greatly restrict the loop's ability to move and re-fold itself to fit into the groove of the DNA helix; p.D121A and p.D121E, which substitute amino acids with, respectively, nonpolar and negatively-charged sidechains for one with a positively-charged sidechain on one of the strands of the beta-sheet comprising another of the MBD's DNA-contacting surfaces; two other fairly common mutations, p.R106W and p.F155S, throw off the protein's overall folding to such an extent that it becomes unstable at body temperature.

Several mutations cause transcription of MECP2 to stop prematurely, leading to the production of an incomplete protein. Depending on where the erroneous "stop" signal occurs, the resulting protein might be missing all or part of its transcription-repressor domain.

Mutations occurring downstream of the transcription-repressor domain have also been associated with problems; this experiment showed that mutant versions of MeCP2 that don't have the long tail following the TRD are less stable than wild-type MeCP2, and tend to break down quickly in the cellular environment.

How common are they?
This article in the European Journal of Human Genetics lists eight MECP2 mutations its authors consider "common," along with each mutation's prevalence among the people with Rett syndrome listed in either the British Isles Rett Survey or the Australian Rett Syndrome Database. Of the 524 cases they looked at, 65 (12.8%) had the mutation p.T158M, which is the substitution of thymine for cytosine at nucleotide #473; 58 (11.1%) had the mutation p.R168X, which is the substitution of thymine for cytosine at nucleotide #502; 44 (8.4%) had the mutation p.R270X, which is the substitution of thymine for cytosine at nucleotide #808; and 42 (8%) had the mutation p.R255X, which is the substitution of thymine for cytosine at nucleotide #763. The other four mutations listed as "common" in this paper --- p.R106W (thymine substituted for cytosine at nucleotide 316), p.R133C (thymine for cytosine at nucleotide 397), p.R294X (thymine for cytosine at nucleotide 880) and p.R306C (thymine for cytosine at nucleotide 916) all account for between 3 and 7 percent of all cases surveyed.

Another article (full text here) also found those eight mutations occurred several times in their sample of 116 people with Rett syndrome; these researchers also found p.T158M to be the most common, present in 12 different people. (The next-most common ones were p.R270X, found in eight people, and p.R255X and p.R106W, each found in seven people). This study also listed three other mutations in its table of "recurring" mutations: a substitution of guanine for cytosine at nucleotide 455 (observed four times), a substitution of thymine for cytosine at nucleotide 965 (observed twice), and a modification of a splice site in exon 4 (an AG sequence becomes GG; this permutation was also observed only twice).

RettBASE also ranks the various mutations by frequency of occurrence: there, too, p.T158M is the most common, with 363 known occurrences and accounting for 8.59% of all mutations identified so far. Most of the mutations (about two-thirds) listed there are unique.

Rett syndrome occurs in between 1:10,000 and 1:22,000 girls, and has only been recorded in 20 boys, ever. (Usually if a boy is born with the kind of mutations that would lead to Rett syndrome in a girl, he dies). So when I say a given mutation is found in, say, 10% of all people with Rett syndrome, that would translate into between 1:100,000 and 1:220,000 for its frequency among all people. So, while some MECP2 mutations might be less rare than others, I'd say they're all rare.

Database entries for this gene: AutDB, Ensembl, Entrez Gene, GeneCards, Genetics Home Reference, WikiGenes

Sources:
Amir RE, Van den Veyver IB, Wan M, Tran CQ, Francke U, & Zoghbi HY (1999). Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2. Nature genetics, 23 (2), 185-188 PMID: 10508514

Bienvenu, T. (2000). MECP2 mutations account for most cases of typical forms of Rett syndrome Human Molecular Genetics, 9 (9), 1377-1384 DOI: 10.1093/hmg/9.9.1377

Bienvenu T, Souville I, Poirier K, Aquaviva C, Burglen L, Amiel J, Héron B, Kaminska A, Couvert P, Beldjord C, & Chelly J (2001). Five novel frameshift mutations in exon 3 and 4 of the MECP2 gene identified in Rett patients: Consequences for the molecular diagnosis strategy. Human mutation, 18 (3), 251-252 PMID: 11524737

Díaz de León-Guerrero, S., Pedraza-Alva, G., & Pérez-Martínez, L. (2011). In sickness and in health: the role of methyl-CpG binding protein 2 in the central nervous system European Journal of Neuroscience, 33 (9), 1563-1574 DOI: 10.1111/j.1460-9568.2011.07658.x

Fendri-Kriaa N, Hsairi I, Kifagi C, Ellouze E, Mkaouar-Rebai E, Triki C, Fakhfakh F, & The Tunisian network on mental retardation study (2011). A case of a Tunisian Rett patient with a novel double-mutation of the MECP2 gene. Biochemical and biophysical research communications, 409 (2), 270-274 PMID: 21575601

Free, Andrew, Robert I. D. Wakefield, Brian O. Smith, David T. F. Dryden, Paul N. Barlow, & Adrian P. Bird (2000). DNA Recognition by the Methyl-CpG Binding Domain of MeCP2 Journal of Biological Chemistry, 276 (5), 3353-3360 DOI: 10.1074/jbc.M007224200

Hite, K., Adams, V., & Hansen, J. (2009). Recent advances in MeCP2 structure and function Biochemistry and Cell Biology, 87 (1), 219-227 DOI: 10.1139/o08-115

Hoffbuhr K, Devaney JM, LaFleur B, Sirianni N, Scacheri C, Giron J, Schuette J, Innis J, Marino M, Philippart M, Narayanan V, Umansky R, Kronn D, Hoffman EP, & Naidu S (2001). MeCP2 mutations in children with and without the phenotype of Rett syndrome. Neurology, 56 (11), 1486-1495 PMID: 11402105

Kudo, S., Y. Nomura, M. Segawa, N. Fujita, M. Nakao, C. Schanen, & M. Tamura (2003). Heterogeneity in residual function of MeCP2 carrying missense mutations in the methyl CpG binding domain Journal of Medical Genetics, 40 (7), 487-493 DOI: 10.1136/jmg.40.7.487

Kumar, A., Kamboj, S., Malone, B., Kudo, S., Twiss, J., Czymmek, K., LaSalle, J., & Schanen, N. (2008). Analysis of protein domains and Rett syndrome mutations indicate that multiple regions influence chromatin-binding dynamics of the chromatin-associated protein MECP2 in vivo Journal of Cell Science, 121 (7), 1128-1137 DOI: 10.1242/jcs.016865

Lee EY, Chung HJ, Ki CS, Yoo JH, & Choi JR (2011). A novel mutation in the MECP2 gene in a Korean patient with Rett syndrome. Annals of clinical and laboratory science, 41 (1), 93-96 PMID: 21325263

Raizis AM, Saleem M, MacKay R, & George PM (2009). Spectrum of MECP2 mutations in New Zealand Rett syndrome patients. The New Zealand medical journal, 122 (1296), 21-28 PMID: 19652677

Singh, J., Saxena, A., Christodoulou, J., & Ravine, D. (2008). MECP2 genomic structure and function: insights from ENCODE Nucleic Acids Research, 36 (19), 6035-6047 DOI: 10.1093/nar/gkn591

Yusufzai, Timur M., & Wolffe, Alan P. (2000). Functional consequences of Rett syndrome mutations on human MeCP2 Nucleic Acids Research, 28 (21), 4172-4179 DOI: 10.1093/nar/28.21.4172

Rhetorical Uses of the Budget Deficit

2011-07-08T15:54:00.004-05:00

This might seem like small potatoes compared with everything else that's going on in Kansas now (which Shakesville has been chronicling), but it's a local story rather than statewide, and thus not going to get the same amount of coverage on the Internet as the Planned Parenthood defunding and the attempt to impose new regulations on abortion clinics, and I also think it's illustrative of a few things, so I'm going to write about it anyway.

The county commission of Johnson County, Kansas (where I live) has just accepted a $500,000 federal grant paying for abstinence-only sex education classes, but has refused the part of the grant subsidizing a more comprehensive sex-ed program (a series of videos) that emphasizes abstinence, contraception, condom use and basic sexual health, and is targeted at "at-risk" teenagers.

The comprehensive program was opposed by the anti-abortion activist group Kansans for Life, which says on its website that it suspects Planned Parenthood of being in some way involved in creating the videos:

One of the two programs --- the curriculum based on for 11-13 year olds, "Making a Difference," seems to be abstinence-based only ... . The one for "at risk" kids aged 13 to 19 revolves around a video named "What Could You Do?" (have a look HERE), which critics believe is inappropriate on its face because it includes a video that includes a couple in bed, has a heavy emphasis on condoms, and a segment with kids putting condoms on cucumbers.

... The point is that 'condom on cucumber' sex ed programs have long been the staple of Planned Parenthood. And, while the program for younger kids appears OK, and does show some effectiveness, is it possible for citizens to be assured that the Jo. Co. Department of Health, using our federal and perhaps state tax dollars, could or would be able to insure that those teaching the program don't use the opportunity to push Planned Parenthood or something similar?
...
... [W]e will be left with two alternatives. Either use all the grant money for the PREP program aimed at younger kids, with some kind of assurance that it will remain pure of Planned Parenthood or abortion influences or references, or ask that our commissioners once again reject this grant altogether.

(I always find it weird, the extent to which Planned Parenthood is seen as a boogeyman, a sort of Pied Piper of abortion, herding unwary girls and women by the score into its clinics. It's like a less overtly misogynistic version of that other widespread myth about abortion, the cartoonishly selfish woman who terminates pregnancies on a whim; only in this version it's the cartoonishly evil and predatory doctor who performs abortions on everyone who comes into his office, whether they want one or not. There also seems to be this idea that everything Planned Parenthood does, or oversees, is going to involve abortion. Which is not true --- most of what Planned Parenthood does has nothing to do with abortion; it's gynecological exams, testing and treatment for STDs, distributing contraception, help managing painful periods, or even giving prenatal care to pregnant women who want to have the baby!)

Kansans for Life's Executive Director, Mary Kay Culp, also brought up the national debt:

Culp and a few others cited the government's huge debt among the reasons for turning down the grant.

"We're borrowing money from China to put condoms on cucumbers," she said.

This is the part I mentioned at the beginning of the post, that I thought was "illustrative" of something. I've been noticing lately (and I haven't been the only one to notice) that concern about the nation's (or sometimes the state's) fiscal health seems to operate as a sort of rhetorical camouflage: when you couch your calls for all sorts of government programs and services to be eliminated in language of scarcity, or of a dire need for any and all cost-cutting measures, you make it harder to argue against them because the usual defense, "But [x] does a lot of good, and people need it!" doesn't refute "There is no money for [x]." If you want to refute that, you have to go a step further, and find a y that could be cut in x's place, yielding equal or greater savings. But usually the x's in this discussion are things that the people pulling the Deficit Gambit want to get rid of just because they don't agree with them philosophically, not because they constitute a serious drain on the budget.

(In this case, I think the Deficit Gambit is functioning a little differently since it is being used in addition to, rather than instead of, philosophical arguments. So I think its purpose is less to disguise the philosophical argument than it is to buttress it, especially to persuade people who might not accept any of the premises on which the philosophical argument is based).

"Zero Degrees of Empathy" Link Roundup

2011-07-04T15:47:00.001-05:00

I'm holding off until I've actually read Zero Degrees of Empathy (or, for the edition I'm most likely to get my hands on, The Science of Evil), but there are plenty of other people writing interesting things about it:

Lili Marlene, who lives in Australia and writes skeptically about psychology on her blog, Incorrect Pleasures, has written several posts about her thoughts on the book as she's been reading it.

Here they are in chronological order:
Just a little bit reductionist don't you think?
A very horrible story that can't be ignored
Mathematician's test score does not add up
A quick word or two regarding the Reading the Mind in the Eyes Test and the Austrian study
Professor Simon Baron-Cohen, empathy expert
Is this guy for real? Baron-Cohen's latest book is a real urban legend!

Indigo Jo has written a double review of Zero Degrees of Empathy and an earlier book on E-S Theory, The Essential Difference. (And Lisa Harney at Questioning Transphobia has enlarged on it; the comment thread on her post is also worth reading).

Rachel Cohen-Rottenberg has a very detailed post about empathy; she has also started a web-anthology of essays addressing myths about autistic people and our capacity for empathy.

On Tumblr (a platform which continues to confuse me, but which is apparently really popular), Emily posted at F*** Yeah Autism Spectrum: So I read the first chapter of Simon Baron-Cohen's new book

This Is Not a Review of "X-Men: First Class" ...

2011-06-26T21:20:00.000-05:00

... if you're looking for one of those, I can direct you to this one by Neil Kapit, a fellow X-fan and author of the webcomic "Ruby's World," who pretty much says what I would say if I were to review this film.

No, I'm going to focus on something much narrower about this movie: its depiction of Angel Salvadore, a relatively minor character in the comics and a supporting character in the film.

I was very surprised to see her in this movie, because 1) she's a very recent character, and wouldn't really belong in a story about the relationship between Professor X and Magneto as young men (not that that's stopped any of the previous movies, where characters from different generations of X-Men have always been thrown together willy-nilly), 2) none of the other characters*, or plotlines, she's involved with make any appearance in this movie, and 3) she's very unphotogenic. She's half-girl, half-fly, and her offensive weapon is super-acidic barf.

Here's what she looks like using that power in the comics:Gross, isn't it?

That's why I was so surprised, before seeing the movie, when I read that she'd be in it. Female characters in movies, especially in comic-book movies, action movies and other movies aimed at a teenage-boy audience, are primarily there as eye candy; when they're allowed to do cool stuff and look pretty it practically counts as a feminist victory, but the look-pretty requirement is not negotiable.

And there's no way to make disgusting green barf look pretty; hence my surprise.

It turns out I underestimated Hollywood's ability to pretty almost anything up: I can't find any video on YouTube that includes this, but when the younger mutants are all showing each other their powers and picking out their X-Men codenames, Angel demonstrates something that looks nothing at all like what's pictured above. She strikes a pose, puckers her lips and releases a smoldering fireball about the size of a Ping-Pong ball, which arcs prettily through the air and lands on the statue's head, where it begins to corrode the metal**.
She uses this power again in a battle near the end of the movie; she's flying through the air breathing fire like a dragon. Less ladylike, but still not gross.

*Except Professor X, obviously, and also Magneto. Though the extent to which Magneto was actually involved in the events of Planet X are debatable ... the character who tried to suborn the Xavier School's "special class" into a reconstituted Brotherhood of Evil Mutants and conquer the world was apparently later revealed to be Not Really Magneto At All. I haven't read the comic where that gets hashed out, though, so I am quite fuzzy on the details. I just know that the whole question of "Does Planet X Count as a 'Magneto Story' or not is very contentious --- see the comment thread on this post.

**For whatever reason, the fireball-spewing part of Angel's power demonstration is missing from all the clips I can find.

Guest Blogging

2011-06-17T16:16:00.000-05:00

I wrote a guest post about Charlotte Perkins Gilman's book Herland for Her Circle Ezine, a website about women, writing and art.

The post is an expansion on one paragraph in this old post I wrote juxtaposing Herland with Marilyn French's book The Women's Room*.

I expanded this paragraph into a longer essay on how masculinity and femininity are portayed in Herland, which is as complementary performances that distort human nature and interactions between the sexes, and which each depend on the other to work. (Particularly, I look at the character of Terry, and how his brand of brash, overbearing hypermasculinity works against him in the all-woman, but not particularly "feminine," society of Herland.)

Here's the link, if you want to go read it!

*Here are a couple of essays on the same blog that deal with that book; there's also another essay on Gilman, this one about The Yellow Wallpaper.

Also

2011-06-15T20:39:00.001-05:00

From Sarah's Tumblr:

In light of the recent John Elder Robison interview clusterfuck, I’ve been thinking about something that has long bothered me: the idea that autism—“Asperger’s autism in particular—is so frequently described as “coming across as a jerk without meaning to.”

I don’t doubt that some autistics do experience this, but that’s never been my reality. For me social impairments aren’t as much of a big deal as other autism-related impairments, and of the social issues that I have, I wouldn’t put “being seen as a jerk” anywhere near the top of the list. In fact, on the occasions that I do have this problem, it’s for completely different reasons than what is commonly described. Sometimes I do, yes, act jerky and even cruel—but that’s usually when I’m in the middle of a meltdown or on the verge of one. This is quite different from what JER and a lot of other autism-related material describes. (Of course in JER’s case, I’m pretty sure that a big reason why he is often perceived as a jerk is because he is one. His first book makes this abundantly clear. Hey, autistics can be not-nice people, too.) I’ve said some pretty blunt and possibly inappropriate things, to be sure, but the people who I interact with on a regular basis know that I’m no jerk. That I am in fact a generally nice and caring person. The closest thing that’s come to this was my family “jokingly” telling me that I cared more about the cats than them. But that wasn’t my doing anything possibly jerky so much as a complete misinterpretation of my need for a lot of alone time.

Obviously my experience isn’t representative of all autistics any more than JER’s is. But I’ve met a lot of autistic people, very few of whom can be fairly described as jerks by any definition. And I would be very surprised if a significant number of autistic people listed “being mistakenly seen as a jerk” as one of their top problems. Yet so much of the literature treats this as a central defining feature of being on the spectrum! It’s befuddling, and most likely the product of incompetent, allistic-centric researchers such as SBC fixating—yes, fixating—on the social aspects of autistic impairments to the exclusion of all else.

I meant to include this in my last post, but there got to be so much just about the bit I quoted from that interview that I figured I'd save it for another post.

Anyway, I've been similarly unaffected (well, most of the time --- I can't say that no one has *ever* assumed I was being rude when I was actually having difficulties stemming from autism, like incipient overload, language-processing issues, or whatever, but it is not really a recurring theme in my life) by this thing where people think I must be very rude, or mean, or aloof, because of the way I speak (or don't speak) or act. Some of this may just be because I am a young woman, rather than a middle-aged man, and candor in a young woman might be read as "innocent" or "naive" rather than "rude" --- because I do share some things with Robison, and unthinking candor is one of them --- but it's also because I have other things going on that just social cluelessness. (See: language-processing issues, uneven ability to produce speech, sensory overload, etc.)

Those other things usually mean I get read as stupid, not as a jerk. (Again, that's not to say I absolutely never get read as a jerk --- I might sometimes! That's just not what always happens, or what happens most of the time).

Apart from sharing that, my other motivation in reposting this was to say I very much agree with Sarah's notion that (many) autism researchers zero in on our social difficulties, to the exclusion of other aspects of being autistic that have more of an impact on what we're able to do, and what our lives are like, and how our particular cognitive styles work.

John Elder Robison Disappoints in Interview

2011-06-15T20:18:00.000-05:00

John Elder Robison may be the second-most-famous autistic person alive now --- Temple Grandin, of course, being the most famous --- and, as such, is treated as something of an authority on autism. He sits on a 30-person scientific review board at Autism Speaks, which makes recommendations about which research to fund, and he is also a bestselling author (Look Me in the Eye, and now Be Different) and speaker.

(In this interview with NeuroTribes blogger Steve Silberman, Robison says that part of the reason he wrote his second book was because people kept asking him how he was able to be successful, and whether he had any advice or wisdom to impart that would help other autistic people achieve similar success).

So I was quite disappointed when I came to this part of the interview:

Silberman: Are there any ways that society could be reformed to make it a more comfortable and supportive place for autistic adults?

Robison: I don't think that's a realistic question, Steve. We represent one percent of the population. Asking what 99 percent of the world should do to make it a better place for that one-percent member --- that's verging on science fiction and fantasy. People who get into that way of thinking become militant about demanding their rights and thinking about what the world owes them. Frankly, I don't think the world perceives that they owe us one single thing.

If you're a guy with severe autistic disability and you can't talk, you cry out for compassion by your very existence. It's obvious when people look at you and listen to you. If you're a person in a wheelchair, nobody can reasonably argue that you should just get your ass across the street. But when you're a person like me and your disability is principally with social functioning, and at the same time you have good language skills, people are going to dismiss you as a jerk if you don't learn to fit in. That's the hard truth. To suggest that someone like me should ask for accommodations is, in my opinion, setting that person up for failure. Because when your language skills are good, there's no external sign of disability, and you act weird --- and then you make demands on people for how they ought to change to accept you? That's a non-starter.

It looks like Steve Silberman was also taken aback by this answer, because he actually starts arguing with Robison about it for a while:

Silberman: But other minority groups have demanded reasonable accommodation from society, such as laws against discrimination in the workplace. Black folks did it by launching the civil rights movement, many other disabled groups have done so, and gay people --- like your brother Augusten [Burroughs] --- have done it, too.

Robison: The race thing is completely different. You can look at someone and right away know if they're black or white. There's been a huge gay rights movement, but look at what there is already for gay accommodation. I don't think there was ever an issue of people refusing to hire gay people in most workplaces.

Silberman: Well, that isn't true. I'm not trying to argue with you ---

Robison: In the autism world, people look at your behavior and say, "He's acting like a jerk, I'm gonna treat him like a jerk." If you're a gay guy and you're acting like a jerk, people think you're a jerk; but if you're a gay guy and you're nice, people think, "He's a nice guy."

Silberman: Not always, but I hear what you're saying. [changes subject]

I think Robison misses the point about a lot of things in this exchange. When he's trying to explain how the neurodiversity movement is fundamentally different from, and less reasonable than, past liberation/civil-rights movements, he greatly overstates mainstream society's willingness to do what those past movements asked of it.

He also overstates the degree to which racism and homophobia aren't still entrenched in mainstream (white, straight) society today. Obviously things are better than they were, but Robison is flatly wrong when he says that today, a gay man can be confident that he'll always be judged according to his personal merits, and not by the fact that he's gay (or a black man by the color of his skin). He's also flatly wrong when he says that gay people were never barred from any form of employment because of their sexuality. (What does he think "Don't Ask, Don't Tell" refers to, one wonders?)

I also have serious problems with this:

If you're a guy with severe autistic disability ... you cry out for compassion by your very existence.

The poetry of this image aside, I find its implications --- that autistic people (or other people with severe disabilities, however we're defining "severity" today) don't need any more rights, legal protections, etc., because other people will automatically take pity on them and give them whatever they need --- disturbing.

They disturb me because I know differently. And it makes me angry, given the extent to which abuse and neglect by caregivers is A HUGE PROBLEM for people with disabilities, to hear that we cannot possibly be abused, neglected, impoverished, or anything else bad because our mere existence appeals so urgently to the better angels of human nature.

Anyway, apart from that, it also bothers me that his argument is essentially, "But it's too hard to change society! We can't ask *THAT* of them!!" and then, when faced with examples of other minority groups who've done just that, and achieved some success, he seems to think ... I don't know what. That society has already adopted those reforms, and since it hasn't adopted the reforms neurodiversity/disability activists are pushing for, that those reforms must be less reasonable than the reforms already (grudgingly, laboriously, slowly, incompletely) adopted?

There's also the fact that his whole "the 99 percent cannot be expected to change the way they do things for the benefit of the 1 percent" essentially amounts to, The Devil take the hindmost! Which is pretty much the way we do things here in Capitalismland, but which I think is a really horrible way to run a society. Horrible for everyone, not just autistic people.

Which brings to mind the last big, philosophical thing that bothered me about his answer. He assumes that the reforms neurodiversity activists want would only be beneficial to autistic people, and would either do nothing for, or actively inconvenience, everyone else. I don't think that would necessarily be the case; I think lots of people would benefit from a more flexible, accommodating workplace or an improved system of caregiving or more walkable communities or whatever else. People who aren't disabled might be able to stay afloat in the current social/economic arrangement; that by no means implies that they're thriving under it, or that their lives couldn't also be improved by tweaking said arrangement. After all, "society" isn't this immutable thing like the laws of gravity or thermodynamics; it's something people make, and can remake as needed.

Beyond Good and Evil: Does Simon Baron-Cohen's E-S Theory Help Us Understand Why People Do Bad Things?

2011-06-13T21:03:00.000-05:00

I found out from browsing Sarah's Tumblr (which I do not regularly read like I used to read her blog, because I find Tumblr annoying, confusing and unreadable with its text-overlapping-text and other format wonkiness*) that Kim Wombles, who writes Countering Age of Autism, has interviewed Simon Baron-Cohen for a website called Science 2.0.

The occasion for this interview is that Baron-Cohen has apparently written a new book, one that extends his ideas about empathizing and systemizing from their usual territory (autism, psychological sex differences) to relatively new ground (explaining the human capacity for antisocial acts).

The American edition of the book is called The Science of Evil: On Empathy and the Origins of Cruelty, and it's reviewed at length (also by Kim Wombles!) here.

I haven't read the book, so I won't bother critiquing it without knowing what it actually says, but I will reproduce some of Wombles's Q&A with Baron-Cohen.

KW: Do you think readers will potentially ... get confused as to why you've placed the ASDs in a book titled The Science of Evil?

SBC: ... [Z]ero degrees of empathy does not necessarily lead to acts of cruelty. In the case of people with autism spectrum conditions, their low empathy usually leads them to avoid other people because they find other people confusing. Their low empathy doesn't lead them to commit acts of cruelty any more than anyone else in the population, but it does often lead them to feel socially isolated, with the added risk of depression.

...

The key difference [between autistics and psychopaths] seems to be that in psychopaths the 'cognitive' component of empathy is intact but the 'affective' component is not. In autism, both components may be impaired, or just the cognitive component. But their strong systemizing leads them, through powerful logic, to develop a moral code based on 'fairness' and 'justice'. Psychopaths lack the moral compass that most people develop using their empathy, and lack the moral compass that people with autism develop using their strong systemizing. People with autism spectrum conditions often end up as 'super-moral', developing a set of rules they expect people to live up to consistently (such as honesty), arriving at the conclusion that one should 'treat others as you would have others treat you' because it is the most logical approach.

...

KW: The online autism community is very vocal (and fairly well in agreement, considering the wide divides usually tearing it apart) that you are incorrect in your belief that autistic people lack empathy (and theory of mind). How do you respond to that charge and what evidence do you have that people with ASDs have zero empathy?

SBC: The online autism community is just one sector of the autistic population: namely, those with at least average intelligence, who can therefore use the internet. They are sometimes referred to as having "high-functioning autism" or Asperger Syndrome. This sector of the autistic population may not have zero degrees of empathy, but they do tend to have below average levels of empathy on different measures that research[ers] have used. These include (but are not restricted to) the 'Reading the Mind in the Eyes' Test, or the Empathy Quotient (EQ).

Many people with autism in the remainder of the spectrum may well have absolutely zero degrees of empathy, as shown in failing the False Belief Test (theory of mind) that even a typical 4 year old child can pass, but which is failed by many children with autism with a mental age above 4 years old. Many may not even show 'joint attention' that even a typical 18 month old toddler can show, such as spontaneously following another person's gaze. A meta-analysis review of false belief studies by Francesca Happe in 1995 found that most children with autism take until the age of 11 years old to pass this test, which is a 7 year delay (see attached graph and the recent paper by Senju, 2011). Even among children with Asperger Syndrome or high functioning autism, delays in 'social sensitivity' (such as detecting faux pas) are seen, despite their average or above average IQ.

...

So why might people with autism in the online community challenge this view? One possibility is that it is in the nature of empathy that people who are low in empathy are often the last people to be aware of it. ... An analogy might be with colour blindness. Many people who are colour blind are the last people to know about it, until they are given a test of it by an optician or vision scientist. They simply assumed that they were seeing the same colours as everyone else.

...

In my experience whilst even adults with Asperger Syndrome may have difficulties figuring out why someone else's remark was considered funny, or why their own remark was considered rude, or may judge others as liars when they simply are inconsistent in not doing what they said they would do, they may nevertheless have a highly developed emotional empathy, caring about how someone feels and not wanting to hurt them. If they do hurt them it is often unintentional and they feel mortified when it is pointed out, and want to rectify this. In this respect, they do have some of the components of empathy.

Many people with autism also form very strong emotional relationships with their pets ... whilst they struggle to 'read' human behaviour and human intentions, they can read the arguably more predictable behaviour of a pet.

Right now, I'm going to restrict myself to a few brief, superficial comments: first, in response to Professor Baron-Cohen's contention that everyone who says they are autistic on the Internet is a highly verbal, high-IQ computer geek with Asperger's --- no, we're not. There's a wide variety of autistic people on the Internet, including people with all sorts of functioning labels. The format of the Internet itself actually makes it easier for the less verbal, likely-to-be-called-low-functioning autistics to participate, since they don't have to produce speech. We might not be represented on the Internet in the exact proportions that we exist in the real world, but neither do we all belong to the same narrow subcategory of autism.

(And yay for him pointing out the difference between cognitive and emotional empathy, and also for pointing out that autistic people can be very emotionally empathic! That often gets lost, even in his own previous discussions of this subject.)

Also, I'm just going to express my skepticism at the idea that most of the abusive state employees described in the New York Times stories I referenced in this post had any psychiatric diagnoses, much less diagnoses that would explain their startling lack of empathy for the developmentally disabled people in their care. While Baron-Cohen does mention that failures of empathy can occur in people whose faculties are theoretically intact, he doesn't go into detail about how this happens. I guess I'll have to read the book to see what kind of case he makes that there is an "empathy circuit" in the brain that is bypassed or otherwise disabled when a person acts in a nasty way toward other people.

Finally, the "moral code[s] based on 'fairness' and 'justice'" that autistic people are supposed to develop through our amazing abilities to reason logically and think abstractly, sound a lot like the "mental widgets" that are so baffling to Amanda Baggs, and to (what seems to be) a significant subset of other autistic/non-neurotypical people! So I very much doubt that *all* of us are intellectualizing our way toward a system of ethics, even if I were to grant that some of us do that.

*I am a living refutation of the common stereotype that being autistic automatically makes you technologically gifted. Oh, how I wish!

Unspeakable

2011-06-11T21:00:00.002-05:00

That's what we call the things that are so awful, so heartbreaking, they stop the words in our throats and the thoughts in our heads. Sometimes they even stop the tears in our eyes; the sadness we feel is so heavy it will not be cried out.

For me, the abuse, neglect and murder of people with disabilities* by the people who are supposed to be taking care of them calls up this heavy sadness.

From Leah Jane's blog:

A lot of my neurotypical friends don't understand why I am so paranoid about going to an institution. They think, for one, that it could never happen to me, because I'm intelligent and express myself eloquently, and secondly, they don't think it could be all that bad for someone like me, who is mostly able-bodied save for troubles with my back from scoliosis, since I could feed myself, ask for private time, and go to the bathroom alone. There is also often this assumption that goes unchallenged that the disabled have it made in the U.S., that we're lucky not to be living in a country where we'd be kept in cages or denied food and water. So I often end up shoving stories like this in their faces, reminding the world that being cognitively, not physically, disabled, or living in America is no guarantee of your human rights being respected.

From the news story she links to:

Jonathan Carey did not die for lack of money.

New York State and the federal government provided $1.4 million annually per person to care for Jonathan and the other residents at the Oswald D. Heck Developmental Center, a warren of low-rise concrete and brick buildings near Albany.

Yet on a February afternoon in 2007, Jonathan, a skinny, autistic 13-year-old, was asphyxiated, slowly crushed to death in the back seat of a van by a state employee who had worked nearly 200 hours without a day off over 15 days. The employee, a ninth-grade dropout with a criminal conviction for selling marijuana, had been on duty during at least one previous episode of alleged abuse involving Jonathan.

"I could be a good king or a bad king," he told the dying boy beneath him, according to court documents.

In the front seat of the van, the driver, another state worker at O.D. Heck, watched through the rear-view mirror but said little. He had been fired from four different private providers of services to the developmentally disabled before the state hired him to care for the same vulnerable population.

O.D. Heck is one of nine large institutions in New York that house the developmentally disabled, those with cerebral palsy, autism, Down syndrome and other conditions.

...

But the institutions are hardly a model: Those who run them have tolerated physical and psychological abuse, knowingly hired unqualified workers, ignored complaints by whistle-blowers and failed to credibly investigate cases of abuse and neglect, according to a review by the New York Times of thousands of state records and court documents, along with interviews of current and former employees.

...

Similar problems can be found across the state. The Broome Developmental Center in Binghamton has been cited for repeatedly failing to protect residents from staff members. One employee there was merely reassigned after encouraging adolescent residents to fight one another.

Patterns of abuse appear embedded in the culture of the Sunmount Developmental Center in the Adirondacks. Last year, one supervisor was accused of four different episodes of physical and psychological abuse of residents within a span of two and a half months; another employee bragged on Facebook about "beating retards."

The most damning accounts of the operations come from employees --- thwarted whistle-blowers from around the state --- and the beleaguered family members of residents.

...

For the Careys, the journey to O.D. Heck was a last resort. ... [They] raised Jonathan until he was 9, but became worried that they could not teach their son basic living skills, like toilet training. They enrolled him at the Anderson Center for Autism, a privately run school in the Hudson Valley overseen by the state.

At first, the school seemed a good fit, until Jonathan, who was always thin, began losing weight. During one visit, an employee told the Careys to take home a duffel bag they had never used. They discovered a logbook inside the bag detailing startling changes to Jonathan's treatment plan. Among other things, the school was withholding food from Jonathan to punish him for taking off his shirt at inappropriate times.

"They literally planned to withhold my son's meals," Mr. Carey said. "And when that was not working, then they began to seclude him in his bedroom for an extended period of time. He missed eight full days of school."

So, to save him from possible death by starvation, Jonathan's parents removed him from that school and tried to take care of him at home again, but his problems had gotten worse. He had tantrums, he would run away, and Mr. and Mrs. Carey didn't think they could keep him safe, so they were referred to O.D. Heck. There was maybe a year and a half between Jonathan's admission to that school and his death in the back of the van. During that period, he was hospitalized three times with unexplained injuries.

It should be obvious from what I've quoted of this (lengthy) article that this is systemic.

It should be equally obvious that this sort of abuse is not restricted to any one kind of institution: the New York Times investigation found that the same culture of abuse detailed above, at the nine large institutions, also pervaded New York's 2,000 smaller group homes. Nor is it just restricted to New York --- last fall, the Chicago Tribune investigated thirteen deaths at a single nursing home, Alden Village North, that occurred over the past ten years. Similarly, stories of people with disabilities being abused, neglected or killed in their homes by family members appear in the news with some regularity. (Most recently, in my area, a young woman was sentenced to eight years and six months in prison for confining her six-year-old son with Down syndrome to an attic and starving him. The boy survived, and is now in foster care with his two sisters).

I think there are a lot of factors that work together to make this such a ubiquitous thing in our culture; the two biggest ones I can come up with now are 1) horrible societal attitudes toward disabled people, and 2) horrible societal attitudes toward caregiving. It's easy to see how the first one would contribute to a culture of abuse: it's always easier to abuse someone if you don't see them as a person. But I also think the undervaluing of caregivers plays a role, too --- the institutions in those news stories wouldn't have hired people with criminal convictions (or previous dismissals from other institutions) if they'd really thought caregiving was an important task that can't be entrusted to just anyone. The chronic understaffing of institutions is another symptom of this undervaluing --- caregiving is hard work, with long, irregular hours, and the pay is low, so they're always short on people who are willing to do it. Then, because of the perennial labor shortage, the people who run institutions are unwilling to fire people even for serious offenses.

I'm also starting to think that "unspeakable" is precisely the wrong word for such atrocities. Unspeakable means something we never talk about, something repressed. It means we can sweep it under the rug and pretend it doesn't happen, or that when it happens it's an aberration. And people want very much to believe institutions are safe, that their children or parents will be happy there.

*I feel similarly about abuse of children or animals by their guardians, or of women by the men they love. But this post deals with issues specific to people with disabilities, so I'm going to restrict my discussion to that.

Link Roundup

2011-06-04T14:52:00.002-05:00

Here's a bunch of stuff I've read that I think my readers --- or, at least, various subsets of my readers --- might like:

Neuroskeptic on the murky relationship between genes and mental illness

A couple of posts --- one from Peter Daou and the other from David Roberts, writing for Grist --- on climate-change denialism

Environmentalist Bill McKibben (author of Deep Economy and Eaarth) writing for the Guardian's Comment Is Free about Barack Obama's environmental policies

Leah Jane at her new blog, nominatissima, on children's rights, why she doesn't see a conflict between being pro-choice and also pro-disability rights, and two posts on sex and romance for autistic people

Amanda Baggs (whose blog has also moved) on animal consciousness

Urocyon on eating disorders, food, gaslighting, colonialism (including a four-part series deconstructing the concept of race based on skin color and a link to this post at Womanist Musings), and how learning about her disabilities has helped her stop thinking of herself as incompetent and weak

Finally, on a blog I just discovered called Sasha Said, two posts on rape, a post on "Poverty in America and the Emerging Slave Class," and a wonderful, eye-opening post on "What Children Learn When They Don't Learn About Patriarchy" --- how children learn to account for male dominance of society when they're being told that men and women have equal rights.

Autism Diagnoses Spread through Social Networks

2011-05-31T17:11:00.005-05:00

EXECUTIVE SUMMARY: A little more than a year ago, a group of sociologists analyzed data from the state of California --- birth records and records from California's Department of Developmental Services --- to look for patterns in where autistic children were most likely to be found. They determined that children living near (defined here as being within 500 meters) a family where one of the children had been diagnosed with autism in the previous year were somewhat (1.26 times) more likely to receive an autism diagnosis themselves. They also found that 1) the effect was stronger for the less severe cases of autism, and also for children who were three years old when they were diagnosed (as opposed to 4, 5, or 6); and 2) children living very close to a family with a recently-diagnosed autistic child were about 28% less likely to be diagnosed with intellectual disability without a concurrent diagnosis of autism. The researchers concluded that parents who know other parents who've had a child diagnosed with autism are more likely to have their own children evaluated, and thus more likely to get a diagnosis for their own children.
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An article published last year in the American Journal of Sociology argues that knowing someone in your neighborhood who has an autistic child makes it likelier that your child, too, will be diagnosed with autism.

The authors' explanation for this is not that autism is "catching," or that people with autistic children are likelier to live in certain places (they investigated both of those possibilities, along with the possibility that some environmental contaminant makes some neighborhoods have more autistic children than others); it's that parents talk to each other about their children, and if one family has an autistic child, and has gotten that child diagnosed and enrolled in services, those parents will tell other parents about that process, and thereby make it easier for other parents to do the same thing. (They may also, by describing their autistic children's behavior, make it more likely that other parents will consider the possibility that their child may be autistic).

What these researchers --- sociologists Peter Shawn Bearman, Marissa D. King (who has conducted a lot of research into autism demographics) and Ka-Yuet Liu --- did to derive this explanation was look at data on all children born in California since 1997, with younger siblings also born in California. (They needed to restrict their sample to children with younger siblings to get information on where the firstborn children spent their early years --- if the family's residence is the same for every child born to that family, the researchers could assume that the firstborn lived in the same place during the years between hir own birth and the birth of hir youngest sibling. That's the information they wanted --- where families lived during their children's early years). This gave them a pool of 533,244 children whose families lived at the same address when they were born as when their younger siblings were born. Then, they used data from the California Department of Developmental Services (I've written about this data set before, in a different context --- it's been used in a lot of studies investigating autism prevalence) to determine which of those children got an autism diagnosis, or a diagnosis of intellectual disability*, between the ages of 2 and 6.

They created a statistical model to see if they could accurately predict which children would end up with a diagnosis of Autistic Disorder**. Their model, which is supposed to predict the odds of any given child being diagnosed with autism in a given year, t, uses the physical proximity of a child diagnosed with autism in the previous year, t - 1, as its predictive variable. They divide this continuous measure --- how far away does [other child with autism] live? --- into six discrete groups: 1 - 250 m; 251 - 500 m; 501 m - 1 km; 1001 m - 2 km; 2001 m - 5 km; and all distances over 5 km. (They used a continuous measure of distance, too). They controlled for a slew of other variables --- sex, maternal age, socioeconomic status (measured by mother's educational attainment and whether she received state assistance with pregnancy- and birth-related medical expenses), proximity to autism-related healthcare services, neighborhood population density, and neighborhood median income --- and predicted that the odds of a child being diagnosed with autism would increase the closer they lived to a child already bearing that diagnosis, and that the odds of a child being diagnosed with intellectual disability independent of any other condition would decrease with increasing proximity to a child diagnosed with autism. They also predicted a pattern in what kind of autistic children would show the greatest change in likelihood of diagnosis: they thought that the "high[est]-functioning" children, who scored the lowest on their measure of autism severity***, would show the greatest effect, along with the youngest children (age 3 or younger). Their reasoning is that, since these are the most ambiguous cases, whether or not their parents knew someone else with an autistic child, and thus got it into their heads to consider whether their child might also be autistic, would make the most difference, since there are less likely to be really obvious, textbook signs of autism. (Or, if signs are present, say, in the very young children, knowing another family with an autistic child might predispose the parents to have their child evaluated sooner, rather than waiting to see if, say, the child is just a late talker).

Sure enough, they found the patterns they'd predicted.

This graph shows the clustering of actual data points around their theoretical curve; you can see it's a pretty close fit.

(Figure 2A, in Bearman, King and Liu, 2010. The x-axis shows distance, in kilometers, from the nearest home with a child with an autism diagnosis, and the y-axis shows the probability that any given child living at that distance will be diagnosed with autism within the next year).

Here's a different representation of the same data:

(Figure 2B, in Bearman, King and Liu, 2010. The x-axis still shows distance, but the y-axis, instead of showing probability of an autism diagnosis in the next year, now shows the odds ratio between each distance category and the reference category, which is 501 m - 1 km. The five different dots in each distance category represent the five different statistical models that were used. You can see that, compared to the middle distance category, the children in the two shorter-distance categories were more likely to receive autism diagnoses, while the children in the three longer-distance categories were less likely to be diagnosed.)

From the Results section:

[W]e also report the effects of proximity as a categorical variable. All odds ratios (ORs) are relative to the reference category of 501 meters - 1 kilometer. ... In figure 2B, we can observe that residing in close proximity to a child diagnosed with autism increases one's chance of being diagnosed with autism in the subsequent year. Compared with children who are 501 meters - 1 kilometer away from their nearest neighbor with autism, those in close proximity (1 - 250 meters) to a child with autism have a 42% higher chance of being diagnosed with autism in the subsequent year. Proximity of 201 - 500 meters increases the chance by 22%. In contrast, being farther away from a child with autism reduces the chance of a diagnosis. Although the last three categories were all significantly associated with the decrease (-21%, -36%, and -49%), there were no statistically significant differences among these three categories. This is consistent with the results in figure 2A, which show that the effect of proximity is strongest within one kilometer, followed by a flat tail.

And here are the graphs showing the effects of proximity to a family with an autistic child on 1) a child being diagnosed with autism (with intellectual disability) rather than with intellectual disability alone ...

(Figure 2C, in Bearman, King and Liu, 2010. The x-axis shows distance; the y-axis shows odds ratios --- compared, again, with the middle-distance "reference" category of 501 m - 1 km --- of being diagnosed with intellectual disability by itself. You can see that living closer to a family with a recently-diagnosed autistic child made it less likely that a given child would be given a sole diagnosis of intellectual disability, although it is only at the farthest distances, 5 kilometers or more, that children become more likely to receive a diagnosis of intellectual disability independent of any other condition).

... and 2) being diagnosed with autism at varying levels of severity:

(Figure 3, in Bearman, King and Liu, 2010. The x-axis shows the percent increase in odds of receiving an autism diagnosis associated with proximity to a recently-diagnosed autistic child; the y-axis shows the child's level of disability as assessed by the state's Client Development Evaluation Reports. The highest-scoring, or least impaired, 20% are compared to the bottom, or most seriously impaired, 20%, and to the middle 60%. You can see that the "highest-functioning" group shows a stronger effect of proximity to another autistic child on their chances of being diagnosed than either the middle group or the "lowest-functioning" group, whose chances of being diagnosed with autism were least affected by proximity to another recently-diagnosed autistic child.)

The researchers were pretty well satisfied that the effect they found for proximity wasn't an artifact of shared environmental contamination because they saw the same pattern in a large, diverse sample of neighborhoods. They looked at rural, urban and suburban communities, which would all have their own distinct toxicological profile. (For instance, pesticide exposure would be a likely risk factor in rural areas, and a possible one in suburban areas, but pretty unlikely in urban areas. Similarly, air pollution is probably only a serious factor in dense urban areas.) There were other patterns that would not be explained by shared environmental risk factors or viral transmission, but that do fit with the social-diffusion hypothesis: first, a strong tendency of people coming in for diagnostic evaluations to have been referred there in the way as their nearest neighbor with an autistic child, and second, for people living on or near a border between school districts, the proximity effect was only seen for children living nearby who also attended school in the same district.

So, I find all this pretty supportive of their idea that social networks play a role in determining who is and who is not diagnosed with autism; what is less clear to me is how much of a role they play compared with other factors, like socioeconomic status, parents' ages, male gender, or having an autistic relative.

What Drs. Bearman, King and Liu did to try and answer that question is calculate the population attributable fractions (PAFs) --- the difference any given risk factor makes in the number of people who develop a certain condition --- for proximity to another autistic child, and also for each of three sociodemographic indicators: mother's age at the time of her child's birth, mother's educational attainment, and whether the state of California paid for her prenatal and obstetric care. By this metric, they found a greater role for proximity than for any other factor: living within 500 meters of a family with a recently-diagnosed autistic child raised children's likelihood of being diagnosed with autism in a given year by 16%.

While this may be a larger effect than any of the other, more-established risk factors, it's not larger by all that much, and in absolute size it's also not very big. I would expect that, though --- most children don't have autism, so the most a social diffusion of autism awareness could do is make the parents of those children who do have autism take them in to be evaluated sooner. (Or, maybe for a few families, at all --- but with schools getting more and more proactive about identifying special-needs children, it's not very likely anymore that a child with autism could get all the way through K-12 without being flagged somewhere along the line).

Liu KY, King M, & Bearman PS (2010). Social influence and the autism epidemic. AJS; American journal of sociology, 115 (5), 1387-434 PMID: 20503647

*They tracked this category as well to look for social/spatial patterns of diagnostic substitution --- are children who are more likely to be diagnosed with autism also less likely to be diagnosed with general (i.e., non-autism-associated) intellectual disability?

**They only counted children in this category, and not any other pervasive developmental disorder, because only Autistic Disorder is a category eligible for state services. The researchers felt that parents' main motivation in pursuing a diagnosis would be to gain access to services, so they didn't bother tracking the diagnoses that wouldn't be useful toward that end.

***Their severity measure involved nine items from the California DDS's Client Development Evaluation Report (CDER) on each child. (Here is a PDF of the complete CDER form, if you want to go and look at what exactly these items are measuring). The overall measure was an equally-weighted average of scores on three "scales" --- communication (made up of 3 CDER items: item # 58, word usage; item # 61, receptive language; and item # 62, expressive language), social interaction (made up of 5 CDER items: item # 27, peer interaction; item # 28, interaction with nonpeers; item # 29, friendship formation; item # 30, friendship maintenance; and item # 31, participation in social activities), and a single CDER item, # 42, measuring repetitive and stereotyped behaviors. (I find it a bit odd that they didn't include self-injurious behavior as part of their severity measure --- there are two items on the CDER addressing that, and the presence or absence of self-harm seems to me a more important measure of how "severe" someone's problems are than, say, being able to interact "normally" with one's peers.)

Gene Expression in Autistic Brain Tissue

2011-05-29T15:33:00.009-05:00

EXECUTIVE SUMMARY: A recent analysis of mRNA extracted from brain tissue samples taken from brains donated to the Autism Tissue Project and the Harvard Brain Bank, with both sources supplying both autistic and neurotypical brains, found two clusters of genes whose expression differs significantly between autistic and NT brain tissues. One of these clusters, whose component genes primarily encode proteins involved in synapse formation and neurotransmission, is expressed less in the autistic brains than it is in the NT ones. The other cluster includes a lot of immune- and inflammation-related genes, and those genes are expressed to a greater degree in autistic brains. This study also unearthed a gene encoding a protein that seems to be involved in splicing the mRNA transcripts of other genes, and the underexpression of this gene in autism may be part of the reason so many of the other genes in the same cluster are also underexpressed.
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This study, published online at Nature.com last Wednesday, strikes me as an interesting hybrid of two kinds of studies that are frequently used in autism research: gene-expression studies (where researchers compare patterns of gene expression in tissue samples taken from autistic people to those in samples taken from neurotypical people) and neuroanatomical studies (where researchers look at differences in size, structure or activation patterns of various brain structures between autistic and neurotypical subjects).

In this study, the researchers took samples from three different regions of the brain (the prefrontal cortex, superior temporal gyrus and cerebellar vermis), using brains donated to the Autism Tissue Project and the Harvard brain bank. From both of those sources, they ended up with 58 cortex samples (29 from autistic brains; 29 from non-autistic brains) and 21 cerebellar samples (11 autistic; 10 not).

They looked for differences in gene expression between autistic and control tissue samples by measuring the amount of RNA present in each sample corresponding to a given sequence of genomic DNA. (Since the mid-to-late 1990s, a tool has existed to do this at quite a high resolution: the DNA microarray. This is a glass or silicon chip covered in tiny wells where a short sequence of DNA is anchored --- in this case, the DNA probes are short, synthesized 50-base snippets made to match specific parts of each gene contained in the National Center for Biotechnology Information's RefSeq database --- to which your sample DNA or RNA will bind if it contains a complementary sequence).

(What a microarray looks like)

This type of experimental design doesn't really allow direct comparison between RNA extracts from different tissue samples --- instead, each sample (from the same region of the brain of either an autistic or neurotypical donor, or from different regions within the same brain) hybridizes (i.e., forms a new, DNA-RNA "hybrid" helix when heated) to the DNA probes on its own separate array. Researchers then compare the intensity of the signal created by each well across the two arrays --- the brighter the color, the more (fluorescent-dye-treated) sample RNA is present on the chip.

(DNA-RNA hybridization)

In this experiment, the researchers found 444 genes that differed significantly between the autistic and control cortex* samples in how much mRNA (the RNA created when DNA is transcribed; used as a template for protein synthesis) there was in a given tissue extract. They decided to concentrate on the 200 most differentially expressed genes for their (more detailed) expression analysis, which included a look into "co-expression networks" of genes whose expression seems to be regulated via the same pathways. They replicated their results by doing a similar microarray experiment on tissue samples from a smaller group of donated brains (nine from autistic donors, five from neurotypical donors), this time taking samples from a different region of the cerebral cortex than either of the cortical regions assayed in the initial experiment.
Figure 1C, in Voineagu et al, 2011 --- scatter plot showing genes found to be up- (red) and down-regulated (green) in both the initial and replication data sets. The bluish lines drawn through each cluster of dots reflects the cutoff for significance; most of the regulation changes are significant, but some aren't. Both axes represent a logarithmic measure of the change from baseline for either data set (Data Set 1, or the initial data, is on the x-axis; Data Set 2, or the replication data, is on the y-axis).

They got additional confirmation of their gene-expression data by using an alternative measure of how much of a given mRNA sequence was present in each tissue extract: for each gene that the microarray experiments identified as being differentially expressed in autistic and non-autistic brain tissues, they made a DNA copy of its array-bound mRNAs, and then amplified those bits of DNA using a process called RT-PCR (real-time polymerase chain reaction). That process uses bacterial enzymes to make huge numbers of copies of a given sequence of DNA, such that the amount of DNA is large enough to be easily quantified. Those amounts could be compared between groups, and thus confirm (or fail to confirm) differences in mRNA production predicted by the microarray experiment.

This figure shows how much more or less mRNA there was from eleven genes whose differential expression levels were validated using PCR:

(Supplementary Figure 2B, in Voineagu et al., 2011 --- top bar graph, in red, shows positive changes in expression of five genes in the tissue samples taken from autistic donors; bottom graph, with green bars, shows the average reduction in expression of six other genes. On both graphs, the numbers on the y-axis represent how many times as much of one kind of mRNA was found in the autistic sample; you can see that the up-regulating produced a more dramatic change --- ten- and twenty-fold, for all but one of the five genes --- than down-regulating, which produced, respectively, one-half, one-fifth, one-eighth, one-third and one-fourth as much mRNA as the control sample).

They found two co-expression modules (networks of genes) whose expression varied in relation to whether the sample came from an autistic or non-autistic donor, and not in relation to any of the other variables they took into account (like age, sex, cause of death, medication history, whether the person also had seizures, and family history of mental illness): M12 and M16.

Here is their drawing of M12, and the relationships between its component genes:
(One of the genes in the middle of this diagram, CNTNAP1, is a close relative of a gene that other genetic studies have tied to autism --- and that I have described on this blog --- CNTNAP2).

... and here is their drawing of M16:
Relative to the samples from neurotypical donors, the brain tissue samples from autistic donors had more mRNA transcripts of genes in M16, and fewer transcripts of genes from M12.

In each of these modules, genes for certain types of proteins predominated: for M12, these are proteins involved in synapse formation, neurotransmission, vesicular transport (importing objects into the cell, or exporting objects from it); while M16 included lots of genes for immune and inflammatory proteins.

One of the major genes in M12, A2BP1, is a splicing regulator. Alternative splicing is one of the ways the cell can make different kinds of proteins from the same mRNA; the mRNA will contain characteristic sequences, called splice sites, where splicing enzymes can bind to it, cut it and put it back together, minus the regions bordered by splice sites.

Like some other instances I've mentioned of proteins playing a role in gene expression themselves being expressed differently in autism, this down-regulation of A2BP1 could have important ramifications for the genes whose transcripts A2BP1 is involved in splicing. The authors of this study thought it would be a good idea to look for A2BP1 splice sites in the RNA samples from those specimens within the autism group with especially low levels of A2BP1 mRNA; to do this, they sequenced all the mRNA from three samples with relatively little A2BP1 mRNA, and also from three control samples with normal A2BP1 expression. They found 212 potential splice sites using this method, which they validated by using RT-PCR (again) to compare relative amounts of various alternatively-spliced mRNAs in autistic and control tissue samples --- first in the same three samples that were sequenced, and then in three other samples from the autism group, which also had low A2BP1 expression. Using this method, they confirmed that the vast majority (85%) of the expected splicing changes were really there in all of the low-A2BP1 samples.

The genes whose alternative splicing depended on A2BP1, and thus whose alternate forms were underexpressed in the low-A2BP1 RNA samples, included a lot of the same genes as the M12 co-expression module. So it looks like, besides finding out that M12 is collectively underexpressed in autism, these researchers have also found at least one of the mechanisms behind this underexpression.

*The cerebellar samples differed significantly in the expression of only two genes, so those data were not included in further analysis.

Irina Voineagu, Xinchen Wang, Patrick Johnston, Jennifer K. Lowe, Yuan Tian, Steve Horvath, Jonathan Mill, Rita M. Cantor, Benjamin J. Blencowe, & Daniel H. Geschwind (2011). Transcriptomic analysis of autistic brain reveals convergent molecular pathology Nature (25 May) : 10.1038/nature10110

Qualified Candidate Barred From Job; U.S. Government Sues Employment Agency

2011-05-28T15:25:00.004-05:00

My heart really goes out to Jason O'Dell; he and I seem to be in similar circumstances.

He recently applied for work as a lab technician in Frederick, Maryland, using an employment agency called Randstad US. Everything had been going pretty well --- Randstad had decided that he was exceptionally well-qualified for this particular job, so they "fast-tracked" his application; the company he had applied to had also expressed interest in hiring him --- until O'Dell let it slip that he had Asperger's.

When that happened, the position he had seemed about to get seemed to evaporate. His contacts at Randstad were telling him it had "been put on hold," but really they were continuing to recruit other candidates, and eventually filled the position with someone who was not Jason O'Dell.

In response to this, the U.S. Equal Employment Opportunity Commission is suing Randstad for discrimination --- in pulling O'Dell out of consideration for employment right after he told them about his disability, they violated the Americans with Disabilities Act's prohibition against employers (or employment agencies!) discriminating against qualified people with disabilities in job application procedures, hiring, promotion, pay, training, firing or any other aspect of employment. They're asking for back pay, compensatory and punitive damages for O'Dell, and revisions to Randstad's employment policies to make the kind of discrimination O'Dell experienced Officially Against The Rules.

Here is the relevant part of the ADA:

Sec. 12112. Discrimination

(a) General rule

No covered entity ["covered entity" meaning an employer, employment agency, labor organization or joint labor-management committee] shall discriminate against a qualified individual [someone who can perform the essential functions of the job with reasonable accommodations] on the basis of disability in regard to job application procedures, the hiring, advancement, or discharge of employees, employee compensation, job training, and other terms, conditions, and privileges of employment.

(b) Construction

As used in subsection (a) of this section, the term "discriminate against a qualified individual on the basis of disability" includes

(1) limiting, segregating, or classifying a job applicant or employee in a way that adversely affects the opportunities or status of such applicant or employee

... and here's a handy little page about employment law; it tells you what your rights are under the ADA, and what you can do if you think they've been violated.

The EEOC also mentions in its press release that fiscal year 2010 has been especially bad for discrimination in employment: they had 99,922 claims, of which 25,165 were disability-related. That constitutes an increase of 17.3% over the number of disability claims filed in fiscal 2009.

I hope they win their suit, and that O'Dell gets those damages ... although even more I hope he manages to get a lab job somewhere!

Stigma

2011-05-28T15:20:00.001-05:00

I thought this paragraph in the Discussion section of the article I posted about yesterday was so interesting it deserved its own post:

Although researchers have not found cultural variability in phenotypic expression of ASDs, cultural variables may affect prevalence estimates. Indications generally suggest ascertainment bias toward lower prevalence in South Korea since Koreans consider autism to be a stigmatizing hereditary disorder; autism (chap'ae) impugns the child's lineage on both sides and threatens the marriage prospects of unaffected relatives. As a result, autism is often untreated, misdiagnosed as attachment disorder, or unreported in records. Although our total population approach avoided clinical and administrative obstacles associated with stigma, it is possible that some parents, fearing a diagnosis, chose not to report ASD symptoms or to participate in diagnostic evaluations.

I don't know if this blog has any Korean readers --- if any of you are reading, I'd love to hear your thoughts on the accuracy of the quoted passage.

Taking the passage at face value, it seems to me that the difference in stigma associated with autism in the U.S. and in Korea is more a matter of where the stigma is directed than whether a stigma exists at all. Autism is very much a stigmatized condition here; it's just that the family members aren't seen as tainted with faulty genetics (and thus less marriageable) as much as they are alternately pitied and lionized for living with an autistic person. The stigma here is directed almost entirely at the autistic person hirself, although of course parents and caregivers who make choices that don't fit with the current ideas of what's best for an autistic child come in for some serious disapproval, too.

1 in 38?

2011-05-27T20:42:00.003-05:00

That's the proportion of school-aged kids found to meet diagnostic criteria for an ASD by this team of mostly Korean researchers --- Drs. Young-Shin Kim, Bennett L. Leventhal, Yun-Joo Koh, Eric Fombonne (who has done a lot of research on the prevalence of autism), Eugene Laska, Keun-Ah Cheon, Soo-Jeong Kim, Young-Key Kim, Dong-Ho Song, and Roy Richard Grinker (the Unstrange Minds guy), along with Eun-Chung Lim and HyunKyung Lee --- when they screened elementary-school children in one district of a fairly large city (Goyang City, pop. 1,073,069; Ilsan district, pop. 488,590) near Seoul, South Korea.

Part of their reasons for doing this study (full text here) was their thought that previous estimates of the prevalence of autism rely too much on documentation from official sources --- national disability offices, special-education registries, autism-specific service providers, etc. --- that wouldn't include children who have not yet been evaluated for ASDs.

To try and get more of a cross-section of Korean children, the researchers recruited from both mainstream elementary schools (41, of which 30 agreed to participate), special-education schools (3), and the city's Disability Registry (all children between 7 and 12 listed as having either ASD or intellectual disability). Children from participating institutions were initially screened for autism using the Autism Spectrum Screening Questionnaire (ASSQ), which parents and/or teachers filled out about each child.

Not surprisingly, the general-population group, recruited from the elementary schools, was much larger than the developmentally-disabled group recruited through the Disability Registry or from special-education schools: in all 30 participating elementary schools, there were 36,592 children between the ages of 7 and 12. Of these, the parents of 23,234 completed the ASSQ and sent it in to the researchers; of the 294 students attending special schools and/or listed in the Disability Registry, 103 had forms submitted for them.

Anyway, following this initial screening, the students who scored high enough on the ASSQ (with a teacher-rated score of at least 10, or a parent-rated score in the top five percentiles*) were offered further diagnostic evaluation. Among the elementary-school students, 1,742 met those screening criteria, and 234 completed the evaluation. All of the special-education students were considered to meet screening criteria, and 52 of them completed the evaluation. Each child was evaluated by two teams, and each team included both Korean- and American-trained practitioners. The evaluators used Korean versions of the Autism Diagnostic Interview (ADI-R), Autism Diagnostic Observation Schedule (ADOS), and two cognitive tests, the WISC-III and a revised version of the Leiter International Performance Scale.

Of the 286 children who were evaluated, 201 met criteria for an ASD**. Just over half of these (101) met criteria for Autistic Disorder; just under half of those (48) had come from the special-education group. All but one of the students in that group who were diagnosed with an ASD were diagnosed with Autistic Disorder, while most of the students in the general-population group were diagnosed with some other ASD, either Asperger's syndrome or PDD-NOS**.

There is one thing I found particularly interesting in their results: the ratio of boys to girls among their ASD "positives" is significantly lower than the 4:1 most commonly cited in the autism literature. These researchers found a ratio of 5.1:1 among the special-education students (who were mostly boys to begin with --- of the 103 special-education students who were screened, 84 were male, so even if *all* of the girls in that group had autism, the ratio would still be skewed in the boys' favor unless relatively few of the boys had it) and a ratio of 2.5:1 among the mainstream elementary-school students.

That number adds some support to the hypothesis that autism remains underdiagnosed among girls --- the lower ratio was only seen in the students who were not flagged as disabled or special-ed, not receiving any services. Among the students known to be developmentally disabled, or already diagnosed with autism (i.e., those registered as ASD in the Disability Registry), the ratio was closer to the current conventional-wisdom ratio of 4:1.

(It also seems like the forms of autism that are most likely to go undiagnosed in girls are the "milder" forms, like Asperger's and PDD-NOS. Very few girls in the general-population sample met criteria for Autistic Disorder; of the 27 children meeting those criteria, only five were female.)

Anyway, back to the number making up the title of this post.

How they got that number is complicated. They divided the number of autistic students they extrapolated there to be based on the number they found (more about this later) by the total number of seven-to-twelve-year-old children living in the Ilsan district of Goyang City, which is 55,266.

So much for the easy part.

There were several steps involved in correcting for the large proportion of nonresponders; first, and easiest, they guesstimated the likely full scores of the people who turned in partial ASSQs. (The simplest method they had for doing this was simply to take the average single-item score on a form in which only some of the items are answered and multiply it by the number of items on the full questionnaire, which is 27). Just doing that gave them 264 more subjects meeting initial screening criteria for an ASD. They also added in all the children listed in the Disability Registry as having ASD who did not participate in this study; this would add 101 subjects to the confirmed-ASD pool. (They left out all the non-participating children listed as having intellectual disability).

They also did some statistical manipulations that I don't understand (I had minimal coursework in statistics, and not even good old Google can tell me what a "weigh-back procedure"*** is) to correct for their only having given some of the people meeting their minimum screening criteria the opportunity for furthere evaluation. (See the Methods section and this supplemental section for their discussion of these techniques).

At the end of all of this, they ended up with an adjusted prevalence figure of 2.64%, or the 1 in 38 referred to in the post title. There are several ways in which this might be an overestimate: chief among them, the researchers assumed that the proportion of children meeting screening criteria who also meet diagnostic criteria for an ASD would be the same for the nonresponders as it was for the responders --- i.e., about 70%. Their basis for this assumption is a logistical regression model they created to try and predict parental consent to, and participation in, diagnostic evaluations. They found that since none of the co-variates they'd chosen for this missing "latent variable" --- child's age, sex and ASSQ score --- predicted whether a given child would end up with an ASD diagnosis or not, that parental willingness to have more tests done did not vary with the likelihood that their child is autistic. But all of those variables are somewhat crude proxies --- even the ASSQ score, when you consider that all of the "screen-positive" children had scores clustered within the same narrow window, and thus variation between them would be minuscule. So I think it's reasonable to think that maybe the model was wrong, and the parents who chose to have their children evaluated might have a higher proportion of autistic children than the parents who opted out.

However, there are just as many reasons to suspect that their numbers are an underestimate --- after all, they did write off all the nonparticipants labeled intellectually disabled, even though their own results show a substantial proportion of intellectually-disabled responders having autism. The authors also suspect underreporting of possible autism by both parents and teachers, because autism is stigmatized in South Korea (thus making parents less likely to want to admit that their child has it) and because the South Korean school day is so rigorous and structured (making teachers less likely to notice the social dysfunction that the ASSQ tests for, because there is so little socializing during a typical school day in Korea).

But the need to extrapolate so much data to make up for low response rates is a serious flaw in this study, though, as Prometheus points out, even when you restrict your gaze to the data that they actually have, you still see that the majority of confirmed ASD cases were in the general-population group, among children who had never seen a mental-health professional before.

Other bloggers posting about this study: Steven Novella at Science-Based Medicine; Sullivan at Left Brain/Right Brain and the Autism Science Foundation blog; Rose at Hard Won Wisdom; Michelle Diament at Disability Scoop; Paul Whiteley at Questioning Answers; Polly Palumbo at Momma Data; Aspie Editorial; Raphael Fraser at Music, Medicine & the Mind; Prometheus at A Photon in the Darkness; and MJ at Autism Jabberwocky (who has a detailed explanation of the ASSQ and its inherent biases)

*Only some of these children were referred for further evaluation: all the children scoring in the top two percentiles, half the children (chosen randomly, not by score) in the percentile third from the top, and one-third of the children in the percentiles fourth and fifth from the top.

**There's another interesting asymmetry within the general-population-derived ASD cases: a much greater proportion of those whose final diagnosis was Autistic Disorder had histories of psychiatric or psychological treatment. A majority (26 of 48) of students attending mainstream elementary schools who both met criteria for an ASD and had seen a psychiatrist or psychologist in the past ended up being diagnosed with Autistic Disorder, while the ASD students from mainstream elementary schools who had never seen a mental-health professional were mostly diagnosed with the other ASDs (27 of 104 with Autistic Disorder; 77 of 104 with either Asperger's or PDD-NOS).

***Perhaps it is how Mr. Peabody travels back in time?

Kim, Y., Leventhal, B., Koh, Y., Fombonne, E., Laska, E., Lim, E., Cheon, K., Kim, S., Kim, Y., Lee, H., Song, D., & Grinker, R. (2011). Prevalence of Autism Spectrum Disorders in a Total Population Sample American Journal of Psychiatry DOI: 10.1176/appi.ajp.2011.10101532

Non-Blog Happenings: Turkey Creek Fest

2011-05-25T14:13:00.003-05:00

Last Saturday, I made my first attempt at selling my jewelry out in the real world. I bought a vendor space at the Merriam Turkey Creek Festival, which includes a fairly large arts-and-crafts market.

Here's what my booth looked like, more or less:
(I say "more or less" because this picture was taken some time before the event, at my house rather than at the actual site. The festival organizers wanted to see what everyone's setup would look like, so I took some pictures in advance. I did not take any pictures on festival day, so this is all I have).

Here's a closer view of the sign I made:
And here's one of my display elements that I think looks cool, although it's really annoying to set up:Unfortunately, I didn't do well at all in terms of selling stuff --- I only sold two items*, and failed even to make back what I had spent on registration fees! Apparently this year's festival had lackluster turnout compared with what the organizers were expecting; they had planned for 10,000 people showing up, and I didn't think there were anywhere near that many. Most of the other vendors I talked to also had poor sales, although a few did really well. I think one of the reasons I had such bad luck was that there were so many other jewelry vendors --- whoever wanted to buy jewelry had maybe a dozen or more places to do it, and had probably already bought some elsewhere before they got around to my booth.

I don't think it was a total loss, because I had fun, distributed some business cards and learned a few things about picking the right festival to sell what you make --- people are more willing to buy stuff near the holidays, when they are looking for gifts, and different festivals attract different kinds of people, some of whom are more likely than others to want fancy beaded jewelry.

You don't find this stuff out if you never try.

*One of the things I sold was the asymmetrical blue necklace with the circular shell beads shown at the bottom of this post; I made two of those and sold one to my sister a while ago, and now someone has bought the other one, too. I was really proud of the design on that one, so I was gratified to see someone take it (even though it means I can't dig it out and wear it anymore).

Autistic Woman Writes Terrible Column; Speculation About Her Capacity for Empathy Ensues

2011-05-23T14:37:00.002-05:00

There's this woman, Penelope Trunk, who writes about climbing the corporate ladder on her blog, and in her book Brazen Careerist: The New Rules for Success. She's founded several startup companies, has worked in marketing and is now a full-time writer, focusing on career advice for young people.

She also has Asperger syndrome.

A few days ago, she wrote a column about Dominique Strauss-Kahn, the former head of the International Monetary Fund who is accused of sexually assaulting a hotel maid. In her column, Trunk advances the bizarre hypothesis that women who occupy the lowest rungs of the socioeconomic ladder, who work low-paying, menial jobs with no possibility of advancement, have greater freedom than higher-paid, professional women do to report sexual abuse by bosses, co-workers or clients.

Her notion is that someone working a low-paying job will not have the same incentive to hold onto that job that someone with a better job would have:

It has been clear for at least a decade that women who want to have a high-flying career should not report sexual harassment. I have written about this a zillion times, and before you argue with me, read the quotes from all the labor lawyers (representing plaintiffs) who agree.

The bottom line is that just about every woman who has entered the workplace has experienced sexual harassment, but the women who report it face retribution. ... [W]omen who complain about harassment generally lose their jobs in some convoluted but ultimately predictable way.
...
But, what about women who don't care if they get fired? Those women hold a lot of power in this equation.

It used to be that women with low-level jobs did not have the socioeconomic backing to stand up for themselves in the face of harassment. Today, women feel more empowered - even women in a low pay grade. And women across the economic spectrum can identify what crosses the line.

These women have nothing to lose when they report men who cross the line sexually. So the maid reported. And then, it turns out, all sorts of women in higher-up positions spoke up against Strauss-Kahn. The women wouldn't report the harassment on their own. They don't want to suffer retribution. But now there will be no retribution, so it's safe to come forward.

This is why men are going to focus harassment at the higher ranks of the corporate ladder. These are the women who have to keep their mouths shut if they want to keep climbing the ladder.

But God help the guy who harasses a woman with nothing to lose.

It's a great moment in history. Poor women are empowered to fight against lecherous men, and rich women can finally come out of the sexual-harassment closet because of it.

Matt Yglesias at Think Progress and Amanda Marcotte at Pandagon have both covered why this is astonishingly, massively wrong --- not just off, but actually the opposite of what's really true, which is that poorer women working menial jobs are more, not less, vulnerable to exploitation and abuse at work, and have fewer options for escaping or combating it. In believing otherwise, Trunk seems to have forgotten that, for some people, losing a job means not being able to pay rent, not having enough money to buy enough food, having to put off needed medical treatments or go without needed medications because they can't pay for them.

She also assumes that, if one quits a menial job, one can quickly and easily find another. This is just not true in an economy where almost one-tenth of all people in the U.S. are officially unemployed, and many more are working fewer hours than they'd like to. These low-wage service jobs are actually really competitive right now, since there are relatively few of them (since companies have mostly been weathering the Great Recession by laying off all the employees they could conceivably do without) and lots of people needing work.

There's a lot of other important stuff she leaves out, but I think the most important failing in her article is her assumption that women working low-paying jobs don't need those jobs. As a commenter on Pandagon noted, it's as if she's assuming that everyone has well-off relatives who can support them for a time, or has a trust fund or significant savings to fall back on. She doesn't seem to understand what poverty is.

Anyway, enough about Trunk. She's ignorant, naive and starry-eyed, and her good fortune and financial security have given her the (mistaken) impression that life is as easy for everyone as it has been for her.

Now, I want to talk about her critics.

It shouldn't surprise anyone reading this blog that commenters on both Pandagon and Yglesias's site have brought up her autism as a possible explanation for her failure to grasp basic economic and social realities.

From Pandagon:

Penelope Trunk's deal is that she has Asperger's and spends a great deal of time and energy figuring out the "rules" for social interaction. (Note: she is open about this and has written a great deal about it.) I got reading her because her perspective can bring some real insight into human interactions. But she can also get things dead, dead wrong.

If Ms. Trunk actually suffers from an illness which damages her ability to feel empathy, that both absolves her (partially) and leads to the next question --- why is she indistinguishable from the average conservative/libertarian?

My understanding is that while the inability to read nonverbal cues is quite acute, the practical effect of Asperger's also includes a lesser capacity for empathy, especially in relatively swift interactions.

From Yglesias's:

Trunk is wrong, obviously. But Asperger's Syndrome makes what she's trying to do here --- put herself in both DSK's and the maid's position and see who's right --- incredibly difficult. This isn't Tom Friedman telling us we gotta say "suck on that" to Iraq b/c he's a dick, this is someone with a legitimate medical condition exercising poor judgment by choosing to comment on something it's very hard for her to understand given that condition.

These comments are actually not representative of the threads in which they appear; these four comments are the only comments on both websites to blame Trunk's classism on her Asperger's diagnosis, and both threads also include other comments telling the quoted commenters that they are wrong to do so.

But it still depresses me that her diagnosis comes up at all in a discussion of why her article is wrong. One of the reasons it depresses me is because --- as the last comment I quote indicates --- it effectively bars all autistic people from participating* in discussions about workplace harassment. "Oh, you're autistic, you don't understand how normal people act." Because our "condition" prevents us from understanding other people, nothing we say about anything other people do --- even things they do to us --- has to be taken seriously. This is especially troubling when it's workplace (or school) harassment we're talking about, since autistic people are especially likely to be targeted for such harassment. (Indeed, we are often blamed for being bullied --- it's our own fault for being so weird, we're told as children.)

It also depresses me somewhat to see Trunk's excessive optimism about most people's ability to quit jobs at will, and find new jobs quickly and easily, attributed to her Asperger's rather than to her having a lot of resources at her disposal that she takes for granted, when most people with autism, when they can work, have terrible trouble finding jobs, and then holding on to those jobs for longer than a few weeks. If anything, we probably have a keener grasp than most people do of the risks inherent in quitting a job, because those risks are heightened for us.

I'd also like to point out, in two of those comments --- both written by the same person --- the use of autism as a metaphor for a self-serving political philosophy.

I've seen this once before, in an article on CommonDreams.org:

The language used in this passage --- citing "self-centered" behavior as the characteristic feature of autism, for example, or saying autistic people lack "linguistic, social, cultural or logical constraints to manage [our] lives" --- draws strong, if implicit, parallels between autism (a neurological condition) and selfishness (a moral quality).

These comments do a similar thing, with the "lack of empathy" that is so often cited as the core deficit of Asperger's syndrome. In the psychological literature on autism, the "empathy" being spoken of is usually cognitive --- we are unable to understand non-autistic people's behavior, feelings or states of mind, even though we are perfectly capable of caring about them. Yet, in the comment quoted above, the implication is that this lack of understanding also entails a lack of feeling for these incomprehensible others.

Autism is not a moral failing. Autistic people have moral failings, but they have them because they are people, not because they are autistic.

*Not in the literal sense of "You are not allowed to speak," but in the more nebulous sense of "You can speak, but if I know that you're autistic, I will attribute everything you say to your being autistic, and if any of it conflicts with what I think is true, or right, I will disregard whatever you say because your mind is diseased and mine is not."

Memento Mori: Thoughts of Mortality Can Subtly Bias People's Ideas about Human Origins

2011-05-05T21:51:00.001-05:00

Death, be not proud, though some have callèd thee
Mighty and dreadful, for thou art not so;
For those, whom thou think'st thou dost overthrow,
Die not, poor Death, nor yet canst thou kill me.

-- John Donne, from Holy Sonnet X (also called "Death, Be Not Proud")

BPS Research Digest described a recent study in which a group of psychologists looked at the influence of thoughts of one's own death on people's attitudes toward two different ideas about human origins: evolutionary theory and the variant of creationism known as Intelligent Design.
The researchers --- Dr. Jessica L. Tracy, who is an assistant professor of social and personality psychology at the University of British Columbia's Vancouver campus, where she is also director of the Emotion and Self Lab, Dr. Joshua J. Hart, who is an assistant professor of psychology at a small liberal arts college in New York called Union College, and UBC graduate student Jason Martens --- went to rather more trouble than is usual in these social-psychology studies in their search for a diverse study population.

Too often, these studies make claims about "people" based on surveys of psychology undergraduates at one university. In this study, one of the five mini-experiments involved people from all over the US who filled out surveys online. They ranged in age from 18 to 75, with a median age of 37, so most of them were substantially older than the college students questioned in the other four experiments. They also came from (one assumes) a broader distribution of socioeconomic classes; socioeconomic data are not given for any of the student groups, but the general-population group includes people from a wide range of income levels: 12% of respondents reported making less than $20,000 a year, 25% made between $20,000 and $40,000, 20% made between $40,000 and $60,000, 11% made between $60,000 and $80,000, 8% made between $80,000 and $100,000, and 9% made more than $100,000 a year. (Fifteen percent of respondents chose not to say how much money they made). The general-population sample also included people with more widely varying educational backgrounds: 26% had a high school diploma or less, 33% had been to college but hadn't gotten a degree, 32% had a college degree, and 9% had a postgraduate degree.

The other four groups consisted entirely of college students; two of the groups were all psychology students recruited from either UBC or Union College, one group was college students recruited online from all over the U.S. and Canada, and the last group was natural-science students* from UBC and Union College.
Each group of participants was asked to specify their religion and rate how religious they thought they were, and then to read a passage written by either Richard Dawkins or Michael Behe discussing either evolution or Intelligent Design, and rate their attitudes toward the two belief systems and their representative authors.

Right before they did this, they were asked to imagine one of two unpleasant things (death vs. painful dental work) and write briefly about their feelings. The reason for including this morbid exercise was to see if bringing mortality to the forefront of people's minds had any effect on their preference for a naturalistic or deistic worldview.
They found that, for most people, being reminded of death does tend to make you more receptive to Intelligent Design and more hostile to evolution. This is true regardless of one's educational attainment, religion or religiosity. It was also true regardless of one's attitude toward evolution as measured before the experiment.
(Some more explanation of that last sentence: yes, being more religious meant you were more likely to be receptive to Intelligent Design whether you were asked to contemplate death or not; likewise with being Christian rather than belonging to any other religious tradition, or claiming no religion. But within each category, the researchers saw the same effect of the memento mori nudging people toward Intelligent Design and away from evolutionary theory. Oddly, being reminded of death did not prompt people to rate themselves as more religious, even though it had a noticeable effect on their ideas about human origins.)

While how much education a person had didn't make any difference in how they responded to the memento mori, the type of education did have some dampening effects. Compared to the general-population and general-student-population groups, the psychology students expressed less hostility to evolutionary theory in response to the memento mori, although they showed the same increase in receptivity to Intelligent Design.

Resistance to these effects was strongest in the natural-science students, who actually responded in the opposite way to the memento mori; when confronted with the thought of death, they reported feeling a stronger affirmation of evolution and repudiation of creationism.

The authors hypothesized that people would react to the thought of death by looking for something that confers some lasting meaning on human life; for most people, a divine Creator fills that role readily enough. One of their experiments --- one of the two using psychology undergraduates as guinea pigs --- addressed this hypothesis directly: they compared the responses of students who had read a passage by Carl Sagan aimed at dispelling fears that the scientific understanding of the universe is nihilistic with those of students who did not read this humanistic passage, looking to see if exposure to a Middle Way between deism and nihilism didn't moderate the shift toward Intelligent Design prompted by the students' meditating on their own deaths.

Here is the Sagan passage:

It is very reasonable for humans to want to understand something of our context in a broader universe, awesome and vast. It is also reasonable for us to want to understand something about ourselves. And understanding the nature of the world and the nature of ourselves is, to a very major degree, I believe, what the human enterprise is about. Truth should be pursued, and science helps us pursue it; science gives us meaning. All we have to do is maintain some tolerance for ambiguity, because right now science does not have all the answers. This tolerance goes with the courageous intent to greet the universe as it really is, not to foist our emotional predispositions on it but to courageously accept what our explorations and knowledge tell us. The more likely we are to assume that the solution comes from something outside science, the less likely we are to solve our problems ourselves. If we are merely matter that is intricately assembled, is this really demeaning? If there's nothing in here but atoms, does that make us less, or does that make matter more? We make our purpose. And we have to work out what that is, for ourselves.

Ahhh. Humanism. (Go on, bask in it!)

Sure enough, students who read this passage did seem to be less threatened by evolution, even with thoughts of their own individual mortality foremost in their minds: they responded to the thought of death by reporting less of a warm feeling for Intelligent Design, and more for evolutionary theory.

Here is the authors' summation of their findings:

The present findings demonstrate that reminders of one's mortality --- inducing a state of mortality salience --- promote relative support for [Intelligent Design Theory], and skepticism toward [Evolutionary Theory]. Individuals respond to existential threat by becoming more accepting of a theory that offers a greater sense of meaning by depicting human life as having ultimate purpose (while appearing consistent with the scientific worldview), and/or less supportive of the theory that is the true mainstay of the scientific worldview but seems to offer little in the way of existential comfort. These findings also suggest that a desire to find greater meaning in human life accounts for this effect (at least the effect of mortality salience on belief in IDT), because it is reversed by making ET more meaningful, and among natural-science students for whom ET is already meaningful. The findings are notable because they (a) help explain why some people are motivated to believe in IDT and doubt ET in terms of fundamental psychological drives; (b) account for the underlying causal process; and (c) emerged regardless of preexisting religious ideologies, religious affiliation, or (with one highly limited exception, discussed below) views of evolution. The last point suggests that although religion influences baseline beliefs in IDT and ET, it cannot account for the impact of MS on these views. Given previous research suggesting that many MS effects are heightened, or occur only, among individuals with certain preexisting belief systems or cultural associations, the fact that we found no moderators of MS effects --- other than the extent to which naturalism is seen as meaningful --- suggests that embracing IDT or rejecting ET may be a unique, broadly appealing mechanism that addresses the existential concerns of religious and, for the most part, more scientifically oriented individuals alike. In contrast, explicitly religious ideologies tend to be fairly parochial, limiting their appeals and making them viable defenses only for those who already believe in a supernatural god.

Yet, an exception emerged in Study 5, where individuals whose life goals require strong acceptance of ET showed the opposite responses. Like those explicitly taught, in Study 4, to view naturalism as a source of meaning, natural-science students responded to MS with stronger antagonism toward IDT. This provides converging support for the causal process found in Study 4, and suggests that rejecting IDT can be a source of existential comfort for a limited population of individuals. These individuals are not simply those steeped in the scientific cultural worldview --- presumably psychology undergraduates fall into that category --- but rather those who more specifically view evolution as a critical part of their understanding of the world and a source of meaning and purpose.

They also point out in the final section of the article that these results might shed some light on why creation-vs.-evolution has remained such an intractable social issue: rather than being solely determined by religious doctrine, political ideology or (lack of) scientific literacy, people's embrace of creationism is also a response to the fear of death. Merely cataloguing the evidence for evolution doesn't address these underlying emotional issues; it tears away the defense mechanism while providing nothing to replace it. To my mind, that goes a long way toward explaining not only the deadlock between sides but also the rancor in this debate.

(Of course, many evolution-defending speakers do emphasize the existential perks of their worldview: a sense of wonder at being part of such a beautiful, intricate, ever-changing universe; the feeling of joy as you discover deeper and deeper layers of life's complexity; a stronger sense of kinship with other forms of animal life, etc. Why, even Richard Dawkins, the theorist featured in this study as representative of the godless, naturalistic worldview, has written a lot --- most notably in his book Unweaving the Rainbow --- about the beauties and benefits of that worldview. So the emotional angle isn't all there is to this, though I think it is important and not usually given the prominence it deserves).

*The authors do not explain what fields are included in this umbrella category "natural sciences." As it is commonly used, it encompasses fields having nothing whatsoever to do with evolution, like physics, or chemistry, or astronomy or geology. So I would quibble a bit with their assertion that strong acceptance of evolutionary theory is necessary for one to progress in the "natural sciences" --- it is quite possible to complete a degree in a non-biological science field without ever encountering it.

Tracy, J., Hart, J., & Martens, J. (2011). Death and Science: The Existential Underpinnings of Belief in Intelligent Design and Discomfort with Evolution PLoS ONE, 6 (3) DOI: 10.1371/journal.pone.0017349

Coming Unstuck in Time

2011-05-02T19:46:00.004-05:00

Neuroskeptic posted about this case study of two autistic young men who experience "time slips" --- extremely vivid memories, as if they are reliving the past instead of just remembering it:

CASE 1

Case 1, a male patient, was 16 years old at the time of his first visit to our hospital. He had not shown any delay in language development but had been isolated and unable to make friends since his infancy. In addition, he was extremely clumsy. He was extremely afraid of developing liver dysfunction. He had been bullied by a classmate when he was in the 8th grade; thereafter he refused to go to school and began to stay indoors. One day, he clearly recalled bullying incident that had occurred a few years earlier and re-experienced the feelings of fear and frustration as if he were once again experiencing that event. Thereafter, he often had similar experiences, even though he did not purposely intend to recall the event, and he became strongly distressed. He and his family stated that the recalled content was always the same. He thought that the distress could only be relieved by obtaining revenge on the boy who had bullied him, and he visited the boy's house with a knife. He was subsequently admitted to the emergency ward of our hospital.
...
The patient continued to experience the [time slip] even after he was hospitalized. If he saw any man with an appearance similar to that of the boy who had bullied him, he recalled the same experience of being bullied and became violent. The patient's doctor and the ward staff observed that the patient made no effort to avoid the recall stimuli but instead seemed to approach the stimuli. ...

CASE 2

Case 2, a male patient, was 27 years old at the time of his first visit. He had shown no marked clinical signs of delayed language development. However, since an early age, he had exhibited disturbed reciprocal sociality and did not have any close friendships. His interest was limited to collecting figures of comic characters. He began to be bullied during junior high school. He entered senior high school but quit during the second year. Thereafter, he tended to seclude himself at home. One day, he watched his neighbor discarding a cigarette butt in front of his home. Thereafter, he began to be annoyed by that memory. Almost every time he heard the voice of that neighbor or saw that man, he would leave his home and curse at the neighbor. His behavior became more violent and he eventually threatened the neighbor with a wooden sword. Because of this event, his family brought him to our hospital as an emergency patient.
...
In this case, an acoustic or visual stimulus (the voice or appearance of the neighbor) provoked the [time slip] resulting in the recollection of the same visual scene accompanied by the vivid emotions that he had experienced at the actual time. He took no measures to avoid remembering the event and tended to advance closer to the neighbor.

The authors of the paper observed four cases of time-slipping autistic patients in all; two of the troublesome recurring memories involved bullying at school, and two involved bad experiences with neighbors. All of the instances of time slipping that they heard about were bad; the memories triggered strong, unpleasant emotions and drove all four young people (three male and one female) to violence.

I mentioned in the comment thread at Neuroskeptic's blog that I experience this kind of vivid, immersive reminiscence --- it can be like those described in the article, where I remember being bullied or some other unpleasant experience with no buffers between me and it, but most often the things that come up are emotionally neutral, and not even necessarily episodes from my life; they might just be something I've seen before.

An example of the latter sort of memory might be my remembering, for decades, a random doodle I drew in preschool. Even now I can call it up --- a monster's face, with scraggly green teeth and a huge lumpy oval of a head. I even remember what color markers I used to draw it. I have similarly clear memories of making colored spinners out of paper plates, cutting off the edges, using a compass to bore a hole through the middle, and drawing a checkered pattern of concentric rings in contrasting colors. I would string a long piece of yarn through it, with a big, bulky knot on one end, and then spin it so that it would climb up the string and into the air, like a brightly colored UFO. This would captivate me for hours; I probably spent most of my schooldays in fifth or sixth grade doing this.

Most of these are really fragmentary, though; a single image, or a single multisensory impression. I don't really have flashbacks where I relive an incident, as the guys in the article seem to be doing. Even when I do recall an episode, it's only fragmented impressions that come back with this immediacy; the whole episode I have to reconstruct with narrative memory, as most people do.

I said on Neuroskeptic's blog that I considered my randomly retrieved archived sensory impressions to be a visual analogue to echolalia --- I hear echoes in my head of many of the things I hear, and sometimes I feel compelled to repeat them aloud; these memories are like visual echoes. However old they are, they persist, and sometimes they'll find their way into my conscious mind and I will hear the sound, or see the image, again. Even if I first saw it ten, fifteen, or twenty years ago.

What a Coincidence

2011-04-22T15:49:00.003-05:00

I just wrote a post about people's attitudes toward vaccination --- particularly the extent to which people worry about vaccines causing autism, and whether that worry leads them to skip recommended shots --- and now I see that Sarah was also moved to write something vaccine-related.

From her Tumblr*:

Pro-vaccine advocacy is not the same as advocating for the rights of autistic people or being anti-ableism. Pro-vaccine advocacy can sometimes repeat the same pernicious, ableist myths about autistic people which are so embedded in the anti-vaccine movement.

She's absolutely 100% right; where the anti-vaccine activists' rhetoric implies that it's better for one's child --- and other people's children, for that matter --- to contract potentially life-threatening, vaccine-preventable diseases than to be autistic, the pro-vaccine camp usually responds with "Nobody wants to have an autistic child, autism is a terrible tragedy and we should hurry up and find a cure, but ..."

It's a conciliatory tactic, meant to convey empathy for the clearly-distraught parents who blame vaccines for their children's disability. And that's good, as far as it goes; everyone deserves to be treated respectfully, and to have their feelings acknowledged and respected when they're debating emotionally-charged subjects.

A discourse that rests on the premise that autistic people should not exist isn't one that respects autistic people. It also implies that there are no autistic people participating in, or watching, the debate, and that's just not true. We're here, we have a personal stake in these issues; we deserve to be equal participants in the public discourse around autism.

*I can link to the post itself, but currently if I do that you're not able to read it --- other text overlaps with it. This is one of the many reasons Tumblr fails to appeal to me.

Poll Data on Vaccines Looks Contradictory, But Isn't

2011-04-21T22:56:00.000-05:00

Yesterday I ran across two seemingly contradictory factoids about public opinion on the autism-vaccine issue: this column in this month's Scientific American cites a poll* finding that just under half of U.S. adults either believe vaccines cause autism or aren't sure whether they do or not, while Left Brain/Right Brain reports on survey data** analyzed in two articles (full text here and here) in Pediatrics that found 79% of U.S. parents believe vaccines are safe.

So, which of these is true?

I'll start by pointing out that the subset of people who said they were "not sure" about the vaccine-autism issue could probably also fall into the subset of people who said they thought vaccines were safe in the other survey --- people's positions on issues can be pretty elastic, depending on how questions are asked and what kind of answers they think the pollsters want to hear. I think people who fall somewhere in the middle might have even more wiggle room than those who come down more strongly on one side or another.

The undecided group in the Harris/HealthDay poll, at 30% of respondents, was quite a bit bigger than the group professing a belief that vaccines cause autism (18%).

Thus, the proportion of all people who don't actively believe that vaccines cause autism in that survey is 82%, similar to the 79% of people who said they considered vaccines to be safe in the survey from two years ago.

Also, the two surveys sampled slightly different subsets of the U.S. population: the Harris/HealthDay poll was open to anyone over 18 (n = 2,026), while the two Pediatrics articles restricted their data set to respondents with minor children (n = 1,552). One of the articles went further, using only data from parents of children younger than 6 (n = 475).

Compared with the general population of the U.S. (reflected in 2010 census data), the group of people studied in the two Pediatrics articles is younger (the all-parents group was split about 60/40 between people under 40 and people 40+; two-thirds of the parents of young children were under 35; in the U.S. as a whole, a little less than half of all people, and about 60% of all adults, are older than 40), a lot richer and more likely to be female (split about 60/40 in favor of women).

What most interested me was the implication, in the article on parents of young children, that some of the people who think vaccines are generally safe, and believed vaccination was important for a child's health, are also worried that vaccines might cause autism:

Parents reported their attitudes regarding the safety and necessity of vaccines (Tables 2 and 3). The majority of the parents were either confident or very confident in vaccine safety (79.0%) and believed that vaccines are important to children's health (79.8%). Similarly, 73% of parents somewhat or strongly believed that the benefits of vaccines outweighed the risks. ...

Parents were asked to respond to a series of 11 potential vaccine-related concerns and were also given the opportunity of stating that they had no vaccine-related concerns (Table 4). Just more than one-fifth (20.8%) of the parents reported that none of the 11 issues listed were of concern to them. The most common concern reported by the parents was that it is painful for children to receive multiple shots during 1 doctor's visit (44.2%). Other concerns reported by >25% of the parents included their child receiving too many vaccines in 1 doctor's visit (34.2%), vaccines causing fevers in their child (28.3%), children getting too many vaccines in their first 2 years of life (27.8%), and vaccines causing learning disabilities such as autism (26.2%).

The article's authors suggest that these parents are probably weighing the potential risk of autism against the protection from disease, and choosing to vaccinate despite their misgivings because they think the benefits outweigh the risks. (Data from the Harris/HealthDay poll would also tend to support this idea of a cost-benefit analysis; even among people who believe that vaccines can cause autism, a majority thinks schools should require children to be vaccinated).

The other article, the one that studied all parents of minor children, also looked into what sources parents considered credible in the matter of vaccine safety.

Overwhelmingly, the person they trusted most was their children's doctor (76% said they trusted their children's doctor "a lot," 22% said "some" and only 2% said they did not trust their children's doctor); just as overwhelmingly, people put very little stock in what celebrities have to say about vaccine safety (in a clean reversal of the figures for doctors, 2% of parents said they trusted celebrities "a lot", 24% said they trusted them "some", and 74% did not trust them at all). For all the other types of people --- health-care providers apart from their children's doctor, government officials, friends and family, and parents who believe their children were harmed by a vaccine --- most people said they felt "some" trust. Similarly, of the people who look at media relating to vaccine safety, most placed "some" trust in all of the media categories listed: medical organizations' websites (the only category that also had a large number of people saying they trusted it "a lot"), government websites, newspaper or magazine articles, TV, vaccine manufacturers' websites and anti-vaccine websites.

These survey results suggest to me that people aren't the gullible sheep skeptics often accuse them of being. They are wary of anecdotal evidence, give more weight to experts' opinions than to laypeople's, and give the most weight to those authorities they consider neutral, or to have their child's best interests specifically in mind. Also, even without an extensive grounding in virology, immunology or epidemiology, they seem to grasp the importance of universal vaccination in maintaining herd immunity.

People are wiser than the conventional wisdom gives them credit for being.

Freed, G., Clark, S., Butchart, A., Singer, D., & Davis, M. (2011). Sources and Perceived Credibility of Vaccine-Safety Information for Parents PEDIATRICS DOI: 10.1542/peds.2010-1722P

Kennedy, A., Basket, M., & Sheedy, K. (2011). Vaccine Attitudes, Concerns, and Information Sources Reported by Parents of Young Children: Results From the 2009 HealthStyles Survey PEDIATRICS DOI: 10.1542/peds.2010-1722N

*Poll conducted by Harris Interactive and HealthDay, on January 11-13, 2011

**The annual HealthStyles survey, conducted by the CDC and the public-relations firm Porter Novelli, throughout the month of January in 2009

More on "The Geneticization of Autism"

2011-04-18T14:04:00.004-05:00

In Saturday's post I quoted at length from Kristin Bumiller's 2009 article "The Geneticization of Autism: From New Reproductive Technologies to the Conception of Genetic Normalcy", which explores the social and political implications of a largely genetic understanding of illness and disability. I think almost all the ideas she develops in that article have merit, especially her points about the limitations of a public-health system modeled on the larger consumer economy, and about coercive, eugenic aspects of genetic testing as it is used today in the U.S.

But there was one part of the article that really bothered me, and that's what I'm going to talk about in this post.

Here's the relevant passage:

The most divisive expression of dissent to geneticization is found among groups that seek to document environmental causes of autism, such as the use of mercury in vaccines. These outsiders, dubbed the "Mercury Moms," are engaged in insurgent activism against the medical establishment and most directly the Centers for Disease Control and Prevention (CDC). They claim that the CDC has perpetuated a cover-up of medical evidence confirming the link between thimerosal (a mercury preservative previously used in many childhood vaccines) and the increase in autism. In stark contrast to professionals, parents and activists who subscribe to a genetic understanding of autism, the Mercury Moms are frequently characterized as hysterical and antiscience (Kennedy 2007; Desmon 2008). As Ken Plummer (2001) has suggested in his account of what he calls "intimate citizenship," this kind of very public debate over controversial issues demonstrates that there is something much grander at stake than the validity of scientific research. For the Mercury Moms, their activities fulfill their role as protectors and provide assurance that they have pursued all avenues to help their children. As activists, the Mercury Moms are often marginalized by the media, national autism advocacy groups, and the professional establishment, not only because they dispute official information but also because they amplify the fears of all parents about the possibility of seemingly benign choices, such as complying with childhood vaccination recommendations. Their advocacy is even seen as dangerous because it could lead to widespread rejection of vaccinations that prevent the resurgence of deadly diseases. In part, the marginalization of the Mercury Moms results from their own tendency toward absolutism, but at the same time there is little mainstream recognition of scientific evidence that supports the possibility of links between exposures to toxins and autism (DeSoto and Hitlan 2007).

I know she's writing an academic paper, and a social-science one at that, so she has to be neutral and objective in her language in a way that a blogger doesn't, and that the truth or falsehood of any given hypothesis about autism's root causes is beyond the scope of her article, but it still reads to me like she's giving the much-discredited thimerosal hypothesis equal weight with the prevailing notion that genetics probably play a role in autism.

(I also think she greatly overstates the extent to which most autism researchers think of autism as being 100% genetic*, or the extent to which genetic variations associated with autism are necessarily inherited.)

Most troubling to me is this phrasing, "... environmental causes of autism, such as the use of mercury in vaccines." Using what may be the most exhaustively debunked hypothesis ever to be proposed as an explanation for autism as an example of bias against research into possible environmental causes, triggers, or correlates of autism strikes me as misguided.

It equates two statements --- "Environmental factors may have something to do with autism, either on their own or in concert with genetic predispositions" and "Mercury in vaccines causes autism" --- treating them as equally viable avenues of inquiry, and implying (by treating the latter as merely an instance of the former, broader category) that refusal to entertain the vaccine hypothesis means that one's mind is closed to all environmental hypotheses of autism. That's just not true.

I don't totally hate her analysis of the "Mercury Moms" movement --- I think she's right that they illustrate the lopsided nature of the partnership between the medical establishment and popular health movements, and also that they represent the loudest dissenting voice to the autism-is-genetic conventional wisdom, and that they are often caricatured in sexist tropes, as hysterical, ignorant women. But I think that if she wants to make the point that the autism-research establishment is ignoring potentially fruitful research into environmental factors, she should not use this group to illustrate it; the alternative explanation of autism that they espouse has been investigated, over and over again, and come up empty. Not wanting to pursue a dead end isn't the same as ideological narrow-mindedness, and many of the researchers who dismiss the Mercury Moms with such contempt are also looking into other environmental factors for a possible link with autism.

I can see why this group appeals to her, since, along with loudly repudiating the genetic understanding of autism, and claiming that a ubiquitous, expert-approved medical practice is actually causing the spread of autism, they are laypeople and mothers rather than doctors or academic researchers. They hit all the right notes as far as opposing the "genetic citizenship" model is concerned; I just don't think you can put aside such things like the ever-increasing weight of evidence against their claims, their indifference to this evidence, and the public-health consequences of their anti-vaccination agenda, to say how much of a role the geneticization narrative also plays in pushing them to the margins. I'm certainly willing to believe it's a factor, but I think the biggest factors are the other ones I mentioned.

Bumiller admits as much in the last sentence of the paragraph I quoted: "In part, the marginalization of the Mercury Moms comes from their own tendency toward absolutism ..."

The other thing that annoyed me somewhat was the positioning of two factions that differ on the matter of what causes autism and what kinds of things are likely to be useful in treating, curing or preventing autism, but that agree in their understanding of autism as a disease that ought to be eradicated, as the two opposite poles of this debate on what autism is and what society ought to do about it. There's a third facet as well, one that I know Bumiller knows about, because she wrote an earlier article about it, and mentions it in passing in this one; it's the neurodiversity movement, which she glosses over as another proponent of the idea that autism is genetically determined.

Many of us do think autism has a genetic component, and some of us think it's entirely genetic and has been around for a very long time, but for the most part we don't give a lot of weight to the matter of what causes autism. It's not critical to our objective, which is acceptance and integration into mainstream society.

And there are premises of the "genetic-citizenship" model that we question, or outright reject, just as the Mercury Moms reject the idea that doctors always know best. Many of us reject the ethic of individual self-care that the genetic-citizenship model revolves around, and we certainly reject the idea that it is every citizen's duty to prevent disabled people from being born. We also have a very fractious relationship with the major autism-advocacy organizations, as a search on the term "Autism Speaks" on most autistic people's blogs will tell you.

It seems to me that this article would've been much the richer had it included more of this stuff, maybe comparing and contrasting the ways in which the Mercury Moms and the neurodiversity and disability-rights movements uphold or challenge (because both groups do some of both, I think) the doctrine of genetic citizenship.

Bumiller, K. (2009). The Geneticization of Autism: From New Reproductive Technologies to the Conception of Genetic Normalcy Signs: Journal of Women in Culture and Society, 34 (4), 875-899 DOI: 10.1086/597130

*Clearly there are plenty of researchers who think genetics is the major factor contributing to autism, and some who do think of autism solely in genetic terms, but the idea that environmental factors also play a role is hardly out of the mainstream. In fact, there are currently several large studies under way of possible environmental correlates of autism, in part because the environmental issue hasn't been as well-explored as the genetic one, and researchers know that and are looking to change it. That hardly seems to me like the idea of autism having environmental triggers is being suppressed by the scientific and medical communities ...

Why is it ...

2011-04-18T14:00:00.002-05:00

... that Blogger always seems to have some weird auto-formatting going on that overrides whatever I'm trying to do? Most of the time, it automatically skips a line whenever I put in a line break, but in my last post it's been ignoring my line breaks completely, and showing my post as a huge unbroken wall of text. (I had this problem with WordPress, too, when I would sometimes write for Here Be Dragons).