Signal Transduction in Autism

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

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

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

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 ...

(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

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

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)
...
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]

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

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

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"

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

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

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

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.