Post #200!

Right now, this is the 200th post on this blog, though that will probably change once I finish up some very old posts in the draft queue --- some of which I'll want to keep backdated so that they will appear in chronological order as part of a series.

There's also another milestone I passed recently: this blog is now a little over three years old.

Two hundred posts over three years means I average about a post a week, with two every third week. Given how long it's taken me to write posts lately, that sounds incredible.

Through a (Brain) Scanner, Darkly

EXECUTIVE SUMMARY: In the August 11 issue of the Journal of Neuroscience, Christine Ecker and her colleagues at the Institute of Psychiatry at King's College in London describe a new tool they've developed for finding differences between autistic and non-autistic brains that go beyond "x brain structure is bigger/smaller in autistic people"; their method takes into account overall patterns of gray matter structure and organization. Their tool not only identifies these subtle, pervasive differences, it also "learns" them, using them to classify individual (computer models of) brains as autistic or not-autistic. The tool works quite well for that kind of classification, doing significantly better than chance on almost all its individual components, and reaching 65 to 85 percent accuracy as a whole. It can also distinguish between autistic brains and some other kind of non-neurotypical brain, in this case ADHD.
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(Still image from the TV show "Dollhouse")

Apart from this brief mention on Amanda's blog, I hadn't read anything at the time about the new multidimensional brain scan described last month in the Journal of Neuroscience. I was intrigued, because one thing that's been awfully elusive to autism researchers is a consistent, reproducible biological marker that's specific to autism.

There've been some hints of neuroanatomical differences between autistic and non-autistic people in previous studies, but those differences --- in, say, the size and activity of the amygdala, the size and shape of the hippocampus, the size of the cerebellar vermis, the distribution of gray matter and white matter, the density of certain cell types within the cerebellum, the thickness of the cerebral cortex, or even in the overall size of the brain --- don't always show up when researchers look for them, nor do they always show up in every member of the (very small, carefully selected and usually quite homogeneous) group of autistic people being studied.

The authors of the recent study --- Christine Ecker, Andre Marquand, Janaina Mourão-Miranda, Patrick Johnston, Eileen M. Daly, Michael J. Brammer, Stefanos Maltezos, Clodagh M. Murphy, Dene Robertson, Steven C. Williams and Declan G. M. Murphy --- suspect that there might be a broader, more pervasive pattern of altered brain structure that underlies all the different, highly variable, changes to individual structures within the brain that are sometimes seen in autism:

[R]eports of region-specific differences in ASD are highly variable [for review, see Toal et al. (2005) and Amaral et al. (2008)]. Such variable findings may simply be explained by confounds such as clinical heterogeneity between studies, or analytical techniques. Alternatively, variability in findings may indicate that differences in brain anatomy in ASD are relatively subtle and spatially distributed, and are difficult to detect using mass-univariate (i.e., voxelwise) approaches. Last, given the multiple etiology of ASD, it is likely that its neuroanatomy is not confined to a single morphological parameter but affects multiple cortical features.

To try to find out what kinds of subtle, structural differences might characterize the brains of autistic adults, the researchers scanned the brains of twenty autistic men*, twenty men without any psychiatric, neurological or developmental disorders, and nineteen men without autism but with ADHD (to provide a non-autism, but also non-neurotypical, control group to try and isolate neuroanatomical variations particular to the autism group), used the MRI data to create three-dimensional computer maps of each subject's brain, and then fed the values of five different measurements taken at each vertex of the computer model (which is made of tiny triangular facets meant to approximate the brain's curved surfaces) into a statistical-analysis algorithm called a Support Vector Machine, which Neuroskeptic describes much better than I could in this post.

The five things they measured at each vertex of their virtual mock-brains are as follows: average convexity/concavity of the cortical surface (i.e., the distance between the cortical surface at a given vertex and where the cortical surface would be if the brain were smooth); cortical thickness; mean (radial) curvature (i.e., the radius of the circle that could be drawn underneath the curve of the cortical surface); metric distortion or Jacobian, which is the ratio of the areas of the triangular facets making up the cortical surface and the gray/white matter interface; and the pial area, which is the average area of the triangular facets touching each vertex.

Since some of these things are very hard to visualize, here's a diagram:

Figure 1, in Ecker et al. (2010)

Overall, this five-parameter model works pretty well at predicting who is autistic** and who isn't, though I was surprised to see how much its accuracy differed from one side of the brain to the other. On all measures, there's a huge gap --- a gap of 20 percentage points or more, in all but one instance --- between the two brain hemispheres in terms of a given measure's accuracy (i.e., its ability to sort all subjects into the correct category), sensitivity (ability to correctly identify autistic subjects --- i.e., having a high number of true positives and a low number of false negatives) and specificity (ability to correctly identify non-autistic subjects --- i.e., having a high number of true negatives and a low number of false positives).

For whatever reason, the left hemisphere much more than the right showed consistent neuroanatomical differences between autistic and non-autistic subjects.

Here's a classification plot showing the two categories as determined by applying the five-variable classifier to the left hemisphere:
Here, all but two autistic subjects are placed into the positive (i.e., autistic) category, and all but four control subjects are correctly placed into the negative category.

Contrast that with the right-brain results ---

--- where you see a lot more crossover between categories, plus several subjects straddling the border line. It is also only in the left hemisphere that any correlation is observed between how far to the right of the dividing line a person is and their ADI scores in the social and communication domains.

Some parameters also performed better than others: cortical thickness had the highest accuracy levels of any parameter (90% in the left hemisphere!), followed by metric distortion.

Finally, in the left hemisphere the model also succeeded in distinguishing ADHD subjects from autistic ones. (In the right hemisphere, it placed about equal numbers of ADHD subjects in each category). That's important because it shows that the model is actually picking up on characteristics of autistic brains, instead of just registering all deviance from "normal."

So, what *ARE* these characteristics of autistic brains? Well, they vary by region --- not only in terms of which parameter is relevant, but also in terms of how autistic people differ from neurotypicals on a given parameter.

For instance, if you look at this map of how the autistic subjects' brains differed from the controls in terms of cortical thickness, you can see that some parts of the brain (mostly on the temporal lobe) tend to have a thicker layer of gray matter in autistic people, while in other areas (mostly on the frontal and parietal lobes), the cortex tends to be thinner in autistic people.

Figure 4 (A), in Ecker et al. (2010); red areas represent more gray matter in relation to average non-autistic brain, blue areas represent less gray matter.

Some of the areas that showed up as having an "excess" of gray matter surprised me, as differential activity in those areas (fusiform gyrus, superior temporal sulcus) had previously been theorized to underlie autistic "deficits" in making sense of faces.

Besides these differences in amount of gray matter, there were also some strong differences in gray matter geometry: first, the autistic subjects showed greater sulcal depth in two regions --- the intraparietal sulcus and the superior frontal cortex --- and second, the inferior parietal lobes and certain regions in the right frontal lobe --- the right supramarginal gyrus, postcentral gyrus, and orbitofrontal cortex --- along with the precuneus, showed different patterns of cortical folding.

For example, here's the right intraparietal sulcus:

From Figure 5 (B), in Ecker et al. (2010)

The blue line represents the cortical surface for the average control subject; the red line represents the average autistic subject's cortex. You can see that the sulcus goes down deeper in the autistic subjects, and also that the gyri on either side are a bit steeper.

I would like to point out, again, that it's not necessarily any single variation at any one region of the brain that this statistical analysis has tied to autism, though --- it's a pattern of gray-matter distribution. It's also a pattern that's so far only been observed in a tiny, rather homogeneous sample of autistic men --- much larger, broader-based studies of this classifier need to be done to see if the same patterns hold up for all of the people currently lumped together under the category "autistic," or whether separate neuroanatomical phenotypes will define autistic subtypes.

I would also like to see future studies done using different diagnostic tools to define the autistic group --- if the goal of this research is to establish a biomarker for autism diagnosis so that we can finally be done with frustratingly ambiguous diagnosing-from-behavior, it will hardly do to have the biomarker be dependent on one of the older behavioral diagnostic tools for its template!

*According to this table showing demographic data on the autistic and control (but not the ADHD) subjects, the autistic subjects were mostly young, and some middle-aged, men (the average age (33) was much closer to the age of the youngest person (20) than it was to that of the oldest person (69)) and had a very wide range of IQ scores as measured by the Weschler Abbreviated Scale of Intelligence. The standard deviation, for full-scale IQ and for verbal and performance IQ, was around 20 points for the autistic group, and scores ranged from 76 (just one point over the cutoff point the authors chose to designate intellectual disability, which is a full-scale IQ of 75) to 141, with verbal IQs ranging from 78 to 133 and performance IQs from 77 to 138. These subjects, I'd like to point out in the spirit of adding to Michelle Dawson's recent post on functioning levels, were all defined as having Asperger's or high-functioning autism.

**Autistic subjects were determined to be such using either the ADI-R (for fifteen subjects), the ADOS (for five) or both (two).

Ecker C, Marquand A, Mourão-Miranda J, Johnston P, Daly EM, Brammer MJ, Maltezos S, Murphy CM, Robertson D, Williams SC, & Murphy DG (2010). Describing the brain in autism in five dimensions--magnetic resonance imaging-assisted diagnosis of autism spectrum disorder using a multiparameter classification approach. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (32), 10612-23 PMID: 20702694

Link Roundup: Fat Is a Feminist Issue Edition

Within the last week or so, there's been a spate of really good feminist blogging about intersections between feminism and fat acceptance.

From Feministe, three guest posts: one by Atheling, who blogs at This Wicked Day, about similarities between slut-shaming and fat-shaming; one by zuzu, who used to be a Feministe contributor and now writes mostly at her own blog, Kindly Póg Mo Thóin, that deals with how fat-shaming health alarmism actually harms fat people's health, both by keeping them out of doctors' offices and by leading doctors to look no further than their patients' BMIs to explain their various health problems; and one by Spilt Milk (who writes an eponymous blog) about how body-shaming permeates mother-daughter relationships and how fat acceptance is radical because it's based on kindness and, well, acceptance, first of yourself and then of others.

There's also this terrific post by Meowser at Fat Fu, which contrasts the reasonable things fat-acceptance advocates are actually saying with the raving denialism everyone else seems to hear:

We say, "Weight is, for the most part, not a very good proxy for health, and there are much better ones, like socioeconomic status." They hear, "Being dozens of pounds over (or under) your baseline weight is just ginchy for you, and your doctor should never bring it up ever." ...

We say, "What causes people to weigh what they do is complex and multifactorial, and varies a lot from one person to another - and you can't tell what people's habits are from their pants size." They hear, "Weight is purely inherited and has nothing whatsoever to do with behavior." ...
...
We say, "Hounding kids about their weight is not likely to result in happier or healthier kids OR adults, for the most part." They hear, "We don't care if all the children lose their toes to dry gangrene by the time they're 12, as long as we can eat all the baby-flavored donuts we want."

Finally, there's this post by Aunt B at Tiny Cat Pants. She talks about two important things that often go unacknowledged in discussions about fat, public health and how U.S. society has changed: first, the class aspects of sitting around waxing oracular about why Those People are so fat and what they must be doing wrong ...

... [W]e talk about obese people having no self-control or being too stupid to know what to put in their bodies or lacking access to experts who could tell them what to do with themselves; the narrative is all about how obese people put all kinds of things in their bodies because they're too stupid (or uneducated to know better) and they thus have really negative life outcomes. Now, read that same sentence and swap out "obese" for "poor."

It works just the same.

I find that interesting. In both cases, it's about a group that has too many people in it, who need education and expertise and guidance, and who are deemed failures or troublemakers if they resist efforts from the outside to improve them.

The word "class" doesn't quite fit, but I think it has to do with demanding people want to strive to remove evidence of what has been deemed their shitty circumstances. Yes, of course, you will be punished for striving. But you will be punished worse for not striving.

It's almost as if the obese/the poor, by their very existence, insult their "betters" by not recognizing and properly responding to their "betters'" expertise on how best to live life.

... and, later, about implicit sexism in how most people --- even most feminists --- talk about fat:

Is it really not clear to feminists how the "obesity epidemic" is about reasserting the right to police women's bodies? Except now, we're doing it for your health!When people talk wistfully about how "nobody cooks at home anymore" who do you think that "nobody" used to be? When people talk about how kids don't get the same free rein of the neighborhoods they used to have, who is the unspoken monitor of all that free time?

Who has, supposedly, fallen down on the job causing us all to be fat?

Spilt Milk also addresses the mother-blaming aspect of obesity panic in her post --- she describes the double bind mothers find themselves in where, if a daughter develops an eating disorder, it's the mother's fault for being too uptight about food and teaching the daughter to hate her body, while, at the same time, if the children are fat, the mother is blamed for being too lazy to cook healthy food and make sure her children get enough exercise!

EDIT: Radical feminist blogger The Bearded Lady has also written two recent posts on fat acceptance: one --- like zuzu's that I linked earlier --- about fat women and doctors, and how doctors both miss underlying conditions that need treatment because they think fat people just need to lose weight, and also how doctors will see a fat woman's fatness as so dangerous, so unhealthy, that they will prescribe extremely aggressive measures to get them to lose weight. Her other entry is about her personal journey toward fat acceptance, and how for her, accepting her body came as part of her radical feminism, and her rejection of heterosexuality:

[A]lthough I had previously strenuously denied any connection between hating my body and wanting men to like me, when I stopped wanting men to like me, I stopped hating my body. Not immediately, in a flash of insight, but gradually, over time, I realised that I was looking at myself in the mirror and not thinking 'ugly' -- not thinking anything at all, really, just looking for toothpaste on my chin or whatever.

Hating my body/self was, for me, expressed not only in extreme dieting and thinking myself deeply ugly, inside and out. I also hated my body by allowing men to use it, by letting men fuck me, when I (the tiny little voice inside me that was barely allowed to speak) knew that I was being violated and used. It was a joyful moment when I realised I could just stop.

I especially liked that entry of hers, because it's probably the closest any other woman has come to describing a relationship to her body, and to the concept of "attractiveness" and whether one possesses it or not, that resembles mine. It's not a total match, and some things are actually very different between the two of us --- I never went through a period of intense dieting and *wanting* to be thin and conventionally attractive like she did, for instance --- the end state she describes is very close to what I have, and it entails a rejection of beauty and attractiveness rather than the reclamation of those things that seems to be a lot more common for large women who learn to love their bodies. I might write more about how that came about for me later, but for now I was just really happy to see someone else articulate these feelings that I also have, and have struggled to characterize accurately.

Neither This Blog Nor My Etsy Store Is Dead ...

... and what better way to demonstrate those two facts than by posting pictures of my latest offering?
One reason I haven't been posting, reading or commenting as much on blogs is because I've been having a glut of ideas for jewelry pieces, and thus have been spending a lot of time making them.

Most of them are sitting around in a half-finished state, as problems arise and have to be troubleshot, worked around or --- sometimes --- the piece in question needs to be started over altogether.

(Problems usually take the form of too many loose ends not staying hidden, too many unsightly knots or awkward bulges, or a bead unexpectedly shattering as I try to force too many strands of thread through it.)

But I have two new projects that *are* totally done, and here's one of them!

As I might have mentioned before, I love geometric shapes. I also love contrasting colors.
This panel bracelet manages to tie both of those things I think are awesome together, with its framed boxes in alternating canary yellow and ... whatever you call a light blue that has a (very slight) hint of teal or turquoise in it. Each of those panels is made of twelve rows of twelve seed beads, all woven together with peyote stitch. (The beads are wider than they are long, so a 12 x 12 matrix ends up being a rectangle, not a square).
Another thing I love --- on bracelets, at least; on necklaces they tend not to stay fastened --- is a button or toggle clasp. Much easier to open or close than those thumb-operated ones with the tiny levers that require you either to have long fingernails (nope) or to never, ever lose your grip (also nope) in order to open them one-handed. Lately, just about everything I make has a button clasp, but I did get a set of toggle clasps recently that I decided to use making these:

(That's my arm --- big, hairy, and stylish!)

I made three of these; two to sell/wear myself until they are sold, and one I gave as a gift.

I really like this motif of the rectangular panels with geometric designs on them strung together on a sort of cuff. I think it's one of the more original design templates I've come up with, and I'm definitely doing a lot more with it.

"I Had to Get Through School by Going Through the Back Door": Temple Grandin on Gatekeeping in Higher Education

Here's an excerpt from Temple Grandin's book Thinking in Pictures, about how educational institutions tend to keep bright but unconventional thinkers out of science, engineering and academia, rather than steering them toward these professions:

There are few Einsteins today. Maybe they all flunk the Graduate Record Exam or get poor grades. I had to get through school by going through the back door, because I failed the math part of the Graduate Record Exam. My grades in high school were poor until I became motivated in my senior year. In college I did well in biology and psychology but had great difficulty with French and math. Most of the great geniuses have had very uneven skills. They are usually terrible in one subject and brilliant in their special area. Richard Feynman had very low scores on the Graduate Record Exam in English and history. His physics score was perfect, but his art score was in the seventh percentile.

Even Einstein, after graduating from the Zurich Federal Institute of Technology, was not able to obtain an academic appointment. He annoyed big important professors when he told them that their theories were wrong. He had to take a job at the Swiss patent office. While he was a patent clerk, he wrote his famous theory of relativity and got it published in a physics journal. Today it would be extremely difficult for a patent clerk to get a paper published in a physics journal. If Einstein had lived today, his paper probably would have been rejected and he would have stayed in the patent office.

There are many examples of great scientists, artists, and writers who were poor students. Charles Darwin, the father of evolutionary theory, was not able to master a foreign language. When he left school, he was considered only an ordinary student. Darwin wrote in his autobiography, Life and Letters, which was edited by his son Francis, "I was considered by all my masters and by my father as a very ordinary boy, rather below the common standard of intellect." He found life at Cambridge University dull and did poorly in mathemathics. Darwin's saving grace was his passion for collecting. This provided the motivation to go on his famous voyage on the Beagle, where he first formulated the theory of evolution.

Gregor Mendel, the father of modern genetics, was unable to pass the exam to get a high school teaching license, according to Guinagh Kevin in his book Inspired Amateurs. He conducted his classic experiments in the corner of a monastery garden with pea plants. When he presented the results at his university thesis defense, he failed to get his degree. Nobody paid any attention to his wild theories, but fortunately 120 copies of his paper survived and were recognized as the works of genius that they are after his death. Today his principles are taught in every high school science class.

During my career, I have met many brilliant visual thinkers working in the maintenance departments of meat plants. Some of these people are great designers and invent all kinds of innovative equipment, but they were disillusioned and frustrated at school. Our educational system weeds these people out of the system instead of turning them into world-class scientists.

Anemone has also covered this issue in some depth: her essays about struggling to find a niche in both the academic and work worlds deal as much with the difficulties of gifted (but not necessarily autistic) people as with those of autistic people (who may or may not also be gifted).

Anemone also has some very similar thoughts about the generalist bias in education and how that puts autistic students at a particular disadvantage:

[Tyler Cowen, writing in the Chronicle of Higher Education] suggests that academia is a favourable environment to the autistic adult, because it allows for specialization in great detail. Personally I found that even an undergraduate education was too generalized for me, and while I did enjoy grad school much more, it was too little too late, and I lacked sufficient training to get into a PhD. Maybe it depends on which department you're in, or maybe it depends on what you look like. Or maybe you need to get into a field where you hit it off with your instructors, so you can tap into the informal half of your education, something I did not do.

I suspect that both science and the arts are favourable to autistic people, precisely because they do allow a person to focus on one thing to the point of excellence. I have pointed out before that this desire to focus on one thing in detail is characteristic of both gifted/successful people and autistic people. I suspect that it is also true of athletes, since a great deal of successful athleticism comes from the brain, too.

I wonder what would happen if all people with specialist brains were put on a different track by high school, on the basis of how their brains worked rather than their interests, with fewer, more concentrated courses each year, so that the generalists could continue to generalize, but the specialists could commit to excellence. As it is now, it's on the basis of whether you're interested or not (at least in North America), and some of us specialists are unable to get into specialized programs because we get elbowed out of the way, or don't know how to make the transition, or don't even know we're allowed to. I wanted to switch to a fine arts high school as a teenager, but I thought you could only switch at the beginning of grade 9, plus I thought you had to be some sort of super-genius, with a portfolio that would knock over God. All without any help from anyone.

I also think a generalist bias might prevent some children who are gifted in one area from being recognized as gifted at all --- with our educational system's focus on grade point averages and standardized test scores (which measure, and average, a person's ability across a wide range of cognitive skills --- sometimes with very different skills lumped together in the same category, like including geometry and algebra questions in a single math category, when geometry and algebra use different kinds of reasoning, and many people find they are good at one and poor at the other), a child who scores very high in some areas and very low in others averages out to be merely mediocre.

I also think it's important to point out that neither Anemone nor Temple Grandin is talking about only autistic people in their discussion of gifted people with wildly uneven abilities; both concede that this sort of cognitive profile is a common one in autistic people, but Anemone stresses that it is also very common among intellectually gifted folks, most of whom are not autistic. Grandin believes that a lot of the same cognitive traits underlie autism, certain mental illnesses and exceptional creativity, and that the balance between giftedness and disability depends on how extremely one manifests a particular trait. A little bit of hyperfocus can enable you to become an expert on something; too much, and you're stuck with unproductive, debilitating obsessions.

PLoS ONE: Children from Wealthier Families More Likely to Meet Criteria for an ASD

EXECUTIVE SUMMARY: A recent study shows that wealthier families are somewhat likelier than middle- and low-income families to have autistic children. The study compares surveillance data on a cohort of eight-year-old children in fourteen areas of the U.S. in 2002 and 2004 whom the CDC decided, based on school and medical records, met diagnostic criteria for ASDs with U.S. Census data from 2000 on eight-year-old children living in those same areas of the U.S. Statistical analyses were done on both groups' demographic data, which showed that the autistic children tended to come from somewhat better-off neighborhoods than the general population of eight-year-old children. Because of the study's use of public-school records, and its inclusion of a sizable group of never-before-diagnosed autistic children, its authors believe the association they found between higher socioeconomic status and higher rates of autism prevalence is not solely due to richer people's unfettered access to diagnostic services, but instead might also reflect some other factor that positively correlates with both autism and higher SES: the authors suggest both advanced parental age and excessive hygiene as potential candidates for this mystery factor.
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This article in the Kansas City Star alerted me to a study published in PLoS ONE on July 12, giving the first indications I've seen that the conventional wisdom about autism and social class --- that autism is mainly a disorder of the upper classes --- might have more to it than just the simple fact that people with unfettered access to health care are a lot more likely than people without such access to get diagnosed with autism-spectrum conditions.

The way I had understood it, there was no big mystery there: people who can afford to see a doctor in non-emergency situations are going to get all sorts of things diagnosed at a higher rate than people who can't afford that kind of preventive care. In that framework, a higher rate of autism diagnoses among children from wealthy families says nothing about autism per se; it just serves as one more example of the huge inequality of access to health care here in the U.S.

The study I mentioned --- carried out by Dr. Maureen S. Durkin and her colleagues --- tries to address how much of the association between autism and higher socioeconomic status (which Durkin says shows up about half the time in the existing literature on the topic) is due to this gap in access to health care and how much may be due to other factors yet to be uncovered.

To try to include autistic children lacking formal diagnoses in their analysis, Durkin et al. relied on the CDC's Autism and Developmental Disabilities Monitoring Network, whose methodology is described here* on the CDC's website:

In 2000, CDC established the Autism and Developmental Disabilities Monitoring (ADDM) Network to track the prevalence and characteristics of ASDs in the United States. The ADDM Network is a multiple-source, active, population-based surveillance system that reviews developmental records at educational and health sources and employs a standardized case algorithm to identify ASD cases.

There is also a flowchart showing where they get their data from and how they decide which children are actually autistic; unfortunately, the flowchart is still pretty vague about which "educational and health sources" they use. It does mention that they use "multiple" of each, though.

So, in the years 2002 and 2004, the ADDM Network collected data on 407,578 (in 2002) and 172,335 (in 2004) eight-year-old children living in fourteen areas around the country: the northern half of Alabama; the central region of North Carolina; the Coastal and PeeDee regions of South Carolina; the entire states of Arkansas and West Virginia; parts of the cities of Denver, Colorado; Atlanta, Georgia; St. Louis, Missouri; and Salt Lake City, Utah; and the cities and surrounding areas of Phoenix, Arizona; Baltimore, Maryland; Newark, New Jersey; Philadelphia, Pennsylvania; and Milwaukee, Wisconsin**. Of these children, 2,685 met diagnostic criteria for an ASD in 2002; in 2004, the number was 1,376.

Durkin et al. took the data on all the children determined to be autistic --- minus the ones living in Utah and West Virginia, since those sites didn't provide enough information to determine socioeconomic status for the children living there --- and compared prevalence rates for ASDs across three socioeconomic "tertiles": high, middle and low socioeconomic status, as determined by three factors: 1) percentage of people in the area living above the poverty line, 2) percentage of adults 25 and over in the area who have at least a bachelor's degree, and 3) median household income for the area. They also compared those factors between the autistic children and the general population of eight-year-olds living in the same areas at the time of the 2000 census.

Compared with the general population of eight-year-olds living in the same areas, autistic eight-year-olds are somewhat less likely to live in "poverty areas," or areas defined in the 2000 census as having 20% or more of its families with children living on poverty-level incomes, with 16.8% of autistic children living in such areas and 25.8% of all children living in them.

Similar small-but-noticeable differences show up with respect to the other two factors, median household income and proportion of adults with college degrees. Among the general population, the median household income was $42,898; among families with autistic children, it was $50,114. Autistic children, on average, tended to live in census blocks where a larger proportion of adults 25 and older had bachelor's degrees; 30.3% had them compared with the general-population figure of 24.8%.

These differences kept showing up, even when the comparisons were set up differently: besides comparing autistic children with their (approximate) peers on measures of socioeconomic status, the researchers also compared autism prevalence rates across the three socioeconomic-status categories they'd created, and found that the richest group had the highest proportion of children meeting criteria for autism, the middle-income group had the second-highest, and the poorest group had the lowest. This pattern showed itself across all the racial categories included in the study, too.

Now, the question is, does the design of this study correct sufficiently for (well-established) class differences in access to specialized medical and educational services? Can its findings of autism prevalence increasing with socioeconomic status be taken at face value?

Part of the reasoning behind the authors' contention that at least part of the association between autism and wealth is real lies in their use of school-based, as well as clinic-based, documentation. Theoretically, all children in the U.S. going to public schools are going to be monitored by their teachers and screened for learning and developmental disabilities if they start to have problems with classwork, behavior or social interaction. But not all schools have the resources to make this sort of individualized attention a reality. It probably won't surprise you to hear that schools in districts where poor people live have less money than schools in districts where richer people live, and accordingly the poorer school districts are less likely to employ psychologists, paraprofessionals or even college-educated teachers. With less space and less staff, also, even very dedicated, insightful and observant teachers aren't able to give individual attention to every student they see struggling.

The U.S. educational system might be more equitable than its health-care system --- last I heard, public schools were still legally required to educate every student living in their districts --- but similar issues of accessibility plague both systems. Even if our educational system is technically socialized --- available for free to everyone, paid for with taxes --- there are still huge differences between the kind of education (including special education) you can get at a well-funded school in a primarily upper- or middle-class district and the kind of education you can get at a school in a poor district. The richer districts can levy additional taxes to give more money to their schools, and students going to those schools also pay student fees to cover equipment and activities.

All of this leads me to suspect that ascertainment bias can be just as big a factor in an educational setting as in a medical setting.

The study authors tackle this issue in their Discussion section:

An important limitation of this study was that the ADDM Network surveillance system relies on information for children who have access to diagnostic services for developmental disabilities. We could not rule out the possibility that the quantity and quality of evaluations and the information available for case ascertainment might have varied by SES. We looked for evidence of this by examining the number of evaluations per child with ASD recorded in the ADDM Network surveillance system, reasoning that if the higher prevalence of ASD among children of higher SES was due to increased access to diagnostic services, high SES might be associated with a higher number of diagnostic evaluations per child. However, we found no association between the number of evaluations per child and SES. We also examined the mean ages at diagnosis by SES and found that children of high SES received an ASD diagnosis at an average age of 58.0 months, 1.1 month earlier than those of middle SES (p = 0.2838) and 2.7 months earlier than those of low SES (p <>

The other important factor that somewhat mitigates the effect of differential access to the educational and medical professionals who can diagnose autism and provide autism-related services on this study's outcome is the inclusion of a subgroup within the group of autistic children they studied who had no prior diagnosis of autism; there were enough of these children (1,244) to do a separate statistical analysis of this group to determine whether the association between autism and socioeconomic status still holds up among children who had never been evaluated. The association did still stand: even among those children with no previous diagnoses of ASDs, the ratio of autism prevalence as determined by the CDC of low- to middle- to high-SES children was 0.78:1:1.09. (That is, the poorest children were somewhat less likely to be autistic than the middle-income children, who in turn were somewhat less likely to be autistic than the wealthiest children). It's worth pointing out that the ratio for children with previous ASD diagnoses is stronger in both directions, at 0.70:1:1.25.

While I'm not sure this study goes far enough to correct for huge systemic inequities in availability of services, those two findings --- that number of evaluations per child does not vary with SES, and that autism prevalence does vary with SES among never-diagnosed children --- introduces some doubt in my mind where there had been none before. Maybe there *is* more to this socioeconomic-status thing than just access to diagnostic services. I remain skeptical, but no longer absolutely convinced that ascertainment bias explains everything.

*A more complete description exists in this 2007 article in Pediatric and Perinatal Epidemiology, for which I cannot find the full text anywhere online for free.

**The list of fourteen areas applies to 2002; in 2004, only eight of those areas participated --- Alabama, Arizona, Georgia, Maryland, Missouri, North Carolina, South Carolina and Wisconsin. That's why the numbers are so much lower for 2004.

Durkin, M., Maenner, M., Meaney, F., Levy, S., DiGuiseppi, C., Nicholas, J., Kirby, R., Pinto-Martin, J., & Schieve, L. (2010). Socioeconomic Inequality in the Prevalence of Autism Spectrum Disorder: Evidence from a U.S. Cross-Sectional Study PLoS ONE, 5 (7) DOI: 10.1371/journal.pone.0011551

On Falsifiability

"You can't prove a negative."

This statement gets tossed around a lot in arguments, especially arguments that lend themselves to the more abstract and theoretical planes, like "Does God exist?" or "Are we alone in the universe?" In those contexts, it's perfectly true --- you can't establish, once and for all, that X (whatever elusive entity X might be) doesn't exist.

A similar precept goes, "Absence of evidence is not evidence of absence."

But if it's true that you can't prove a negative, why is science news so regularly coming out with stories announcing such proofs? "Danish researchers find no link between thimerosal and autism," say, or "Mozart's music does not make you smarter," or "[G]iving up caffeine does not relieve tinnitus" --- all of these statements imply that something has been shown not to be the case.

I think the difference between those statements and the kind of "proving a negative" that's supposed to be impossible lies in how the questions are phrased. For a hypothesis to be testable, it has to have a set of conditions that must also be true --- and are measurable --- if the hypothesis is true. If you can make a prediction based on your hypothesis --- say, that if it's true that thimerosal in vaccines causes autism in children, then autism rates among school-aged children should fall as people stop using thimerosal in vaccines --- and if that prediction's failing to come true necessarily means your hypothesis was wrong, you can falsify the hypothesis. Based on what happens, your hypothesis can be proved wrong or right.

There's nothing inherently impossible about proving that a hypothesis is not true; usually, the statements that cannot be disproven are so vague, or deal with such a vast array of possibilities (i.e., "Space aliens exist somewhere in the universe") that there's no way to test them.

"Autism Science Blogging"

In the comments section of this final post at Here Be Dragons, Riel and Yarrow^Amorpha articulated some things that had always bothered them about the Autism Hub:

There's a lot on the Hub that doesn't seem to have much to do with ethics or reality. We occasionally got the impression that it was really by and for this clique of people who all had this thing they called "autism science blogging." Which seemed to have little to do with what we understood science to be or with autistic people's lives, and to be mostly about making repetitive snarky debunking posts every time anyone anywhere says anything about autism being caused by vaccines and/or mercury poisoning, no matter how many times they have previously established that it is not. Often with ignorant to downright appalling attitudes about disability in general mixed in, and oh-so-fun ableist language. I think you [Kowalski] blogged about that previously, actually.

(Here are several of Kowalski's previous posts dealing with unexamined biases and unchecked privilege in the skeptical, atheist, autism, liberal- and radical-feminist blogospheres).

I don't have a problem with autism- and/or science-related blogs (or blogs devoted to other topics that sometimes dabble in science) writing a lot of anti-vaccine-debunking posts; debunking posts help make a whole field somewhat accessible to laypeople, by sketching the outlines of whole complicated bodies of evidence that it would be really hard or time-consuming to discover on one's own, and sometimes debunking each permutation of the vaccines-cause-autism meme requires you to talk about very different things.

It it's the thimerosal-in-vaccines-causes-autism incarnation, you can get into the pathophysiology of mercury poisoning and how it differs from what's generally been observed about the brains of autistic people, and you can also get into all the different epidemiological studies comparing autism prevalence before and after thimerosal was phased out of a given country's vaccines. If it's the measles-DNA-in-MMR-causes-autism variant, though, you get into very different matters: how the immune system works, how measles virus infects a host and causes disease, what viral DNA can and can't do inside a human cell.

I love this kind of writing, and do a fair amount of it myself. (Indeed, this was one of the first things I wanted to do on the Internet! My first-ever plan for a website, which I had to abandon as being way too ambitious, was to create one big webpage indexing *all* of the autism-related research articles I knew of; this blog was to be separate, dealing only with autism in fiction. I later decided to just write about whatever research interested me on this blog, too, since my rudimentary computer skills do not allow me to build a website from scratch!)

I certainly understand what Riel and Yarrow^Amorpha are talking about when they mention the ignorant, intolerant attitudes toward autism, and toward disability in general, in much autism-related science blogging, though. Most writing I've seen debunking the vaccines-cause-autism conspiracy theory* includes at least one disclaimer about how the writer is totally not suggesting that autism is anything less than a terrible disease that ought to be eradicated, and the writer understands the desperation parents of autistic children feel, especially since autism is incurable. Our existence is a terrible tragedy that ought to have been averted; that's the common ground on which reasonable people are encouraged to meet in these discussions.

That's to say nothing of the casual ableism that permeates so many of these posts, and especially their comment threads. Armchair diagnosis of quacks and Internet cranks with various mental illnesses masquerades as critique, serving no purpose but registering the author's and commenters' disdain for whomever is being discussed while at the same time making readers who are actually diagnosed with whatever mental illness is being bandied about as a slur feel shut out of the discussion.

Anyway, I just wanted to reproduce, and endorse, those observations of Riel and Yarrow^Amorpha's while also defending debunking.

*Anymore, I suspect I'm doing that particular belief too much credit by calling it a "hypothesis"; hypotheses are for testing, and get modified or discarded when the evidence proves them wrong. The "hypothesis" that vaccines cause autism seems to be impervious to evidence.

A Little Bit More About Empathy

EXECUTIVE SUMMARY: I'm reproducing a table from one of the (freely available, so I think I'm in the clear, copyright-wise) articles I cited in my last post, with commentary. The table shows average scores --- totals and subscales --- from the three alexithymia- and empathy-related questionnaires used in those studies: the Toronto Alexithymia Scale (TAS-20), the Bermond-Vorst Alexithymia Questionnaire (BVAQ) and the Interpersonal Reactivity Index (IRI). The places where autistic people do, and don't, differ from non-autistic people in Silani et al.'s (2008) use of these questionnaires don't mesh with the stereotypical, extreme-systemizer understanding of autism popularized by Simon Baron-Cohen.
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I couldn't fit it into this post, but there was something else I wanted to highlight in the results of this study (full text here).

It isn't all that important to the conclusions of the research itself, and it doesn't have much more than anecdotal value, since it's drawing from such a small sample, but because it runs somewhat counter to the conventional understanding of empathy in autism I wanted to showcase it anyway.

Think of it as a numerical version of Michelle Dawson's "Verbatim" series.

Anyway, here are the mean scores (totals and subscales; standard deviations shown in parentheses) of the fourteen autistic (there were fifteen, but one didn't finish all the tests) and fifteen control subjects on the Toronto Alexithymia Scale (TAS), Bermond-Vorst Alexithymia Questionnaire (BVAQ), and Interpersonal Reactivity Index (IRI)*.

Toronto Alexithymia Scale

(Total)

______________________________________

Controls (n = 15)..................................43.7 (12.7)

Autism/Asperger (n = 14)........................55.6 (9.7)

(Subscale F1 - difficulty identifying feelings)

______________________________________

Controls............................................14.3 (5.3)

Autism/Asperger..................................18.5 (6.5)

(Subscale F2 - difficulty describing feelings to others)

______________________________________

Controls............................................11.8 (4.4)

Autism/Asperger..................................17.2 (4.2)

(Subscale F3 - externally oriented thinking**)

______________________________________

Controls............................................17.6 (5.3)

Autism/Asperger..................................19.9 (3.1)

Total TAS scores were significantly higher for the autistic group than for the control group, but only one subscale showed significant differences: the "difficulty describing feelings" subscale. This is not at all surprising when you consider how many autistic people --- even speaking autistic people --- even speaking autistic people who never exactly lose their capacity for speech; they're just better at it some days and worse at it other days --- say they have a lot of trouble with language, especially in the "finding the right words for whatever it is I'd like to communicate" sector.

Bermond-Vorst Alexithymia Questionnaire

(Total)

______________________________________

Controls............................................47.0 (11.1)

Autism/Asperger..................................53.2 (8.7)

(Subtotal - Cognitive Component)

______________________________________

Controls............................................27.0 (7.6)

Autism/Aspeger...................................32.4 (4.9)

(Subtotal - Emotional Component)

______________________________________

Controls............................................20.0 (5.4)

Autism/Asperger..................................20.9 (6.0)

(Subscale 1 - Verbalizing)

______________________________________

Controls............................................9.7 (3.5)

Autism/Asperger..................................11.7 (2.3)

(Subscale 2 - Fantasizing)

_______________________________________

Controls............................................10.2 (3.5)

Autism/Asperger..................................10.6 (2.8)

(Subscale 3 - Insight)

_______________________________________

Controls............................................8.9 (2.9)

Autism/Asperger..................................12.4 (3.0)

(Subscale 4 - Emotional Excitability)

_______________________________________

Controls............................................9.8 (2.7)

Autism/Asperger..................................10.2 (3.9)

(Subscale 5 - Concrete Thinking)

_______________________________________

Controls............................................8.4 (3.1)

Autism/Asperger..................................8.2 (3.0)

On the BVAQ, total scores do not differ significantly between the autistic and non-autistic groups; significant differences between groups only appear on one of the five subscales --- the Insight subscale, which in other versions of the test might be called Analyzing. It reflects your ability to think about what you're feeling and why you might be feeling it. There is also a significant disparity in the whole cognitive component of the BVAQ, which is the sum of the Insight, Verbalizing and Concrete Thinking subscales. (While only the Insight subscale showed a significant difference between the autistic and non-autistic groups' average scores, the Verbalizing subscale showed a difference that, while it did not rise to statistical significance, wasn't negligible either; by contrast, scores on the Concrete Thinking subscale are virtually identical).

Interpersonal Reactivity Index

(Total)

_______________________________________

Controls...........................................59.6 (8.8)

Autism/Asperger.................................52.8 (11.0)

(Perspective-Taking Scale)

_______________________________________

Controls...........................................16.1 (4.5)

Autism/Asperger.................................9.8 (3.1)

(Fantasy Scale)

_______________________________________

Controls...........................................14.7 (4.3)

Autism/Asperger.................................12.2 (5.0)

(Empathic Concern Scale)

_______________________________________

Controls...........................................17.7 (4.2)

Autism/Asperger.................................16.4 (4.2)

(Personal Distress Scale)

_______________________________________

Controls...........................................11.3 (5.0)

Autism/Asperger.................................14.6 (6.3)

Several things are worth pointing out about the IRI scores. First, there's no significant difference in overall scores --- according to this measure of empathy, in this instance, autistic people are not significantly less empathetic than non-autistic people. Second, only one of the subscales shows a significant difference between autistic and NT study participants, and that's the perspective-taking subscale, which measures the (cognitive and imaginative) ability to put oneself in another's shoes. This disparity could be explained by invoking Baron-Cohen's (and, I think, also Uta Frith's --- she's an author of both of the studies I just finished writing about) idea that autistic people are lacking in Theory of Mind; it could also be explained by pointing out that autistic people and non-autistic people have very different experiences, even of the simplest and most fundamental sorts. Our emotions and senses work differently from theirs, and we have to work hard adjusting for that in our attempts to consider things from a non-autistic person's perspective. (Curiously, non-autistic people are never asked to consider things from an autistic person's perspective. Maybe if some researchers asked them to do that, they would find a corresponding impairment in neurotypicals' Theory of (Autistic) Minds!) On the more purely emotional measures --- the empathic-concern subscale, which measures one's capacity for pity, tenderness and worry on another person's behalf, and the personal-distress scale, which measures the extent to which you become upset at another person's distress --- the differences are either vanishingly small (the difference between the average scores of the autistic group and the control group on the empathic-concern subscale is just a little over one-quarter of a standard deviation) or favor the autistic group (on the personal-distress subscale, the autistic group scores about three points higher --- about half a standard deviation --- than the non-autistic group).

So, while according to these measures we do indeed have trouble "mind-reading," we are not any more concrete, literal-minded or fantasy-deprived than non-autistics, and even if we can't infer another person's state of mind, we feel for them just the same. In fact, our distress when they are unhappy might even be greater than non-autistic people's.

Autistic people are emotionless robots?

Myth busted.

*Anemone has posted the IRI as an interactive quiz on her website, so, if you want to, you can go there and take it yourself.

**This refers to a preference for thinking and talking about concrete, external objects or events rather than feelings. An example question from this subscale asks whether, when you're talking with someone about your day, you prefer to focus on what happened rather than on how you felt about it.

Silani, G., Bird, G., Brindley, R., Singer, T., Frith, C., & Frith, U. (2007). Levels of emotional awareness and autism: An fMRI study Social Neuroscience, 3 (2), 97-112 DOI: 10.1080/17470910701577020

Autism, Alexithymia and Empathy

EXECUTIVE SUMMARY: Earlier this year, a group of psychologists and neuroscientists published a paper showing a relationship between alexithymia (difficulty identifying and expressing feelings) and lower levels of activity in a part of the brain that previous studies have linked with the capacity to feel empathy for another person. They did not find any such relationship between autism and decreased activity in this region of the brain, although autistic people do experience alexithymia at much higher rates than the general population. This paper builds on a similar article from 2008, by most of the same authors, that sought to measure autistic people's levels of emotional self-awareness by, first, measuring their self-reported levels of alexithymia and empathy, and then having them undergo fMRI scanning while looking at, and reporting their response to, strongly emotionally charged images. That study's results were somewhat ambiguous, since there wasn't a group of strongly alexithymic subjects who were not autistic, so, while levels of alexithymia were shown to correlate with reduced brain activity in both the autistic and control groups, there were also some differences between the autistic group's results and those of the control group that might result from multiple factors. The later study seems to suggest that much of this difference arises from the autistic group's higher overall scores on measures of alexithymia.
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Emotions --- whether they're one's own or another person's --- are widely believed to be terra incognita for autistic people. Many of us believe this about ourselves; Data and Spock are the "Star Trek" characters in whom autistic fans tend to see themselves.

To a degree, this is true of us more than it is true of non-autistic people. We have much higher rates of alexithymia --- the inability to put emotional states into words --- than the general population. Just because we can't talk about what we're feeling doesn't mean we don't understand it, though; it just means we have a much harder time explaining it to other people. (Also, even when we're not alexithymic, it's fairly common for autistic people to have all sorts of problems with language in general). It's also made even harder by the fact that the kinds of things that we feel tend to be a lot different from the kinds of things non-autistic people are likely to feel in any given situation. We are usually very much aware that our experiences are different from theirs, even if we might not have much of an idea how they might differ.

I've already discussed the role of shared experience, or lack thereof, in the "empathy gap" between autistic and non-autistic people. (Other people have, too). What I'm going to do in this post is discuss two recent fMRI studies comparing brain activity during tasks designed to elicit empathic emotional responses between groups of autistic and non-autistic study participants.

Both of these studies start from the assumption that autistic people really are objectively impaired at picking up on emotional cues, and seek to identify neural and psychological factors specific to autistic people that might explain this.

The first study --- Silani et al., 2008 (full text here) --- involved two groups of fifteen participants (thirteen men and two women), one made up of people with diagnosed autism-spectrum conditions and the other of age-, sex- and IQ-matched controls. The researchers had both groups fill out several questionnaires --- the Toronto Alexithymia Scale (TAS-20), the Bermond-Vorst Alexithymia Questionnaire (BVAQ-B) and the Interpersonal Reactivity Index (IRI) --- and then look at images on a screen and evaluate something about them on a sliding scale (either their own emotional response to the image, or the balance of light and dark colors within the image) while having their brain activity measured by fMRI.

In their Introduction, the authors propose a three-tiered model of emotional experience: the first layer is the emotion itself, and the changes in mental and physical state associated with it (e.g., racing heart, sweating, agitation, excitement, shivers, lethargy or tears); the second layer is the awareness of what is happening to you physically; and the third is awareness of the emotional reasons for what is happening to you physically. They cite previous fMRI studies (and reviews) implicating the amygdala and orbitofrontal cortex in first-order emotional experience, and the anterior insula and anterior cingulate cortex in what they call "interoceptive awareness" --- awareness of bodily changes, including those brought on by emotions.

They didn't find very much different between the autistic and control subjects' patterns of brain activity, and the major correlations they established --- between low scores on the alexithymia indices, high scores on the empathy index, and higher levels of activity in the mid-anterior insula during the emotion-rating part of the experiment --- held equally true for both groups of subjects. The autistic participants also showed a correlation between those test scores and increased activity in the left amygdala; no such pattern occurred, even to a diminished extent, among the non-autistic ones. Another area of the brain --- a circuit consisting of the medial prefrontal cortex, anterior cingulate cortex, precuneus, frontal inferior orbital cortex, temporal poles and cerebellum, collectively called the "mentalizing network" --- also lit up during this task, and showed lower overall activation for the autistic group than for the control group, although its activity was not correlated to either measure of alexithymia, which surprised the researchers.

So, while this study helped shed some light on why some people --- including many autistic people --- have such poor insight into their own states of mind (to say nothing of others'), it raised almost as many questions as it answered. To what extent are the differences in empathizing between autistic and non-autistic people attributable to autistic people's greater chances of being alexithymic? Why are autistic people so much more likely to be alexithymic? Why didn't alexithymia correspond to lower activity levels in the mentalizing network while the subjects were supposed to be mentalizing?

The second study --- by Bird et al., 2010 (full text here) --- was designed to try to make the relationship between autism, alexithymia, cognitive empathy and emotional empathy a bit clearer. It involved two groups of eighteen men: one whose members all had diagnoses of autism or Asperger syndrome, and most (13 of the 18) of whom also met Autism Diagnostic Observational Schedule (ADOS-G) criteria for either autism or autism-spectrum disorder; and another group of neurotypical men matched with the experimental subjects for age, IQ and degree of alexithymia. Within both groups, participants ranged from low scorers to very high scorers on the Toronto Alexithymia Scale (TAS-20): within the autistic group, scores ranged from 37 to 80, with a standard deviation of 11.8 and an average score of 57.2; within the control group, the average score was 50.3, the standard deviation 14.5, and the range 27 to 72. A TAS-20 score of 60 indicates alexithymia; scores between 52 and 60 are considered borderline.

Here is the authors' own assessment of what they're trying to find out:

To determine whether the often-reported empathy deficit in autism spectrum conditions is due to the alexithymia comorbidity within this group or to the presence of an autism spectrum condition, we sought to investigate: (i) whether empathic brain responses were correlated with degree of alexithymia in autism spectrum condition and control groups; (ii) whether the relationship between degree of alexithymia and empathic brain response varied as a function of autism spectrum condition diagnosis; and (iii) whether the autism spectrum condition and control groups exhibited differential levels of empathic brain activity after accounting for levels of alexithymia.

The experiment in the second study was actually kind of disturbing: they tried to measure empathy directly --- rather than relying on self-reported answers to questionnaires --- by having the participants bring someone they cared about into the lab with them, and then tracking their brain activity as that person received mild electric shocks on the back of their right hand.

I hadn't thought researchers were allowed to cause pain in experiments anymore. This worries me.

Whether or not I am personally creeped out by this experiment, though, it did furnish some pretty solid evidence that it's alexithymia, and not autism per se, that dampens people's capacity to feel other people's emotions as if they were their own.

Among members of both groups, seeing their partners in pain (before one member of each pair was to be shocked, a symbol would appear on the screen in front of them telling them who the unlucky person was and how intense the shock would be, so the researchers had a way to compare their subjects' reaction to different levels of vicarious distress) triggered activity in the left anterior insula, which intensified in proportion to the severity of the shock their loved one was getting. That activity --- the "empathic brain response" the researchers are talking about --- also correlated negatively with the subjects' scores on the alexithymia questionnaire: the more alexithymic the men in either group were, the less intense their brain activity in response to their loved ones' pain was.

Besides shoring up the hypothesis that alexithymia (or whatever its absence is called --- lexithymia?) has something to do with empathy, this newer study also throws up some roadblocks on the free-association superhighway pop psychology has built between autism (particularly Asperger syndrome) and lack of empathy.

After correcting for degree of alexithymia, all significant between-group differences in brain activity vanished. The researchers also looked for a correlation between degree of alexithymia and severity of autistic symptoms as measured by the ADOS, and found none:

A final analysis was conducted to investigate a possible concern with respect to the current study: that alexithymia scores are a proxy for symptom severity in autism spectrum conditions. If true, the present findings could be explained by hypothesizing that controlling for degree of alexithymia before testing for group differences in empathy causes all variance due to autism spectrum condition symptom severity to be removed. This would result in a spurious null result and a false conclusion of there being no empathy deficit in autism spectrum conditions after controlling for alexithymia. Such a possibility is made plausible by the inclusion of participants who, despite having received a clinical diagnosis of autism or Asperger's syndrome, do not meet ADOS-G cut-off [criteria] in the sample of individuals with autism spectrum conditions. These individuals may raise the mean empathic brain response in the autism spectrum condition group and mask any differences in empathy due to diagnosis of an autism spectrum condition (if alexithymia scores are a proxy for autism spectrum condition symptom severity the corollary of this would also be true; highly alexithymic participants in the control group may also have high levels of autism spectrum condition symptoms). To guard against the possibility that any null effects observed in the data could be caused by overly inclusive diagnostic classification, or statistical covariance between ADOS scores and alexithymia scores, the ADOS scores were regressed against empathy-related brain data and alexithymia scores as measured by the TAS. ADOS scores were unrelated to all these measures (all correlations P > 0.4). Inspection of scatterplots (Supplementary Figs. 1-3) showing the relationship between the ADOS and empathy-related brain data, TAS and BVAQ scores, reveals that it is not the case that participants with low ADOS scores are clustered at the extremes of the distributions of any measure. In addition, the relationship between alexithymia (TAS scores) and empathic brain response was found in both the autism spectrum condition and the control groups, who were matched for degree of alexithymia. Thus, it is unlikely that any of the observed effects are an artefact of inappropriate diagnosis, or a statistical artefact due to high covariance between autism spectrum condition symptom severity and degree of alexithymia.

So, autism and alexithymia are distinct, unrelated, though overlapping things, and only one of them --- alexithymia --- seems to have any bearing on affective empathy. (Cognitive empathy might be a different story; questionnaire data from both studies show significant differences between autistic and control subjects on subscales specific to cognitive empathy/Theory of Mind, like the perspective-taking subscale on the Interpersonal Reactivity Index and the cognitive component of the Bermond-Vorst Alexithymia Questionnaire. There's still plenty to criticize about this measure of empathy, too, particularly its one-sidedness, but that's not the focus of this post).

Bird, G., Silani, G., Brindley, R., White, S., Frith, U., & Singer, T. (2010). Empathic brain responses in insula are modulated by levels of alexithymia but not autism. Brain, 133 (5), 1515-1525 DOI: 10.1093/brain/awq060

Silani G, Bird G, Brindley R, Singer T, Frith C, & Frith U (2008). Levels of emotional awareness and autism: an fMRI study. Social neuroscience, 3 (2), 97-112 PMID: 18633852