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

Does Teaching Emotional Literacy Foster Compassion?

EXECUTIVE SUMMARY: Time magazine ran an article this week describing a radical new anti-bullying program that tries to teach young children empathy by having them observe a mother and baby, and try to figure out what the baby is feeling. This is supposed to help them imagine themselves in another's place, and also to help them learn to put their own feelings into words. Evaluations of the program show that it does decrease "aggressive behavior" and increase "pro-social behavior," but I have doubts that it's really all that effective against the kind of cruel harrassment and intimidation campaigns so many of us remember from middle and high school. It doesn't seem to me like that's anger boiling over so much as a decision coolly reached that some people just aren't worth treating like people. And I'm not sure empathy training can address that.

An antibullying initiative sure to give Counselor Troi the warm fuzzies

I read this article in this week's Time magazine with great interest --- it describes an educational program called Roots of Empathy that aims to make children kinder, more peaceful and more considerate of others by teaching them to pay attention to how other people are feeling, and to the ways one's own behavior can affect other people's feelings.

Here's a description of how it works from Roots of Empathy's own "About" page:

At the heart of the program are a neighbourhood infant and parent who visit the classroom every three weeks over the school year. A trained ROE Instructor [link] coaches students to observe the baby's development and to label the baby's feelings. In this experiential learning, the baby is the "Teacher" and a lever, which the instructor uses to help children identify and reflect on their own feelings and the feelings of others. This "emotional literacy" taught in the program lays the foundation for more safe and caring classrooms, where children are the "Changers". They are more competent in understanding their own feelings and the feelings of others (empathy) and are therefore less likely to physically, psychologically and emotionally hurt each other through bullying and other cruelties. In the ROE program children learn how to challenge cruelty and injustice. Messages of social inclusion and activities that are consensus building contribute to a culture of caring that changes the tone of the classroom. The ROE Instructor also visits before and after each family visit to prepare and reinforce teachings using a specialized lesson plan for each visit. Research results from national and international evaluations of ROE indicate significant reductions in aggression and increases in pro-social behaviour.

That's the theory; here's a bit from the Time article describing how it works in practice:

At a public school in Toronto, 25 third- and fourth-graders circle a green blanket and focus intently on a 10-month-old baby with serious brown eyes. Baby Stephana, as they call her, crawls back toward the center of the blanket, then turns to glance at her mother. "When she looks back to her mom, we know she's checking in to see if everything's cool," explains one boy, who is learning how to understand and respond to the emotions of the baby --- and to those of his classmates --- in a program called Roots of Empathy (ROE).

...

One of the most promising antibullying programs, ROE (along with its sister program, Seeds of Empathy) starts as early as preschool and brings a loving parent and a baby to classrooms to help children learn to understand the perspective of others. The nonprofit program is based in part on social neuroscience, a field that has exploded in the past 10 years, with hundreds of new findings on how our brains are built to care, compete and cooperate. Once a month, students watch the same mom and baby interact on the blanket. Special ROE instructors also hold related classes and discussions before and after these visits throughout the course of the school year.

"We love when we get a colicky baby," says founder Mary Gordon. Then the mother will usually tell the class how frustrating and annoying it is when she can't figure out what to do to get the baby to stop crying. That gives children insight into the parent's perspective --- and into how children's behavior can affect adults, often something they have never thought about.

When Baby Stephana cries, an ROE instructor helps students consider what might be bothering her. They are taught that a crying baby isn't a bad baby but a baby with a problem. By trying to figure out how to help, they learn to see the world through the infant's eyes and understand what it is like to have needs but no ability to express them clearly.

That last part, the part I highlighted in bold text? I think that's a crucial thing to understand, but I'm not sure children are the ones who most urgently need remedial lessons in it.

Failing to grasp that someone without language will still have needs, and will use whatever other means of communication they have to try to call other people's attention to their need, underlies a lot of the most abusive, callous treatment of developmentally disabled people by their caregivers.

Accordingly, I'd love to see a similar empathy-building program for would-be paraprofessionals, special-ed teachers, home health aides, etc. I think caregivers often fail to put themselves in their clients' shoes, and appreciate the anxiety/stress/pain/hunger/whatever that the client was feeling, and the added stress of not being able to tell the caregiver what they needed, and instead either blame the client for "acting out" or, worse, consider hir beneath blame, so broken and messed up by virtue of hir disability that nothing ze does could ever possibly be a response to anything, just a "behavior" that happens randomly, like error messages from a glitchy computer.

Anyway, back to Time, and back to (some more of) the theoretical underpinnings of Roots of Empathy:

[L]ike language acquisition, the inherent capacity to empathize can be profoundly affected by early experience. The first five years of life are now known to be a critical time for emotional as well as linguistic development. Although children can be astonishingly resilient, studies show that those who experience early abuse or neglect are at much greater risk of becoming aggressive or even psychopathic, bullying other children or being bullied themselves.

That helps explain why simply punishing bullies doesn't work. Most already know what it's like to be victimized. Instead of identifying with the victims, some kids learn to use violence to express anger or assert power. [Bolding and italics mine]

After a child has hurt someone, "we always think we should start with 'How do you think so-and-so felt?'" Gordon says. "But you will be more successful if you start with 'You must have felt very upset.'" The trick, she says, is to "help children describe how they felt, so that the next time this happens, they've got language. How they can say 'I'm feeling like I did when I bit Johnny.'"

When children are able to understand their own feelings, they are closer to being able to understand that Johnny was also hurt and upset by being bitten. Empathy is based on our ability to mirror others' emotions, and ROE helps children recognize and describe what they're seeing.

I really like this idea in general, and think it's based on some pretty sound principles --- especially the ones about giving people the verbal tools to help vent their frustrations, or ask for help dealing with them, and about understanding that much of what we experience as "problem behavior" from others comes when they are experiencing stresses that overwhelm their ability to cope.

I have no trouble at all believing that this type of training greatly helps kids learn to handle their own feelings in a safe, non-destructive way, and to be more considerate of their classmates' needs and feelings. (This is indeed what independent evaluations of ROE --- there have been nine so far --- have shown: lasting increases in prosocial behaviors like sharing, helping others, being fair and trying to include everyone; in social and emotional knowledge; in kids' sense of their classroom as a caring, safe place; and lasting decreases in aggressive behavior).

But I am not sure that bullying --- a sustained, calculated campaign of terror against targets chosen for their vulnerability --- is in the same category as the aggressive behaviors ROE nips in the bud. Bullying doesn't seem to me like a spontaneous outpouring of emotion too intense to be contained, from a person too inarticulate or emotionally illiterate to express it without violence. Most bullies know exactly what they're doing, and have enough self-control not to do it; I know this because they're able to keep the worst of their violence hidden from authority figures. Some bullies are also very articulate and emotionally intelligent, convincing their victims that they are "friends," and guilt-tripping victims for not doing everything they ask. (The comments section of this old post on Pandagon is full of useful insights about bullying, and similarities between bullying and spousal abuse).

I think bullying comes because the bullies have keen insight into social dynamics --- they see that some people are less powerful, less well-liked, less noticed, less valued than others. They see that, they realize they could do just about anything to one of those unfortunates, and they decide, coolly and rationally, that so-and-so isn't a person, or at least isn't anyone worth treating like a person.

In most cases, there might not be any deep emotional turmoil underlying their cruel treatment of so-and-so; they do it because they can, end of story. Empathy training might help somewhat by making potential bystanders more likely to intervene, and stick up for the person being bullied, and it might also make it harder for potential bullies to tune out their targets' feelings if they've been trained from preschool to notice people's feelings.

I also think one of the major factors emboldening bullies is the larger culture's tacit (and sometimes explicit) endorsement of the very ideas bullies are experimenting with: specifically, that there are people who matter and people who don't and that you treat people differently according to which group they're in. All the empathy training in the world won't wipe out bullying if that doesn't change.

Fat Panic as Front-Page News (Again)

EXECUTIVE SUMMARY: An article in my local newspaper reporting on the most recent of a long series of studies analyzing data from a large national survey of U.S. children's health has managed to reduce that study's findings to boilerplate obesity-scare rhetoric. The study's author, Gopal Singh, has found that lots and lots of things contribute to a region's, or demographic group's, relative prevalence of childhood obesity, and a lot of those things have to do with economic inequality. But the newspaper article ignores these larger, systemic aspects of public health and seems to promote constant vigilance over children's diet, lifestyle and body size as The Answer to the Childhood Obesity Epidemic. I don't think that's the answer, because dieting for weight loss --- i.e., chronic low-level undernutrition --- is also very bad for people, and it's especially dangerous for children, who are not yet done building the bodies they're going to have to live in for the rest of their lives.
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This article in today's Kansas City Star is a pretty good (and by "good" I mean "aggravating") example of the above formula (i.e., fat panic as front-page news).

Let's start with the title: "Study reveals soaring obesity rates among girls." I like those two verbs --- "soaring" obesity rates! It seems like every obesity-related news story uses some kind of dramatic, exciting action verb like that --- soaring, skyrocketing, ballooning, exploding --- or, more rarely, an adjective that conjures similar images of rapid expansion or upward motion, like "stratospheric." And then there's "reveals." While "reveal" is a perfectly good word for talking about research findings --- being a synonym for "show," "demonstrate," "present," etc. --- it also has connotations that whatever is revealed had been hidden, as opposed to merely there waiting for someone to call attention to it. This idea of a menace lurking insidiously under our noses is a staple of alarmist journalism, and has often been used before in equally panicky stories about an Obesity Epidemic.

The study they're talking about is this article in this month's Archives of Pediatric and Adolescent Medicine, which looks at the prevalence of obesity (BMI at or above the 95th percentile for the child's age) and overweight (BMI between 85th and 95th percentiles) among children all over the US in 2003 and 2007, as determined by parents' responses to a nationwide telephone survey about their children's health conducted in both of those years.

The article is actually one of several, all based on different statistical analyses of the same survey data. The lead author of all these studies, Dr. Gopal Singh, is looking at all sorts of different structural and demographic factors for things that correlate to greater rates of obesity within certain groups of people: things like whether people live in walkable communities, how poor they are, their race* and ethnicity, what kind of food they can afford/have time to prepare, how much crime there is in their neighborhoods, whether there are parks nearby, etc.

Here is ScienceDaily's summation of Dr. Singh's most recent findings:

The geographic patterns in childhood obesity are similar to those observed among adult populations, the authors note. Several Southern states -- including Mississippi, Georgia, Kentucky, Louisiana and Tennessee -- were in the top one-fifth of both childhood and adult obesity rates in 2007. For both adults and children, obesity rates were highest in the Southern region and lowest in the Western region.

"Individual, household and neighborhood social and built environmental characteristics accounted for 45 and 42 percent of the state variance in childhood obesity and overweight, respectively," the authors write. "Prevention programs for reducing disparities in childhood obesity should not only include behavioral interventions aimed at reducing children's physical inactivity levels and limiting their television viewing and recreational screen time but also should include social policy measures aimed at improving the broader social and physical environments that create obesogenic conditions that put children at risk for poor diet, physical inactivity and other sedentary activities," they conclude.

(Semantic aside: I love how merely not engaging in physical activity is deemed a "sedentary activit[y]" in its own right in that last sentence. I had no idea you could be so busy not doing something!)

Anyway, one of the weirder things Dr. Singh found in his comparison of the 2003 and 2007 National Children's Health Survey data was two states whose childhood obesity-prevalence numbers almost doubled in those four years. Those states were Arizona and Kansas, with 2007 rates 90.9% and 91.4% higher than their respective rates in 2003.

Also, this increase (which is humongous when compared with the national increase of just 10% over the same period) was only observed in girls. Boys' rates of overweight and obesity did not change significantly between 2003 and 2007.

One thing that has definitely changed between the early and late '00s is the level of sheer panic that's crept into people's attitudes about weight; where maybe before, you might know your child was overweight, and maybe you worried a little about how much weight they might continue to gain once they stopped growing and their metabolism slowed down (or, alternatively, you didn't worry at all because they were still growing!) whereas now, being even a little bit overweight is seen as a life-threatening condition. (You think I exaggerate? Read this. And this. And this. And this. And this. And also, this entire blog).

The study's design protects it somewhat from undue influence of parental attitudes about their children's weight because the parents are not asked whether their child is overweight or obese; they're just asked the child's height and weight (along with, obviously, their age). There's still some room for parental interpretation, in that the parents might have an imperfect notion of what their children actually weigh, and some overly-worried, perfectionist parents might overestimate the weight of a healthy child they're convinced is too chubby. (Or, alternatively, more parents might be actively monitoring their children's weight, due to scaremongering awareness campaigns about Childhood Obesity, and thus more kids who are overweight are having their weights accurately reported). Girls would be particularly prone to this sort of thing, since thinness is so highly prized in girls, and the size of a girl's body is frequently a subject of contention between that girl and her controlling, abusive, judgmental or over-involved parents.

Those factors are more or less constant throughout society, though, and tend --- especially the parental-perfectionism one --- to be concentrated in the demographic categories that didn't see much of an increase in girlhood obesity: white, middle- and upper-class families. The abstract of this other study of the same data makes it clear that most of the increase was seen in poorer children of color.

In general, the groups of people seeing the sharpest increases in childhood obesity over the past four years were the same groups within which obesity is especially prevalent: this is stated explicitly in a study Singh, along with coauthors Michael D. Kogan and Mohammad Siahpush (Kogan, but not Siahpush, is also a coauthor of the state-by-state study) conducted last year, finding that "[s]ocial inequalities in obesity and overweight prevalence increased because of more rapid increases in prevalence among children in lower socioeconomic groups."

However, there is very little discussion of social, economic or policy implications of this research in the Star article; when one social factors do come up is typically in the context of laws mandating certain behaviors at the individual level, rather than addressing any of these underlying systemic inequalities:

Nobody knows why for sure, but girls in Kansas have been gaining weight at an alarming rate.

From 2003 to 2007, the percentage of Kansas girls 10 to 17 years old who were obese nearly doubled, a new federal study shows.
...
Most of the increase in obesity in Kansas may have been among girls who were below high school age, [study author Gopal Singh] said.

About one in three children in the United States is now considered overweight or obese, which is raising concerns about their future health and even their longevity. Many children already are developing diabetes or showing early signs of heart disease that typically are found in adults.

First lady Michelle Obama recently initiated the "Let's Move" campaign against childhood obesity. A government report last week offered 70 recommendations, including healthier food at schools and getting children to exercise more, to combat weight gain.

People who are obese are well above normal weight and have large amounts of body fat. Obesity is usually measured by a calculation based on height and weight called the body mass index, or BMI.

For example, a 12-year-old girl who is 5 feet tall would be considered to be a healthy weight at 110 pounds and obese at 130 pounds.

Singh's study found wide variations in obesity rates among states, even after accounting for ethnic and economic differences.

Kids in Kansas, for example, were twice as likely to be obese as kids in Oregon, which had the lowest obesity rate.

Differences in the availability of parks and playgrounds and in state policies promoting healthy weight among children may play a role, Singh said.

State policies could be a factor in Kansas, said Sarah Hampl, a pediatrician who directs weight management services at Children's Mercy Hospital.

She pointed to a 2009 report by the Trust for America's Health that noted which states had nutrition standards for foods available to children at school or policies for measuring students' BMIs.

"Notably, Kansas was one of the only states in the nation that doesn't have this kind of legislation," Hampl said.

So, while the article does allude to some of the social and environmental factors Singh found accounted for some of the state and regional variation --- it mentions the issue of access to safe outdoor spaces --- it gives more emphasis to solutions addressing children's behavior: restrict what kinds of foods they can get at school, regularly weigh them, etc.

I was particularly distressed to see Dr. Hampl's suggestion that Kansas's lack of school BMI-monitoring policies might explain the state's "alarming" increase in childhood obesity rates appearing just a few inches below Dr. Singh's claim that most of the newly obese or overweight girls in his study are probably preteens; the last thing girls need right as they're going through puberty is some adult scrutinizing their bodies and warning them not to gain any more weight!

*While there is certainly a big role for systemic, economic racism in explaining why people in some racial and ethnic categories tend to be both fatter and less healthy than people in others --- African-Americans, Latin@s and Native Americans are all much likelier than white Anglo-Americans to be poor, unable to afford enough food, and to live in food deserts --- another factor might just be variation in average body type among different ethnic groups. Urocyon has several eye-opening posts about how her body type, which she shares with her relatives and with lots of other people, living and historical, with Cherokee/Tutelo heritage, has been deemed ugly, fat and dangerously unhealthy throughout her life because it doesn't match the thin, willowy ideal of beauty and health that, while it might be unrealistic for most white, European women, too, is even further removed from the actual bodies of most women of color.

Bizarre Things Purported to Cause Autism: Cells from Aborted Fetuses

EXECUTIVE SUMMARY: A pro-life advocacy group called Sound Choice Pharmaceutical Institute has claimed that the increase in autism-spectrum diagnoses in the U.S. over the past two decades is due to the presence of cells from aborted fetuses in vaccines introduced during that period. The evidence they have for this consists of chronological "change points": years after which the rate of autism incidence begins to rise more sharply than it has before. They connect these change points with developments in U.S. immunization practices that might mean more exposure to vaccines made from fetal cells.

I think the idea that those two developments are related is a ridiculous one, first because it is physically impossible that the trace amounts of human cell components still found in the finished vaccines could trigger such a massive immune response even in very sensitive children, and second, because the timing of the change points they've chosen to highlight is an artifact of the autism-incidence statistics they've chosen to use, and third, because many other factors track with those change points that have a more obvious, immediate effect on reported autism incidence, like revisions of the Diagnostic and Statistical Manual (DSM), changes in special-education policy, etc.
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There's a blog I used to read occasionally called Autistic Conjecture of the Day --- sadly, it's now open only to invited readers --- that dealt with every idea the blogger had ever encountered for what causes autism. Some of these ideas would be mainstream, some would be cutting-edge, some would be controversial, and some would be just plain off-the-wall.

Since discovering that blog, though, I've loved that idea: simply collecting all the different ideas in one place.

So I've decided I'm going to do my own (intermittent, open-ended) series on Bizarre Things that have been Purported to Cause Autism! Because this is a perseveration of mine, as well, and you can never have too much debunking of wacky ideas on the Internet.

The subject of this inaugural post in the series comes courtesy of fellow feminist skepticblogger Amanda Marcotte: according to pro-life columnist Jill Stanek, and this story on the LifeNews website, the "worldwide jump in the incidence of autism beginning in 1988" can be traced to the use of human fetal cells in the measles-mumps-rubella (MMR) vaccine.

Quoting the pro-life advocacy group Sound Choice Pharmaceutical Institute, Stanek argues that the three "change points" --- points at which the slope of the line on a graph of autism incidence changes --- occurring in 1981, 1988 and 1995 coincide with three changes in which vaccines are recommended for very young children. In 1981, the CDC's Advisory Committee on Immunization Practices (ACIP) approved a rubella vaccine called Meruvax, which is made from live attenuated rubella viruses that have been incubated in human fetal cells from the cell line WI-38; in 1988, a second dose of the MMR vaccine was added to the recommendations; and in 1995, a chicken-pox vaccine (Varivax) was approved that, like the rubella vaccine, contains live attenuated viruses that are grown in human lung cells. The chicken-pox vaccine used cells from two different cell lines, WI-38 and MRC-5, both of which were cultured from lung cells taken from human fetuses* that had been aborted.

I'm going to address the autism-incidence statistics Stanek's sources relied on later in this post; for now, I'd like to concentrate on what is, for me, the biggest problem with her claim that human fetal cells used to grow the viruses used in common childhood vaccines are causing autism: where is the mechanism? The mercury and MMR hypotheses, flawed as they are, at least propose some physical process by which the brain's development can be disrupted as a result of vaccine exposure.

Though neither Stanek nor the newsletter from which she quotes goes into how residual fetal cells in vaccines might have such an effect on an infant's nervous system, this July, 2009 editorial by Sound Choice Pharmaceutical Institute president Theresa A. Deisher makes a bold suggestion:

How could the contaminating aborted fetal DNA create problems? It creates the potential for autoimmune responses and/or inappropriate insertion into our own genomes through a process called recombination. There are groups researching the potential link between this DNA and autoimmune diseases such as juvenile (type I) diabetes, multiple sclerosis and lupus. Our organization, Sound Choice Pharmaceutical Institute (SCPI), is focused on studying the quantity, characteristics and genomic recombination of the aborted fetal DNA found in many of our vaccines.

Preliminary bioinformatics research conducted as SCPI indicates that "hot spots" for DNA recombination are found in nine autism-associated genes on the X chromosome. These nine genes are involved in nerve-cell synapse formation, central nervous system development and mitochondrial function.

So, the hypothesis here is that fetal DNA left in the sample of live virus that makes up the MMR and chickenpox vaccines is merging with people's own genomic DNA and scrambling their genes.

Like all good science fiction, this fantastical scenario springs from fairly plausible conceptual roots: it's true that one type of virus --- the retroviruses (like HIV) --- can embed its tiny genome within its (human) host's much-larger genome, and that some other viruses, like herpesviruses, can keep their genetic material dormant within a host cell, and thereby persist in that host for years, or even decades, with periodic reactivation of its infectious cycle when the host is under physiological stress; it's also true that a few people do suffer severe allergic reactions to some of the ingredients in vaccines, including --- what's most relevant to this post --- cells used to incubate the vaccine's active component, the virus.

In this 2003 article in Pediatrics on vaccine safety, Drs. Paul Offit and Rita K. Jew discuss the relative dangers posed by all the different vaccine additives: preservatives (like thimerosal, phenol, and 2-phenoxyethanol), adjuvants (aluminum salts), stabilizers (sugars, amino acids like glycine or monosodium glutamate, proteins like gelatin or human serum albumin), and manufacturing residuals (into which category the fetal cells Dr. Deisher is so worried about would fall, along with egg proteins, yeast proteins, formaldehyde and various antibiotic drugs).

Residual quantities of reagents that are used to make vaccines are clearly defined and well regulated by the FDA. Inactivating agents (eg, formaldehyde), antibiotics, and cellular residuals (eg, egg and yeast proteins) may be contained in the final product.
...
Cellular Residuals

Egg Proteins
Egg allergies occur in approximately 0.5% of the population and in approximately 5% of atopic [i.e., allergically hypersensitive] children. Because influenza and yellow fever vaccines both are propagated in the allantoic sacs of chick embryos (eggs), egg proteins (primarily ovalbumin) are present in the final product. Residual quantities of egg proteins found in the influenza vaccine (approximately 0.02-1.0 μg/dose) are sufficient to induce severe and rarely fatal hypersensitivity reactions in children with egg allergies. Unfortunately, children with egg allergies often have other diseases (eg, asthma) that are associated with a high risk of severe and occasionally fatal influenza infection. For this reason, children who have egg allergies and are at high risk of severe influenza infection should be given influenza vaccine through a strict protocol.

In contrast to influenza vaccine, measles and mumps vaccines are propagated in chick embryo fibroblast cells in culture. The quantity of residual egg proteins found in measles- and mumps-containing vaccines is approximately 40 pg --- a quantity at least 500-fold less than those found for influenza vaccines. The quantity of egg proteins found in measles- and mumps-containing vaccines is not sufficient to induce immediate-type hypersensitivity reactions, and children with severe egg allergies can receive these vaccines safely.

This article does not mention the rubella vaccine, Meruvax, which is propagated in human fibroblast cells in culture, but because the vaccine is prepared in the same way as the measles and mumps vaccines (just using cultures of a different cell type), it's probably safe to assume that residual human cell components are present in the same minute quantities. Chances of severe immune response to residual cell components should be even lower for the rubella vaccine than for the measles or mumps vaccines since the attenuated rubella viruses are grown in human cells as opposed to chicken cells, and human cells are less likely to trigger an immune response in humans than nonhuman cells, since our immune systems work by distinguishing "self" from "non-self" antigens.

As for the DNA from those residual cells somehow integrating itself into people's genomes, I don't think that's even possible. DNA rearrangement like that doesn't happen on its own, whenever two different molecules of DNA encounter each other; retroviruses that inject their genomes into a host cell's genome are able to do so because their protein shells (capsids) also include all the requisite enzymes for doing this --- reverse transcriptase, for converting the virus's RNA genome into a length of double-stranded DNA suitable for patching into a host cell's chromosomal DNA, and, crucially, an enzyme called integrase, which cuts the ends off of both viral and host DNA and then pastes them together. This enzyme exists only in retroviruses and some bacteriophages --- humans have nothing like it, and neither do any of the viruses present in the MMR or chicken-pox vaccines.

Expecting one piece of DNA spontaneously to insert itself into another because they're in the same cell and might happen to bump into each other is as misguided as placing, say, two whole eggs, a bag of flour and a bag of sugar out on your kitchen counter and leaving them there overnight, with the expectation that they will have turned into a cake by the time you get up the next morning.

Finally, let's look at the graph Jill Stanek reproduces in her column, that purports to show an increase in autism incidence coinciding with those three additions to the list of recommended vaccines.

The smaller, inset graph making up this image comes from this 2008 article in the Archives of General Psychiatry, tracking the number of children in California who are a) diagnosed with autism or a related condition like Asperger's syndrome or PDD-NOS, and b) receiving services from the California Department of Developmental Supports.
You can see that this graph has three pairs of lines representing three different age cohorts of children (with the incidence of autism measured two ways for each group; hence the double lines) where the modified version in the SCPI graphic has only one --- the (merged) middle pair of lines, representing the rate of autism diagnoses occurring among four-year-old children each year. The top two sets of lines --- showing the incidence data for four- and five-year-olds --- do trend sharply upward starting around 1995, but for the third set --- three-year-olds --- the rise is much less pronounced, and starts later.

The larger, background graph comes from this article (full text here) in the March 15, 2010 issue of Environmental Science & Technology, in which two EPA researchers look at autism-incidence trends worldwide over the past fifty years or so by looking at three large autism-incidence studies from the U.S. (this report from the California state Department of Health and Human Services' Department of Developmental Supports), Denmark (Lauritsen et al., 2004), and Japan (Honda et al., 2005; full text here) and estimating each subject's year of birth, and then plotting the number of autistic people born between 1960 and 2000.

The EPA study found just one "changepoint year": 1988. After that point, the slope of each line representing each of their four data sets (each of the three already cited, plus a "worldwide" data set that includes all of those three put together, plus a bunch of other studies too small, or too variable in timing or methodology, to be analyzed on their own) jumps to a value several times that of the slope of the line prior to that point.

That discrepancy is also reflected in the raw data pre- and post-1988: in California, the average incidence of DSM-IV Autistic Disorder was 5.7 cases per 10,000 children in the years before 1988; after 1988, it was 20.8 cases. In Denmark, 1988 marked an increase from 0.6 to 6.6 cases of ICD-10 Autistic Disorder per 10,000 children; worldwide, the change was from 6.0 to 24.2 autistic children per 10,000 live births.

I did not forget to mention Japan; the Japanese data starts in 1988.

No changepoint data could be calculated for the Kohoku Ward, Japan, data set (Table 1), as AD cumulative incidence increased continuously over the entire period of study (1988-1996)(Figure 1a).

As Mark Chu-Carroll of Good Math, Bad Math remarks about another crucial data discrepancy*** hinging on that unlucky year:

[T]he earliest data in their analysis comes from a different source than the latest data. They've got some data from the US Department of Education (1970->1987) and some data from the California Department of Developmental Services (1973->1997). And those two are measuring different things; the US DOE statistic is based on a count of the number of 19 year olds who have a diagnosis of autism (so it was data collected in 1989 through 2006); the California DDS statistic is based on the autism diagnosis rate for children living in California.

So - guess where one of their slope changes occurs? Go on, guess.

1988.

The slope changed in the year when they switched from mixed data to California DDS data exclusively. Gosh, you don't think that might be a confounding factor, do you?

While the absence of any Japanese data from before 1988 wouldn't affect the change-point calculations for California or Denmark, it does make me a bit more skeptical of the worldwide changepoint, which was around 1989. It does help a bit to know that there are other bits and pieces of data from around the world helping to fill in the patchwork --- while it still might be a bit lopsided, depending on how the various studies are distributed in time, it's at least not as much of a foregone conclusion that the slope will change in 1988.

Besides the statistical uncertainties arising from such an uneven, patched-together data set, there are also some confounding factors arising from the fact that all this data came from administrative databases maintained by government human-services agencies. This introduces changes in policy as other potential influences on how many people show up labeled "autistic" (see this old post by Michelle Dawson for more on how this works).

The authors of the EPA study, Michael E. McDonald and John F. Paul, understand this and are accordingly cautious about whether their observed increase in autism incidence is "real" or not:

The three studies that were selected for inclusion in our analysis had sufficient record length for time trend analysis because they collected administrative data for programmatic services to autistic children. Each of these studies, which showed cumulative incidence of autism increasing (Figure 1a), had the advantage of using the data collections from a single administrative database that covered a well-defined geographic region. This was not true of our worldwide data set, where differences in method of data collection, record length, and geographic area may all have contributed substantially to an increase in AD cumulative incidence (Figure 1b).

Administrative databases also have the advantage of a relatively consistent methodology over periods of time. However, all three of our selected databases have some methodological changes associated with their long-term data collections. A changing of the diagnostic criteria and the broadening of the definition of autism to PDD occurred during the data collection within the Danish and California databases, but a single diagnostic criterion was applied consistently within the Kohoku Ward study. As we were aware of the issues with broadening and changing diagnostic criteria, in our study selection criteria we chose explicitly to focus on AD, which has had relatively consistent diagnostic criteria since about 1978. However, this does not necessarily mean that the diagnostic criteria have been consistently applied in practice over this time frame. It does appear that AD criteria have been applied fairly consistently since about 1994 in the Danish database and across the United States with the use of ICD-10 and DSM-IV, respectively. A recent analysis of the California database from the early 1990s through about 2006 suggests that changing diagnostic criteria may account for a 2.2-fold higher cumulative incidence of autism, relative to the 7-fold increase observed over 11 birth cohorts. It is unknown how consistently previous AD criteria were applied or how the application of the current criteria compare with past criteria.

Administrative data may also be prone to diagnostic substitution, where children with multiple diagnoses may be identified differently over time depending on which diagnosis allows the individual to receive administrative services. In British Columbia, Canada, changes in the assignment of special education codes may account for at least one-third of the increase in autism prevalence from 1996 to 2004. However, in the California data set, diagnostic substitution from the category of mental retardation to autism could not account for increased autism from 1987 to 1994.

...

Studies with AD assessment in children occurring before age 10 may show an apparent increase in autism because of earlier ages of diagnosis in recent years, relative to historic underidentification at the same assessment age. In fact, Parner and coinvestigators examined recent cohorts (1996 and 1997; 1998 and 1999) in the Danish database and found that at least some of the AD increase was attributable to earlier diagnosis. In the California database, a shift toward a younger age at diagnosis also was found and contributed to about 12% of the observed increase in autism from 1990 to 1996, based on assessment at age 10. Thus, earlier diagnosis contributed to increase in AD cumulative incidence in at least two of our selected studies and, likely, to studies in our worldwide data set (Table S1, Supporting Information).

In addition to finding that changes in diagnostic criteria and earlier age at diagnosis do contribute to some of the observed increase in cumulative AD incidence in the California database for 1990-2006, Hertz-Picciotto and Delwiche also found that the inclusion of milder cases of autism contributed to the increase. This contribution was not as much as that resulting from changing diagnostic criteria but was more than that contributed by earlier age at diagnosis. Differential migration of autistic children into the state was also found to play a minor role in the increase. The investigators suggest that wider awareness of autism, greater motivation to seek services, and increased funding for services also may contribute to increasing cumulative AD incidence, but these factors could not be documented or quantified.

I've already spent a ridiculously long time**** writing this post, so I'm not going to try to unearth every single policy change that might affect autistic children's enrollment in state disability programs. I can tell you, though, that each of the change points SCPI identifies corresponds with historical events much likelier to account for changes in how many people receive a given DSM diagnosis than the addition of a few new vaccines to the recommended vaccine regimen: in 1980, 1987 and 1994 the DSM underwent major revisions. While I'm not sure about the DSM-III, I know for sure that the DSM-IV greatly relaxed the diagnostic requirements for Autistic Disorder from what they were in the DSM-III-R, and added the category of Asperger's syndrome. (The 1995 changepoint, identified by SCPI and taken from a study not used by the EPA analysts, reflects all the different autism-spectrum diagnoses, not just Autistic Disorder). Changing diagnostic criteria, as well as a sea change in people's ideas about what sort of person might be called "autistic," seem to me much more likely to be behind the increasing rate of autism diagnosis than exposure to a few femtograms of human fetal DNA fragments via vaccines.

*(It is hard to find sources on the Internet that can verify that claim --- while most laboratories that use those cell lines, or sell them for other researchers to use, will classify the cells as human fetal cells, and describe their cell type, growth characteristics and other things it would be useful to know if you were going to try to culture those cells, they don't go into huge detail about the circumstances of those cell lines' establishment. Why would they? But I was able to find original articles describing the cell lines --- MRC-5 was established in 1970 by British researchers J. P. Jacobs, C. M. Jones and J. P. Baille, and described in this 1970 letter to Nature; WI-38 was established sometime in the 1960s at the Wistar Institute in Philadelphia, Pennsylvania, by cell biologists Leonard Hayflick** and Paul S. Moorhead, according to a method described in this 1961 article (full text here) in Experimental Cell Research. That paper only describes the creation of cell lines WI-1 through WI-25, though; WI-38 came later. Papers using WI-38 cells usually cite either Hayflick and Moorhead (1961), or this later article by Hayflick (1965), also published in Experimental Cell Research. Hayflick and Moorhead (1961) do not go into detail about the source of their human tissue cells; they only mention that the source of the lung tissue used to establish some of the cell lines, which would include WI-38, is a three-month-old fetus. So, weird as it might sound, it's actually true that some vaccines are produced using cells derived from aborted fetuses.)

**AnneC, if you're reading, you might have heard of this guy! He discovered the "Hayflick limit," or the maximum number of times a given cell can divide before it deteriorates past functioning. He's done lots of research on the biology of aging and life extension, the latter of which I know is one of your perseverations.

***He seems to be using the SCPI newsletter as his reference, and not trying to tease out which errors are theirs and which were already in the EPA's somewhat more conservative analysis. The problems with the Department of Education data he mentions would apply only to the SCPI's findings, since the EPA researchers did not use any of that data. The problems he has with "hockey-stick analysis" in general, though, would seem to apply to both parties. SCPI just compounds the EPA's error by doing multiple such analyses on their already-too-small data set.

****A little over two weeks.

McDonald, M., & Paul, J. (2010). Timing of Increased Autistic Disorder Cumulative Incidence Environmental Science & Technology, 44 (6), 2112-2118 DOI: 10.1021/es902057k