Emma, Intense World Theory, and Science Nerd Throwdown Action (here’s Part One)
My primary scientific issue with the theory is that the research behind it is all either procedurally/experimentally shaky or totally nonexistent. And I dislike that it takes attention and kudos away from better-researched, theoretically sound theories—most of which come from researchers that have done more than the Markrams ever will for the autistic community, and for scientific dialogue about autism. I’m thinking of scientists like Michelle Dawson (representtttt!), Laurent Mottron and Morton Ann Gernsbacher. If you don’t know them, or at least know of them, please look up their work. I would be happy to share articles, and I can’t say enough good things about the work Dawson, Mottron and their colleagues have done to put together their theories concerning “Enhanced Perceptual Function” and “Veridical Mapping” as models of autistic cognition.
To give examples of specific issues I have with the Markrams research, I’m just going to quote a comment I wrote on a post from Landon at thAutcast where he linked (with trepidation) to an article quoting the Markrams. Here’s the section of that article I commented on:
The intense world theory is based on data from two experimental studies using the valproic acid (VPA) rat model of autism. Exposure to VPA, an epilepsy drug, during pregnancy results in reduced social interactions, increased repetitive behaviors and loss of cerebellar neurons in the rat pups.
The Markrams and their colleagues found that the amygdalae and medial prefrontal cortices of these rats are hyperreactive, hyperconnected and hyperplastic. Their brains show a change in the balance of excitatory and inhibitory nerve signals, and in the efficiency of communication between neurons, which may have significant behavioral effects.
The Markrams extrapolated these findings to suggest the presence of increased activity in certain regions of the brains of humans with autism, leading to overactive perception, memory and attentional processes. These, they say, are hypercapabilities that all individuals with autism possess. These features manifest as extreme sensitivity to sensory stimuli, elevated fear and over-emotionality. The intense world theory suggests that to deal with this intensity, people with autism tend to shut down and withdraw from the world. (Link)
And here’s my comment:
Super classy bad science is my favorite thing. Though I vaguely appreciate that, in this case, it at least seems like well-meaning bad science. There are just so many methodological and theoretical fails in this…It’s a perfect example of confirmation bias fucking up experimental design.
Anyone familiar with rat and mouse models in neurological/psychiatric research will tell you that “decreased social interaction” and “increased repetitive behaviors” are the two traits most commonly seen in every rodent model of every DSM diagnosis ever. And the neurological “signs” they describe in the amygdala and MPFC are, similarly, universally correlated with heightened emotional states and/or stress.
This is priceless though: “Their brains show a change in the balance of excitatory and inhibitory nerve signals, and in the efficiency of communication between neurons, which may have significant behavioral effects…The Markrams extrapolated these findings to suggest the presence of increased activity in certain regions of the brains of humans with autism, leading to overactive perception, memory and attentional processes.”
Look at how they use all those big science words! Allow me to translate: “In the brains it was like some electrical stuff was different, and also some chemical stuff was different. This could make brains do stuff different. So we made up a theory that autistic people are different because some of their brain parts are hella intense. The neurons that do thoughts in autistic people are just, like, intense.” Groundbreaking.
Apologies for being absurd; but I couldn’t help myself.
What I want to add to this is…well, a lot.
- The valproic acid model of autism is one of many models, it’s not just used to model autism, and it’s probably the oldest model…the fact that the Markrams are using this model (not to mention trying to come up with a theory of autistic sensory experience using animal model experiments) is a sign that they are really not up to date on appropriate experimental procedure for neuropsychiatric research concerning humans.
- I can’t even explain how many different models of psychiatric diagnoses display the “decreased social interaction” and “increased repetitive behavior” profile. Like, I can’t even. And, like…99% of daily rodent life involves A. Social interaction and B. Playing with your food and/or eating it. So basically, anything that causes changes in rat behavior that aren’t violence/psychosis or increased sex drive will result in alterations in their social interactions and food hoarding. And since most psychiatric diagnoses modeled cause stress for the organism, the changes in social interaction and food hoarding almost always take the form of reduced socialization and increased, extra-repetitive food/object stashing.
- Not all autistic people have good attentional capacity. I do not. Not all autistic people are overly emotional, not all autistic people are hyperreactive, not all…I could go on for ages. The theory is full of overgeneralizations.
- I was not at all exaggerating in my translation of the “science-speak” the Markrams used when describing their fMRI results. That is truly how broad and vague the language they were using actually is.
- Things this doesn’t explain: The high levels of heritable risk for autism spectrum disorders when there is a family history of schizophrenia, bipolar disorder, and depression, all of which can be characterized, at times, as disorders that involve a marked decrease in the sensitivity and receptivity to sensory information. With schizophrenia spectrum disorders, I’m thinking of how psychosis (or hallucination in general) requires a lack of awareness of actually externally present sensory information in favor of internally generated information, and how often catatonia and anhedonia are exhibited by schizophrenic people. With bipolar disorder and depression, anhedonia and frequent lack of sensitivity to previously vivid sensory perceptions are both consistent aspects of severe depression, while manic states often involve a lack of awareness of physical needs (sleep, food, etc.) and, in some cases, hallucinations.
- Other things this doesn’t explain: Like…95% of autistic people and their lives. Sorry, couldn’t help the sarcasm on this one.
I could keep going on this, but I think that this is probably a long enough science rant for now. Now I know, by this time, anyone who is still reading is going to be like “Well, obviously you have issues with this theory, but are you going to offer any alternative explanations?” To that, I first want to say that I don’t think you need to have a better idea to point out the flaws in someone else’s shitty theory. And secondly, yes. I do have a better explanation. It’ll probably (hopefully) be my next post, and will include both a sciencey part and and experiencey-metaphory-concrete part, so that everyone can engage with it. So…stay tuned?