A major limitation of psychotherapy is that I can’t change the behavior of other people. I could become resilient and self-accepting and flexible and able to love like you wouldn’t believe, and I’d still be handicapped in my social relationships. I’ve always known that, without always understanding why.
This data from OkCupid was a revelation:
That’s not accounting for things like mixed-race issues, being vegan, or not being black enough in other people’s opinions. I thought I had a complex and unusual social background, which made it very difficult to succinctly explain who I was. My friend with social skills agreed it would be hard to introduce me without just summarizing my life story.
I felt like I was being socially disabled before, but it definitely explains a lot that I’m autistic in addition to the already-listed factors.
Individuals with autism spectrum disorder (ASD), including those who otherwise require less support, face severe difficulties in everyday social interactions. Research in this area has primarily focused on identifying the cognitive and neurological differences that contribute to these social impairments, but social interaction by definition involves more than one person and social difficulties may arise not just from people with ASD themselves, but also from the perceptions, judgments, and social decisions made by those around them. Here, across three studies, we find that first impressions of individuals with ASD made from thin slices of real-world social behavior by typically-developing observers are not only far less favorable across a range of trait judgments compared to controls, but also are associated with reduced intentions to pursue social interaction. These patterns are remarkably robust, occur within seconds, do not change with increased exposure, and persist across both child and adult age groups. However, these biases disappear when impressions are based on conversational content lacking audio-visual cues, suggesting that style, not substance, drives negative impressions of ASD. Collectively, these findings advocate for a broader perspective of social difficulties in ASD that considers both the individual’s impairments and the biases of potential social partners.
Thank you, Sasson et al. The images help:
Even if I were an otherwise-normal white person, people would be starting to automatically, subconsciously reject me within seconds, before I’ve had a chance to even DO anything, even if what I’m saying is acceptable.
When I first tried describing my TFW NO GF problems to my first therapist, her reaction was to deploy a Normalization Intervention: I’m not a unique snowflake; everyone is pretty fail at relationships if I look around me. I understand that, now. My intuition was also correct: other people just are NOT dealing with what I’m dealing with. They’re CREATING what I’m dealing with.
It’s worth pointing out that the social model of disability led to improved scientific conclusions, here. It’s a political thing, very SJW, but research is always already political. The prevailing model is built by normal people, and I don’t see why the effects shown in this post’s figures wouldn’t apply to autism researchers. As absurd as it sounds, science been held back by normal people assuming they do everything right and autistic people do everything wrong, a priori.
It’s similar to the way that (recreational) drug research has been held back by the a priori assumption that drugs produce deficits rather than tradeoffs. Consider that antidepressants and MDMA produce similar changes in serotonin morphology, but only one of those things led to officially-sanctioned hysteria about brain damage:
We compared the effects of treatment with high doses of fluoxetine, sibutramine, sertraline, and dexfenfluramine for 4 days on brain serotonergic nerve terminals in rats. Methylenedioxymethamphetamine (MDMA) and 5,7-dihydroxytryptamine (5,7-DHT) were used as positive controls because both compounds deplete brain serotonin. Food intake and body weight changes were also monitored and yoked, pair-fed animals were used to control for possible changes in morphology due to nutritional deficits. Fluoxetine, sibutramine, sertraline and dexfenfluramine all produced a significant reduction in body weight. Fluoxetine, sibutramine and sertraline treatment resulted in no depletion of brain serotonin but produced morphological abnormalities in the serotonergic immunoreactive nerve network. In contrast, dexfenfluramine and MDMA depleted brain serotonin and produced morphological changes in the serotonin nerve network. These results indicate that even though fluoxetine, sibutramine and sertraline do not deplete brain serotonin, they do produce morphological changes in several brain regions (as identified by serotonin immunohistochemistry). Dexfenfluramine and MDMA, on the other hand, markedly deplete brain serotonin and also produce morphological changes. Collectively, these results lend support to the concept that all compounds acting on brain serotonin systems, whether capable of producing serotonin depletion or not, could produce similar effects on the morphology of cerebral serotonin systems.
Now it’s uncontroversial that MDMA can do good things for people, 17 years later (my adult lifetime).
In light of the above, the neurodiversity movement asks a fair question: is the best use of limited resources proving that I have a few more genes in common with chimpanzees than everyone else, who share most of their genes with chimpanzees?