The newsletter of Spectrum News this morning re-linked two older articles about kids who “lost” their autism diagnosis having all sorts of developmental, learning, psychological, or psychiatric issues “to the researchers’ surprise”. One of the articles is about research I’ve mentioned before, and I just wanted to underscore here what I said there, which is that if you’re “surprised” at a result, you should be asking why — and the crucial why here would be asking whether or not the “early intervention” treatments to which these kids were subjected in fact might be responsible for all of these other problems they have after they “lose” the diagnostic label of autistic. By which I mean: perhaps they are still in fact autistic and you’ve simply trained them to suppress it, leading to all the other things you’re “surprised” by afterward.
Robert P. Jones, adapting from a forthcoming book, writes that white Christianity in America continues to have some unaddressed reckoning to do with its role in racism and slavery, and some uncomfortable but lingering effects of that role.
In my day job, I am the CEO and founder of Public Religion Research Institute (PRRI), a nonprofit, nonpartisan organization that conducts research on issues at the intersection of religion, culture, and politics. I’m a social scientist by training and have always been fascinated by the ways in which beliefs, institutional belonging, and culture impact opinions and behaviors in public space. I strive to conduct research and write as an impartial observer. In our work at PRRI, we’ve found that white Christian groups—including evangelicals, mainline Protestants, and Catholics—consistently hold views that are at odds with African American Protestants’ views. The attitudes of nonreligious white Americans, conversely, tend to be more aligned with African Americans’. For white Americans, the data suggest that Christian identity limits their ability to see structural injustice, and even influences them to see themselves, rather than African Americans, as a persecuted group.
Popping up in On This Day today is this post about research suggesting that autistic brains aren’t capable, or are less capable than neurotypical brains, of habituation, potentially helping explain autistics’ sensory overload and hypervigilance, and potentially ruling out exposure therapy for autistics. This is a good starter post if you want to know what I think about my brain, as it’s one of those posts where I draw several previous posts together in a sort of unified, “Aha! See, I told you.”
Some new polling of Oregonians from DHM Research and the Oregon Values and Beliefs Center includes some fairly interesting results when it comes to various proposed changes to how we structure policing.
As noted by Aaron Michael Brown, whether they understand it in these terms or not, 58% of Oregonians support defunding the police, while 37% support abolishing police departments outright.
On a sitenote: one of my pet peeves is polling a question that demands ungathered context in order to understand the results. In this instance, the matter of approval or disapproval “of the way police have responded to the protests”. People who think police should be more tough and those who think police should be more lenient can state that they disapprove of the police response.
These types of poll questions are effectively useless for public policy discussions, unless you’ve got the per-respondent answers on whether or not they support the protests; even then, it’s not going to precisely correlate and give you a full sense.
I guess my peevish sidenote ended up being longer than my main point of interest.
First, our immune system is a mysterious place, and the KCL study looked at only one part of it. When a new pathogen enters the body, our adaptive immune system calls up a team of B cells, which produce antibodies, and T cells. To oversimplify a bit, the B cells’ antibodies intercept and bind to invading molecules, and the killer T cells seek and destroy infected cells. Evaluating an immune response without accounting for T cells is like inventorying a national air force but leaving out the bomber jets. And, in the case of COVID-19, those bomber jets could make the biggest difference. A growing collection of evidence suggests that T cells provide the strongest and longest-lasting immunity to COVID-19—but this study didn’t measure them at all.
So, the study likely remains an important piece of answering the immunity question, but only partially addresses what our immune system does.
If you weren’t depressed enough, a new study suggests that post-infection immunity to SARS-CoV-2 could be lost within months.
Blood tests revealed that while 60% of people marshalled a “potent” antibody response at the height of their battle with the virus, only 17% retained the same potency three months later. Antibody levels fell as much as 23-fold over the period. In some cases, they became undetectable.
Interesting news to drop right before James Hamblin’s discussion of various herd immunity models, wherein he issues this caveat.
Models like Britton’s and Gomes’s also assume that, after infection, people obtain immunity. This is a clear caveat that all the researchers make. COVID-19 is a new disease, so no one can be sure that infected people become immune reliably, or how long immunity lasts. But Britton noted that there are no clear instances of double infections so far, which suggests that this virus creates immunity for at least some meaningful length of time, as most viruses do.
It’s getting to be time we start thinking of the coronavirus as the setting, not the story.
While browsing more than a hundred pages of WordPress plugins for something I still don’t have a solution for, I ran across something more scholarly bloggers might be interested in: Cite, a plugin to “help readers know how to cite your article correctly”.
“Most of us assume visual imagery is something everyone has, something fundamental to the way we see and move through the world. But what does having a ‘blind mind’ mean for the mental journeys we take every day when we imagine, remember, feel and dream?”
Mr Dawes was the lead author on a new aphantasia study, published overnight in Scientific Reports. It surveyed over 250 people who self-identified as having aphantasia, making it one of the largest studies on aphantasia yet.
“We found that aphantasia isn’t just associated with absent visual imagery, but also with a widespread pattern of changes to other important cognitive processes,” he says.
“People with aphantasia reported a reduced ability to remember the past, imagine the future, and even dream.”
Interesting to me is Dawes’ note that this general lack of visualization impacts not just projection into the past but into the future as well — which I’ve been suggesting might be the case (links to blog search for aphantasia), because it appears to be so with me.
I’ve been wondering also about the issue of dreams, because I definitely dream in visuals despite being otherwise aphantasic; but I wonder now about other people’s general sensory experience of dreaming, and to what degree my own in fact is lacking by comparison.
The other write-up linked at MeFi notes other linkages which suggest to me now that there’s an entire range ways in which my cognitive sensory experience simply does not match nor mirror most everyone else’s.
To slightly paraphrase the Spectrum News link copy about this study, “autistic people value research on quality of life and social well-being, according to a large online survey, two large meetings[,] three focus groups[, and literally any other autistic adult I’ve ever seen talk about this]”.
Through a variety of methods including a large online survey, two large stakeholder meetings, and three face-to-face focus groups, the project team identified five top priorities for mental health research which should be incorporated by researchers and practitioners in their work with autistic adults. These included research to inform trauma-informed care approaches; societal approaches for inclusion and acceptance of autistic individuals; community-available approaches for self-management of mental health; evaluation of adverse mental health outcomes of existing interventions; and improvements in measurement of quality of life, social well-being, and other preferred outcomes in autistic adults.
Far from discouraging Botha, these ignorant statements only solidified their resolve to change the scientific conversation about autistic people. Now associate lecturer in psychology at the University of Surrey, Botha studies the effects of stigma and discrimination on autistic people. The importance of Botha’s mission goes beyond principle. Autistic people are at risk for numerous mental health issues and suicide — much of it likely propelled by prejudice. Amid the coronavirus outbreak, some doctors in the U.K. have pushed for blanket ‘do not resuscitate’ orders for autistic adults without their or their family’s consent. As long as the scientific literature casts autistic people as less than human, “it facilitates maltreatment of autistic people,” Botha says. “It legitimizes violence.”
From Meet the autistic scientists redefining autism research by Rachel Nuwer
Wasn’t this “minimally invasive technique […] to activate neurons in the brains […] by using a light source located outside of the head” literally Topher Brink’s contribution to the technology of the Dollhouse?
And while findings from past epidemics can give researchers like him a good place to start, they’re not exact parallels. In general, studies specifically on the long-term, society-wide impacts of pandemics are limited, according to Taylor. It was only in the last 20 years that academics began looking at the psychological aftermath of the 1918 Spanish Flu — one of the deadliest pandemics in modern history and one that often gets compared to the current crisis — and even then, he says, its similar timing to World War I complicates the findings.
From What Our Post-Pandemic Behavior Might Look Like by Linda Poon
STAT has a fascinating, disturbing look at how SARS-CoV-2 works upon cells; behavior apparently not seen before: blocking the “call-to-arms” genes which would trigger process to restrict viral replication, but triggering the “call-for-reinforcement” genes, creating “a storm of inflammatory molecules in the lungs”.