Yet another condition—one that is primarily marked by 1) psychological symptoms, 2) chronic fatigue, and 3) chronic pain—is found to be neuroinflammatory in origin!
This paper is FASCINATING, because the condition is associated...
1/11
...with a history of traumatic events (including emotional trauma).
This shows that—even for psychological disorders that are known to directly result from psychological trauma—the etiology of the disorder is PHYSIOLOGICAL, not "mental."
2/11
They again confirmed that serious psychological disorders can result from trauma such as:
- serious accidents, employment issues, witnessing violence, etc.
- in childhood: exposure to neglect, abuse, domestic violence, loss of a parent, substance abuse, incarcerated family
3/11
Critically, "ACE [adverse childhood event] + NLE [negative life event] score had a significant effect on all symptom domains.... The results . . . show that cytokines/chemokines/growth factors had significant effects on the symptom domains beyond the effects of ACE+NLEs"
4/11
This led to a handful of conclusions, which I find absolutely fascinating:
First up, for MDMD (major dysmood disorder), the factor driving physiosomatic, fatigue-fibromyalgia, and gastrointestinal symptoms is the same factor driving pure depression, anxiety, and insomnia!
5/11
Here's a visual representation of the statistical model that led to this result.
This is what's called a latent variable model, and this approach is just beautiful. It shows that about 40% of the psychological symptoms can be explained by history, and 60% are PHYSIOLOGICAL.
6/11
Then, when they treat the immune network as a single latent variable, they once again find that over half of the variance in physio-affective symptoms can be explained by activation of the immune system.
7/11
Here's my favorite part: this finding fits in with a variety of results that basically show that depressive and fatigue-fibromyalgia symptoms are directly related to the level of immune activation!
8/11
The implication is simple: "Together, ACEs and NLEs appear to induce a pro-inflammatory network composed of cytokines, chemokines, and growth factors."
That is, psychological trauma can induce dysregulation of immune processes, leading to physiological symptoms.
9/11
They conclude: "A larger part of the variances in the physioaffective phenome, and the physiosomatic FF and GIS symptom domains is explained by immune variables."
10/11
To put it another way, psychological factors can lead to physiological dysfunction, but it's highly unlikely that further psychological intervention alone would make a difference without addressing the induced physiological dysfunction!
13/11 I think large swathes of OTHER fields need to start adopting latent factor analysis and moderated mediation models. If history follows the pattern of how long it took other statistical methods developed by psychology to become common in other fields, we have like 20 years
14/11 Here's the entire thread on a single page. I use Readwise for this purpose, because if there are corrections or retractions in the future (or I notice that I made an error), I can add an annotation to the page
15/11 My annotated copy of this paper is available at this link (as well as a related paper by the same research group, which I discussed in another thread):
The annotations are mostly just what's included in the screenshots, but in a more useful formdropbox.com/t/3FMrkI5nURsy…
16/11 A few people have asked about what this means practically/for treatment, but at this point, the research is only demonstrating that this method of building a model is superior to the existing methods. However, it does suggest psych pharmaceuticals are worth looking at!
17/11 What's *new* about this paper is how it shows the inextricable relationship between psychology and physiology! The serotonin model is flawed, but SSRI, etc. research shows they do have an effect—it's just likely that a DEPENDENT variable was being interpreted as INDEPENDENT
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Here's a thread about a paper that build a more accurate model of depression—as an outcome of PHYSIOLOGICAL factors! I'm genuinely impressed by the robustness of their method, and I'm usually nitpicky as fuck about research methods!
They come in HOT in the abstract…
1/
They point out that, fundamentally, it's a mistake to represent a complex spectrum of factors with a single binary metric.
When they actually account for these complex factors, they end up with a robust statistical model that explains how the factors interact.
2/
I think I love this paper so much because it really drives home something I'm always saying, which is "everything is a gradient; all categories are artificial constructs."
They point out that using rigid criteria as a variable in the experimental design is a terrible idea.
Here's a thread about a paper I recently read that made me genuinely *furious*.
It's a paper from 1980.
You know... 40 years before the pandemic began.
You wanna know the title?
"Coronavirus Infections of Man Associated With Diseases Other Than the Common Cold"
1/
If you're now thinking "well, it probably can also cause pneumonia and acute respiratory distress syndrome," you'd be correct. If you guessed another major LC issue, neurological symptoms, YOU'RE CORRECT AGAIN.
But it gets worse! Let's take a little tour of the method...
2/
It had a small number of participants drawn from a HUGE pool:
- 14,000 paired sera samples (1 pair=1 person, 2 time points) were screened for changes in HCoV-OC43 antibodies
I want to point out some highlights from this piece that totally surprised me while researching it. A bunch of things were offhandedly mentioned in a paper, and then when I looked at the source, it opened up a tanker-truck-sized can of worms
People with an asymptomatic acute infections can develop Long Covid. The risk from asymptomatic infections is definitely *lower* than symptomatic infections, but it's NOT ZERO.
What the hell, amiright?
Loss of smell is a symptom that strongly suggests viral entry into the nervous system. My mental model up until like two months ago was that anosmia was caused by inflammation of the cranial nerves, but NOPE, it's actually very covid-specific.