Michael Joyce produces multimedia for HealthNewsReview.org and tweets as @mlmjoyce
Having a bad day? Feeling down? Wouldn’t it be great to just hit a ‘reset’ button?
It’s an appealing notion, but a dangerous analogy for journalists to latch on to in reporting about depression.
But that’s exactly what’s happened over the past week or so as a host of reporters jumped on very preliminary findings from a British study investigating the role of hallucinogenic mushrooms (active ingredient: psilocybin) in treating ‘treatment-resistant depression,’ or TRD:
Magic mushrooms ‘reboot’ brain in depressed people — study (The Guardian)
First, the basics of this study published by researchers from the Psychedelic Research Group at the Imperial College London: A group of 20 patients were given two doses of psilocybin and were followed for 5 weeks. Changes in mood were assessed using patient questionnaires. Subjects’ brains were scanned with functional magnetic resonance imaging (fMRI) before and after taking psilocybin.
Researchers found that all the patients reported feeling better immediately after taking the drug, and about half still felt better 5 weeks later. Brain scans showed decreased blood flow to the amygdala — two clusters of nerves located deep in our temporal lobes that play a role in modulating memory, decision-making, and emotions.
That reporters jumped all over these very preliminary findings — from a very small study, no less — is not surprising. We’ve reported before on how news organizations not only seem to be smitten with magic mushroom studies, but will often hype the findings at the expense of neglecting some very important caveats and cautions.
Coverage of this British study was no exception and brings up three such cautions worth mentioning.
It was the patients in this study that actually used these computer analogies. Then Imperial College put them in its news release headline (“Magic mushrooms may ‘reset’ the brains of depressed patients”) and the lead author of the study, Robin Carhart-Harris, PhD, started using them in interviews:
“Psilocybin may be giving these individuals the temporary ‘kick-start’ they need to break out of their depressive states and these imaging results do tentatively support a reset analogy.”
The italics are mine because I want to underscore not only that these results do NOT prove a therapeutic benefit of psilocybin (see below), but that the very notion of a ‘reboot’ is an analogy and nothing more. A very powerful one at that. Most of the news coverage I saw featured this analogy prominently. But as illustrative as this analogy is, is it responsible?
“This kind of discourse has become increasingly popular,” says Lisa Cosgrove, PhD, a clinical psychologist at the University of Massachusetts Boston.
“We ‘talk’ in computer terms but the brain doesn’t operate like a computer — there is no neuroanatomical or neurotransmitter ‘rebooting.’ There is an attempt to maintain homeostasis. So if we take a (licit or illicit) drug that increases dopamine, our brains decrease dopaminergic activity. Then, if we stop taking the drug, our brains will respond by increasing dopaminergic activity. But that is a far cry from saying our brains have ‘rebooted.’ Such language is thus reductive and misleading — as if there was some ‘normal’ to get back to (that could be measured).”
You could argue that if such computer analogies come from patient experiences they have some value, albeit very subjective. But the language also carries significant risk. Could a reader — in particular one desperate with intractable depression — walk away with the idea that by taking hallucinogenic mushrooms they could “start over …. get a clean slate …. a fresh start … and get rid of my depression”? The risks they would assume by taking an illegal Schedule I drug, with no knowledge of dosing, and without supervision, would be considerable. They might also be led to believe that there is such a ‘reset button’ in their brain. And since there is no proof of such a mechanism, that would be a false hope — something people with major depression don’t need.
There’s something about fMRI images; especially when it comes to the subjective nature of the signs and symptoms of mental illness. The general public can erroneously believe that whatever changes are seen on the scans, somehow prove that there is a cause-and-effect relationship they can now point to … that spot, lighting up, right there!
But what lights up (or doesn’t light up) on a fMRI scan — even if it appears to correlate with something observed clinically — does not prove causation in any way. For example, the amygdala is associated with emotions. It is not necessarily a center or controller of emotions as some might imply. Even if you could prove that a substance like psilocybin decreased (or increased) blood flow to it, that may have no impact on emotions whatsoever.
“Not to say this isn’t interesting research,” says psychiatrist Susan Molchan MD, a frequent contributor to this blog. “But simply looking at the ups and downs of blood flow — or having the scientists pick various brain regions and look to see if the signal strength gets stronger or weaker, with or without the drug — gives somewhat meaningless measures that no one really knows what they mean.”
Writing in Slate about the public’s superficial fascination with MRI’s, Matthew Huston said:
“I think people expect neuro-imaging studies to tell us more about psychology than they actually do or even can.”
None of the articles I read about this study — and it was well covered — even mentioned the limitations of fMRI as a surrogate marker. It’s a common oversight. So common that we wrote this primer on surrogate markers.
The answer is: We don’t know. And the authors of this study would be the first to admit this.
Many stories also picked up the researchers’ framing of a “sustained benefit” from magic mushrooms. But again, this study lasted only 5 weeks, and the participants all had long-standing depression that wasn’t helped by other treatments. It will take a much longer follow-up to know if patients experience benefits that are truly lasting.
Proving an established benefit of psilocybin on depression won’t be easy says psychiatrist Molchan:
“Admittedly it would be impossible to do a placebo-controlled study with a psychedelic drug. You would need another psychedelic to compare with. And that would be OK, since you’d be exploring mechanisms of actions and hopefully longer-term effects on depression.”
But, at this point, this is not the next step of the Psychedelic Research Group. Instead, next year they are planning to start a 2-arm, double-blind, randomized trial comparing a single does of psilocybin with 4 weeks of daily escitalopram (brand name: Lexapro).
And once again, they plan to use fMRI.