Very interesting article about why Ketamine works

I’m not sure if this has been shared here:

https://www.psypost.org/2020/12/ketamine-may-ease-depression-by-restoring-the-brains-sensitivity-to-prediction-error-study-suggests-58912

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Some of you may be familiar with the books by Carlos Castaneda. In those, Don Juan told Carlos that he only had to blast him with power plants to shake the solidity of his world view, because moments of serious sorcery were always done in sober consciousness. My personal take is that psychedelics work on depression for the same reason-they shake the solidity of the depressive world view. My take on this article is that it appears to agree.

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Thanks for sharing Phamer28…

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Jim, we should go to Peru…

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Hey Sojourner,
Been actually thinking about that all day…LOL

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Count me in! :wink:

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Thanks for posting that phamer28. I think most of us here are always interested to read about research regarding depression/anxiety. We’re all still hoping for the magic bullet that will let us say we’re now feel 9/10 on the happiness scale.

I swear I’m not trying to be contrarian for the sake of it, but having gone through a mid-sized public library worth of psychiatry research I’m a bit jaded with such hypotheses, not because they are egregiously wrongheaded or anything, but precisely because they are so innocuous so as to be entirely tautological.

Basically, it’s a sufficiency vs. necessity fallacy; take any depression trait X, then say, agent K cures depression because of some property Y->-X. Then you say when X is treated so is depression (D). So you (falsely) conclude, if K->X and K->-D by mechanism Y, then Y->-D, and more crucially Y->-X. So K->-D implies -X->-D.

Now here’s the mistake, you can’t conclude that statement -X->-D from that, as the implication actually goes the other way, meaning if ketamine treats X (here we say brain plasticity which could be one of many characteristic biomarkers of depression), that’s necessary but not necessarily sufficient for treating depression: it could easily be just an epiphenomenon of depression disappearing of which we have some transparency. Now by itself that’s not such a terrible mistake, and yeah I’m nitpicking but that’s kinda the only game in town science; it’s when they go from that to start talking about CBT or whatnot, which if you read the data critically has simply been a dead-end for TRD, and mostly good at taking credit in cases where patients would’ve recovered from an interventional treatment anyway.

So just my 0.02 rubles, don’t take too serious. I just like sometimes to give voice to the fact that this shit is hard, and if we were having this conversation only 5-10 years ago, everyone would wax poetic about the monoamine hypothesis and how our biggest problem is due to serotonin deficiency. We’ve made progress, but it’s slow, and sadly researchers/doctors/pharma isn’t really always aligned with our best interests.

I hear that, Hoping in big way!