Ketamine and Psychedelic Drugs Change Structure of Neurons

I thought this was generally interesting, shedding some light, as it does, on how ketamine and psychedelics affect the brain structurally, and suggesting the possibility of new drugs for depression and anxiety based on these chemicals.

Ketamine was also suggested and tried as a treatment for ME by Dr Jay Goldstein; he found it useful for patients, but I think did not publish peer-reviewed work.

https://neurosciencenews.com/ketamine-psychedelics-neuron-structure-9314

And an article with more detail,

https://www.google.co.uk/amp/s/medi...-psychedelic-drugs-neural-plasticity-rats.amp

 

Interesting that they choose to indicate the potential use for depression but don't mention other cases where increasing neural plasticity would be helpful, such as stroke victims.

 

Michael Pollan just wrote a book on psychedelics (out May 2018, see amazon). He's doing a big publicity tour. I haven't dug into it yet, but here's the info.

Here's the NPR interview
https://www.npr.org/sections/health...llan-embraces-the-new-science-of-psychedelics

....And 3 re-broadcasts next week of the interview he had in SF recently as part of the City Arts & Lectures series
https://www.cityarts.net/radio-broadcasts/

 

In general, I am not a fan of psychedelics, I had too much interaction with the walking wounded from the initial enthusiasm for LSD. I have some wild stories based on direct experience with the people, not the drugs.

That said, there is a possibility the entire idea of changing what is going on in the brain is based of misunderstanding of the mechanism of action. For example some people with antibodies to NMDA receptors have had the kind of symptoms that would have permanently confined them to locked wards prior to sophisticated biochemical tests. Resetting immune response to NMDA receptors might benefit them.

Of course the whole idea of "psychological problems" being centered inside the brain ignores the substantial nervous system interacting with other parts of the body. I've known people who had the vagus nerve surgically cut in an attempt to treat ulcers. Their gut went right on digesting food with no input from upper management.

Still another subsystem controls vascular response. Again, this takes place in the walls of blood vessels, without waiting to consult the brain.

You could make a checklist for symptoms deriving from parts of the nervous system least connected to the brain. Compare this with standard medical advice for diagnosing "mental problems" and you would find a surprising overlap. Gut disturbances, sphincter control, blood pressure, circulation and even sweating (diaphoresis/hidrosis) are all considered signs of emotional problems. Maybe we have cause and effect reversed.

A friend sometimes shows me things that Paul Cheney is exploring. I am cautious about separating his enthusiasms from replicable evidence. He has long said that ME/CFS patients show a distinctive pattern of changes on echocardiograms, and I've been frustrated that nobody else has even tried to reproduce this, so far as I know. The changes he describes fit with the work by David Systrom et al. about low pressure on venous return and exertional dyspnea. In both cases we are talking about measurements independent of assumptions about patient emotional state.

I will also note that the brain is highly sensitive to changes in the supply of oxygenated blood, even in people thought to have no fundamental psychological problems. There is a considerable literature on weird symptoms of hypoxia. ME/CFS patients don't have ordinary hypoxia, but there seems to be a problem at the tissue or cellular level in using oxygen.

Cheney has recently run before and after echocardiograms on a few patients treated via ketamine infusion for presumed psychological problems. The known dissociative effects of ketamine were significant negative factors in the treatment, and were not necessary for improvement. It looks like lower doses that don't produce dissociation still have a substantial measurable effect on cardiovascular function, seen on echocardiograms, and this is quickly apparent in orthostatic tolerance.

This is very early, and not ready for publication. Still, I think the idea that the drug is acting directly on a neglected part of the nervous system having little interaction with the brain, and producing measurable changes in a key symptom, is worth investigation.

I'm sorry that I can't link any references to sources. Perhaps others can turn up useful research.