GUEST ESSAY: Further Response to the Psychedelic Neuroimaging Researchers

By Prof. Edward F. Kelly

(This is a guest essay by Prof. Edward F. Kelly, University of Virginia School of Medicine, Department of Psychiatry and Neurobehavioral Sciences. It follows up on an earlier essay and disclosure.)

Bernardo has already provided a swift and trenchant response to the critique of our recent Scientific American blog on psychedelic neuroimaging by six leading figures in that rapidly bourgeoning area of research. Here I wish only to add a few further comments, focusing primarily on issues of particular interest or concern to me.

It is noteworthy first that the authors do very little to address directly the intriguing topic announced in their title – “What Psychedelic Research Can and Cannot Tell Us About Consciousness” – and devote most of their attention instead to the theme of their subtitle – “A recent Scientific American blog misconstrues and oversimplifies the research”.

Let me speak immediately to our allegedly oversimplifying “the details” of the studies we discussed. These studies are all enormously complex, and within the constraints of the Scientific American blog forum (strict word limits, technical discussions discouraged) there is no realistic possibility of getting into the details of any one of them, let alone the whole lot. The best we could hope to accomplish was to convey a faithful overall impression of what has been accomplished to date and to indicate where the research seems to us to be heading. I believe we succeeded in that, but our critics do not.

They go on to give two primary examples of how we supposedly misconstrued the available findings. One, which Bernardo has already dealt with at some length, concerns the observed sharp reductions by various agents of activity in brain networks associated with ordinary conscious awareness – in effect, the neural embodiment of the everyday self or ego. Amazingly to us, the researchers now want to back away from their own early findings of this sort, which as Bernardo shows again in his rejoinder are anything but subtle. The observed reductions, that is, are big effects, easily detected using conventional and straightforward analysis techniques. They satisfy what statisticians sometimes jokingly refer to as the IOT test (InterOcular Trauma – it socks you right between the eyes). Those results are certainly not going away.

Even relatively simple neuroimaging methods can easily distinguish between wakeful and drowsy states and other commonplace conditions, yet here we seem to be having difficulty finding anything in patterns of brain activity that is even remotely commensurate with the extraordinary phenomenology of psychedelic states.

Now consider by contrast their other example, which involves possible increases in other aspects of brain activity that they think might help us understand the extraordinary phenomenology of psychedelic states. They accuse us of misrepresenting the observed increases in multichannel MEG signal “diversity” produced by several agents as “small” effects. What really matters, they now declare, are the statistical significance and effect sizes (using Cohen’s d) of the observed increases. Those results, however, depend strongly upon the very large numbers of 2-second MEG data segments that enter into the analyses. The exact Ns are not explicitly stated, but given information provided elsewhere in the report they likely range from something like several hundred for the psilocybin data to several thousand for the ketamine data. These large numbers are what drive successful statistical discrimination of mean differences between drug and placebo conditions that in absolute magnitude are in fact appropriately described as “tiny” rather than merely “small”. Specifically, on a diversity scale of 0 to 100 they average on the order of .005 across all drug/placebo pairs, and occupy the interval between .98 and .99 (see Fig. 2 in Schartner et al., 2017). For several subjects the observed mean differences between drug and placebo conditions even go in the wrong direction.

Now, an enormous amount of unusually sophisticated computation went into the generation of these results, and to both Bernardo and me they seem puzzlingly meagre. After all, even relatively simple neuroimaging methods can easily distinguish between wakeful and drowsy states and other commonplace conditions, yet here we seem to be having difficulty finding anything in patterns of brain activity that is even remotely commensurate with the extraordinary phenomenology of psychedelic states. Our critics are not troubled by this; instead they go on to describe some of the relevant experiential properties and simply urge us to believe that they will all somehow, someday, be “accounted for” or “underpinned”, or “explained by” physical properties such as the “diversity” of the accompanying brain states.

Let me remark here parenthetically that I don’t think “diversity” in the sense of unpredictability or randomness in multichannel neuroelectric signals is by itself a very good candidate for such a property. To me the facile equation of brain signal diversity with experiential richness and complexity seems at best premature, and reminiscent of the many instances since publication of Shannon and Weaver’s original treatise on information theory in which cognitive scientists and neuroscientists have glibly conflated technical and everyday meanings of the word “information”.

Be that as it may, however, Bernardo and I can certainly agree with our critics that psychedelic neuroimaging research is at a very early stage in its development, and we certainly don’t profess to know how far it may ultimately get. Indeed, in the original blog we even offered a concrete suggestion of our own as to how to carry it further.

But our critics don’t know either, and here we arrive at the bottom-level disagreement. All of them are apparently conventional physicalists, and for persons of that persuasion it is simply axiomatic, a given, that everything in mind and consciousness must be manufactured by, or in some mysterious way identical to, neurophysiological events and processes in the brain. In our original blog we had provided indications that not only popular interpreters of psychedelic neuroimaging research but the researchers themselves were showing signs of bias in favor of this physicalist picture, and Bernardo has already demonstrated that this 6-person response to our blog amounts to more of the same.

Everything comes to a head in their final paragraph, where they now start by accusing us not merely of misrepresenting but of deliberately misrepresenting their findings in order to motivate an alternative non-physicalist view. That accusation is false and offensive. To set the record straight, Bernardo and I began our very different scientific careers as conventional physicalists ourselves, but we have long since changed our minds in light of arguments and evidence presented in voluminous detail in earlier publications. We approached psychedelic neuroimaging research as genuinely interested and admiring outside observers, viewing the subject through that independently justified lens, and we could not help noticing the evident tensions between physicalist expectations and the experimental results that had started coming in. As a scientist with long-time involvement in the field of psychical research, I also noticed that the most prominent reported physiological effect of psychedelics, the reduction or disruption of activity in networks that stabilize ordinary everyday consciousness, has parallels in recent neuroimaging research with advanced practitioners of various kinds of meditation, and that both of those situations could be viewed as steps on the way toward one of the main empirical challenges to physicalist neuroscience – namely, mystical-type near-death experiences (NDEs) occurring under extreme circumstances such as deep general anesthesia and/or cardiac arrest in which physiological conditions regarded by virtually all contemporary neuroscientists as necessary for consciousness have been abolished.

Our critics end by openly revealing themselves as guardians of the physicalist faith, intent upon defending it against potentially dangerous infidels. It seems to them that merely by entertaining any possibility of an alternative conceptual framework or worldview we are somehow putting at risk the legitimacy of the emerging neuroscience of consciousness. That in my opinion is patent nonsense. Their own efforts in psychedelic neuroimaging are certainly not at risk. Indeed, one of the most exciting developments in contemporary neuroscience is surely the rapid intensification of efforts to relate improved measures of brain activity to improved measures of the phenomenological character of associated states of consciousness, and psychedelic neuroimaging provides an ideal arena in which to pursue and deepen that inquiry precisely because of the extreme character of the states involved. Friendly criticism ought not be perceived as a threat. The research will certainly go on unabated, and all of us – we and our critics alike – are enthusiastically supportive of that. Let the empirical chips fall where they may.

Bernardo and I have evidently had no impact whatsoever on these six critics, at least not yet, but perhaps other readers will prove more open-minded.

Copyright © 2018 by Edward F. Kelly. Published with permission.

Setting the record straight with Robin Carhart-Harris and Enzo Tagliazucchi

Clouds on the horizon shall not obscure the light of facts.
(Photo by Bernardo Kastrup, hereby released into the public domain.)
As many of you know, I have been recently embroiled in a public exchange with a number of neuroscientists involved in the study of psychedelics. The exchange is about what I believe to be misinterpretations and misrepresentations of their results, as Prof. Edward Kelly and I argued in an opinion piece on Scientific American. Two days ago, the researchers replied on that same forum. I have commented on and rebutted their reply in this blog.

Yesterday, one of the researchers—Enzo Tagliazucchi—engaged in a de facto Twitter debate with me. Those interested can go on Twitter to peruse the many threads of that conversation. Here, however, I want to focus on a particular point, which I feel forced to vigorously counter. You will soon understand why.

First, a little background: about four years ago, one of the researchers, Robin Carhart-Harris, was busy promoting the results of the then latest psychedelic study of his team. This included a piece he wrote for The Conversation and an interview he gave to the Washington Post, amongst a number of other media engagements. Upon comparing his media statements with the actual study in question, however, I realized that things didn't add up: what the study actually said did not—either directly or by implication—support what Carhart-Harris was telling to the media.

The issue here seemed to be a basic misunderstanding of the signal processing analysis carried out in the study. Carhart-Harris was conflating changes in BOLD—a proxy for brain activity—level with changes in BOLD variance. I even went on to explain this difference in a 2014 post in this blog. I emailed Carhart-Harris to try and clarify the situation. Carhart-Harris then added Tagliazucchi to the discussion and, in a 2014 email to me, Tagliazucchi confirmed that I was correct.

But in my Twitter exchange with Tagliazucchi, I was accused of having been the party who misunderstood the issue in the first place! Here are the relevant tweets:

The initial accusation of my having misunderstood the relationship between oscillatory activity and brain activation did not bear out upon further debate, as you can see if you peruse the broader Twitter exchanges. The salient issue here, however, is the accusation that—precisely opposite to fact—I was the party that conflated BOLD level with BOLD variance: in actuality, I was the one who noticed Carhart-Harris' conflation of the two and sought the authors out via private email to alert them to it.

Carhart-Harris had asked, after the fact, that I not make our email exchange public. I have honored this request for about four years now. Yet, here is Tagliazucchi publicly claiming the opposite of what actually happened in those emails, portraying me as someone confused with the neuroscience in question and in need of redressing. This puts me in a very uncomfortable position.

He proceeded to double-down on his claim and dare me:

For clarity, I don't doubt that he was being honest in these tweets, in the sense that he truly recalls the story in a distorted manner. Admittedly, the actual story is somewhat surprising: a philosopher, with no formal background in neuroscience, suddenly emailing the authors of a neuroscience study to correct their interpretation of their own study? The opposite would be more expectable, of course. Nonetheless, facts are facts. So I accepted the challenge:

Let me be absolutely honest and clear: I had agreed to Carhart-Harris' after-the-fact request not to make the emails public. I stick to my word and the very idea of disclosing those emails gives me a wrenching feeling in my gut. I don't take this at all lightly. But put yourself in my position now:
  1. One of the people involved in that email exchange is now publicly claiming—without maliciousness, as I believe the case to be, but nonetheless publicly—that what happened was the opposite of what actually did. This inversion of the truth publicly portrays me as the ignorant and confused party, instead of the party that found the misunderstanding and then informed the authors about it. I have the emails to prove it. Should I continue to sit on them while Tagliazucchi's incorrect tweet stays online for all to see?
  2. These same people—Carhart-Harris and Tagliazucchi are both co-authors of the Scientific American reply attacking me and Prof. Kelly—are now publicly accusing me of misrepresenting their psychedelic studies. I have the emails to prove that Carhart-Harris himself has been—and continues to be, insofar as he has never amended his erroneous earlier statements, as I shall discuss below—the chief misrepresenter of the work. Should I continue to sit on them?
  3. In my Twitter exchange with him, Tagliazucchi repeatedly accused me of being ignorant of the basics of neuroscience. Consider this tweet, for instance:
    I address the false accusation that I "identify 'alpha power' with 'brain activity'" in other tweets of the exchange. But be that as it may, should I continue to sit on an email exchange that demonstrates that, although some 101 basics were indeed misunderstood, it was not me who misunderstood them?
  4. Tagliazucchi, one of the people involved in the original 2014 email exchange, has now given me public permission to disclose those emails. Should I continue to sit on them?
I feel Carhart-Harris and Tagliazucchi have left me no alternative but to defend myself and disclose the emails, for the reasons above. The record must be set straight. I can't remain silent in face of this onslaught.

(Post-publication clarification: In private correspondence after the original publication of this post, Tagliazucchi told me that his intent was to give me permission to publish only his own messages in the three-way exchange of 2014, not the messages he was commenting on. I acknowledge the clarification. But Tagliazucchi's messages alone would lack all context and much of the substance they refer to, thereby making it impossible for me to defend myself against his claims in point 1 above. Let it be clear, nonetheless, that I have four reasons to publish the 2014 exchange, only one of which is Tagliazucchi's permission. It has also been claimed, in private correspondence to me, that I am publishing messages originally shared with me in confidence. This, however, is not true. The messages were originally exchanged freely and openly, without any prior understanding regarding confidentiality, either explicit or implicit. I simply emailed Carhart-Harris asking for clarifications regarding public articles of his. There was no reason to think of confidentiality or for him to treat me any differently than any member of the public; he didn't know me back then. Only thereafter did Carhart-Harris ask me to not divulge the exchange. More specifically, this happened after he read the draft of an essay I sent to him, which was eventually published in my book Brief Peeks Beyond. In that draft, it was clear that my interest in Carhart-Harris' work was motivated by a metaphysical position I was trying to argue for. I shared the draft with him because I wanted to clarify in it, by reference to passages of our email exchange, that there was actually no finding of increased brain activity in the technical paper in question, despite how it was portrayed in the media. Carhart-Harris did not agree to it. My having not disclosed this material since then was a gesture of respect and courtesy towards Carhart-Harris and Tagliazucchi. But since Tagliazucchi, out of the blue and without prompting by me, now chose to refer to that original 2014 email exchange and characterize it as the opposite of what it actually was, the basis for that courtesy is nullified and I feel effectively forced to publish the exchange.)

Below, I reproduce the 2014 emails verbatim. I didn't correct even the typos, so I apologize if the text looks sloppy at times. I did remove email headers to avoid disclosing email addresses, SMTP servers and other sensitive information. But if any of the parties involved in the exchange questions the accuracy of what I am reproducing below, I can make the entire email files public.

Here is my original email to Carhart-Harris, dated Monday, 17 November 2014, sent at 10:52am Central European Time:
Dear Robin,
I've been following your studies with psilocybin with interest since the preliminary publications in 2011. I've been reading mostly your technical publications but, today, read a popular science article you wrote here:
In your 2012 PNAS paper you explicitly say that psilocybin decreases brain activity mostly in the DMN and doesn't increase it anywhere in the brain. In your new HBM study you talk of an increase in variability and spectral power of activity in dream-associated areas. Naturally, an increase in variability is not necessarily an increase in activity. Similarly, an increase in spectral density is also not necessarily an increase in activity, since phase information is ignored. I've concluded then that your new study in no way contradicts your earlier findings: psilocybin has NOT been found to increase sheer brain activity (metabolism, BOLD signal) in dream-associated areas, even though the media seems to have described the study that way. I've attributed the inaccuracy to journalists.
Yet, in your own myscienceacademy writeup you wrote "that psilocybin increased the amplitude (or “volume”) of activity in regions of the brain that are reliably activated during dream sleep and form part of the brain’s ancient emotion system." You also wrote of "the principle that the psychedelic state rests on disorganised activity in the ego system permitting disinhibited activity in the emotion system." Both statements are at least highly suggestive of a direct increase in brain activity ("amplitude," "volume," "reduced disinhibition"), even though no indication of this seems to be found in your technical papers (the HBM paper, for instances, talks of an increase in amplitude of variations).
I wonder if you could help me understand the discrepancy. Have you ever found that psilocybin increases sheer brain activity (BOLD signal, metabolism) anywhere in the brain?
Kind regards, Bernardo.
Carhart-Harris replied kindly and attentively on Tuesday, 18 November 2014, in an email I received at 12:12pm Central European Time:
Dear Bernardo,
Thanks for your email. The questions you raise are entirely valid and I would summarise it thus: the term 'activity' is generic and non-specific and not really that helpful or informative. With fMRI and FDG PET do not measure neural activity directly but instead via proxies, e.g. cerebral blood flow or glucose metabolism to index 'activity'. However, 'activity' used in this way is vague and we should probably not use it and instead just refer to the proxies. It is not certain for example that ASL fMRI and FDG PET measure the same 'activity'. My preference would be to move away from any reference to absolute increases or decreases in activity in relation to the action of psychedelic drugs. We get more information in the spontaneous oscillations and fluctuations in neural activity than we do in any absolute increases or drops in cerebral blood flow for example. If we observe increases in signal variance, this means the spontaneous signal fluctuations have a higher amplitude. You could interpret this as an increase in 'activity' but like I said, I'd prefer to avoid this and instead use a more specific term, i.e. an increase in signal variance or signal amplitude.
In short, we have mostly seen decreases in our measures of neural activity when looking at the brain effects of psychedelic drugs but it would be too simplistic to say all of these measures measure something that we can generically call 'activity' - as if it is something that is absolute, a quantitative thing that rises or falls. Instead, we need to think of these signals as dynamic and then think how best to describe the specific measures. My preference is to move towards referring to increases or decreases in the 'order' or 'organisation' of the systems from which the signal is recorded. I've attached an article that may help. When trying to communicate the results in the simplest terms, we often succumb to references to increases or decreases in activity but as I've said above, this isn't really the full picture and so, it can be misleading. It's a difficult trade off, knowing when to be specific but risk people not understanding what you're talking about or being generic but then over-simplifying the matter. If ever I make the 'mistake' of referring to increases or decreases in activity (which I do) then I need to hold my hands up and say yes, this is an over-simplification. You may find evidence of this over-simplification in what I have just sent you.
With best wishes,
Kind as it is, this answer is evasive. It renders it virtually impossible to pin down what Carhart-Harris means whenever he uses the term 'activity.' How can it sometimes denote short-term fluctuations of metabolism and other times (such as in association with their 2012 PNAS paper) metabolism itself? Why use the term 'activity' repeatedly towards the media (e.g.: "psilocybin increased the amplitude (or “volume”) of activity in regions of the brain," and "You’re seeing these areas getting louder, and more active," etc.) if one means by it different things at different times? What are we to make of it, as readers? The need to simplify things towards the general public is acknowledged, but the simplification should still preserve internal consistency and comply to the standard meaning of terms used without further definition, lest the communications become at least misleading.

In any case, comparing brain activity levels between placebo and psychedelic conditions must somehow involve a time-averaged mean amplitude of the signal for each respective condition, not merely the signal's short-term fluctuations within a condition. But an analysis of variance says nothing about the signal's time-averaged mean amplitude. I therefore insisted on my point, in an email to Carhart-Harris and his supervisor, Prof. David Nutt, dated Tuesday, 18 November 2014, 1:10pm Central European Time:
Dear Robin and Prof. Nutt,
Thank you both for your prompt and thoughtful replies, which I much appreciate. Without meaning to abuse, I have a couple of very brief comments.

>> We get more information in the spontaneous oscillations and fluctuations in neural activity than we do in any absolute increases or drops in cerebral blood flow for example. <<

This is paradigmatically very significant and has profound implications as far as the biological basis of consciousness, as I am sure you realize.

>> If we observe increases in signal variance, this means the spontaneous signal fluctuations have a higher amplitude. You could interpret this as an increase in 'activity' <<

An increase in variance (and spectral power) can be tied to higher-frequency fluctuations, not only fluctuations of higher amplitude. An increase in variance can lead to signals of lower amplitude, if the frequency components are not in phase and thus interfere destructively. Isn't this correct? Assuming it is, I will be as bold as to disagree with you here. I acknowledge the ambiguity behind proxy measurements of activity, but activity itself is a clean concept tied to metabolism. Variations of levels of metabolism are not activity; metabolism is. Personally, I find it confusing to conflate these terms.

>> I'd prefer to avoid this and instead use a more specific term, i.e. an increase in signal variance or signal amplitude. <<

I concur. I have a brief question: in the HBM paper you report increases in the amplitude of fluctuations of the BOLD signal (i.e. amplitude of the delta in time). This leaves it unclear whether the amplitude of the BOLD signal itself, during bursts, was higher than in placebo controls. I could imagine that, even though time-averaged BOLD is not higher in the psychedelic state, brief bursts could be. Did you observe higher-amplitude bursts of the BOLD signal in the psychedelic state as compared to placebo controls?
On a more personal note, Robin, I enormously appreciate the work you and Prof. Nutt have been doing. You are pioneers in the full sense of the word. I am keenly aware of the pressures you are probably under, given the sensitivity of your work for our scientific and philosophical worldviews in general, way beyond neuroscience. Though I am critical of the ambiguity of your recent communications, I am very understanding of the potential motivations behind it, and tend to believe I would not have done better than you are doing.
Sincere regards,
Carhart-Harris replied very openly and honestly in an email dated Tuesday, 18 November 2014, which I received at 2:09pm Central European Time:
Dear Bernado,
I've copied in Enzo, first author of the HBM paper to address your questions re signal variance. My understanding is that an increase in signal variance as it was measured in the HBM paper is equivalent to an increase in signal amplitude. Enzo may wish to comment on this.
As for reproducing my email response in print. If it's ok, I'd rather it not be. It was written somewhat in haste and I'd consider this more free communication rather than something sufficiently considered for publication. Perhaps if I could review and edit however, it could it principle be ok.
As for the issue re bursts. The increase in signal variance applies for a 5 min continuous period of scanning (post-infusion) and so is time-averaged. We did not specifically look at periodic bursts but this would be something interesting to look at. Would this be a Wavelet-like analysis Enzo? We'd need to know how to define a 'burst' in a systematic way. Since scanning was pure 'rest' there are no behavioural 'tags' to time lock 'bursts' to - but this is not to say they do not occur or that they are not behaviourally relevant. We'd have to be careful not to interpret motion artefact as a neurally generated burst. We have looked at 1 min time bins (see entropy analysis in HBM paper) Enzo is an expert on these more dynamic measures.
Best wishes,
Carhart-Harris admits here that his "understanding is that an increase in signal variance as it was measured in the HBM paper is equivalent to an increase in signal amplitude." This is not true. Signal variance is equivalent only to the RMS (not peak) amplitude of the fluctuations of the signal; that is, what is left of the signal after one first subtracts the signal's mean value from it. Performing this subtraction, however, amounts to discarding the core information about the difference in time-averaged brain activity levels between placebo and psychedelic conditions, which can't then be compared. There seems to be, as such, a misunderstanding here on Carhart-Harris' part, which could explain the consistent media misreporting (e.g. this and this) claiming that the study in question found increases in activity in dream-related regions of the brain. The 'activity' reported to increase in these dream-related regions is, at any rate, something quite different from the activity proper reported to decrease in his 2012 PNAS paper. Under the normal denotation of 'activity' as a measure of metabolism, this 2014 paper showed no increases in activity—which, by the way, renders it consistent with the earlier 2012 results—despite Carhart-Harris' messages to the media.

Upon this email, Tagliazucchi, lead author of the study in question, replied on Tuesday, 18 November 2014, in an email I received at 2:57pm. In the email, he confirms my assessment:
Dear all,
Bernardo: indeed, variance is in this context just a measure of variability in the signal. Increased variance implies increased fluctuations of the signal, as opposed to a constant, unchanging signal. My interpretation of these fluctuations is that spontaneously occurring processes in the affected regions are engaging and disengaging more often under the psilocybin condition, so even if subjects are resting, spontaneous processes are more "active" and thus increase the variability of the signal. Following this line of thought, I'm interpreting signal variance as a sort of equivalent of BOLD signal amplitude but during rest (i.e. a measure of "something going on" you can apply during rest, as opposed to BOLD signal amplitude, for which you need a task paradigm).
I find Tagliazucchi's "interpreting signal variance as a sort of equivalent of BOLD signal amplitude but during rest" misleading. Activity variability is not the same as activity proper; acceleration is not the same as speed. But never mind: the salient point in the context of this exchange is that Tagliazucchi recognized that my assessment was correct.

Misunderstandings do happen. I surely have misunderstood many things in my life and continue to do so. I don't think it can ever be avoided. My problem here is not Carhart-Harris' misunderstanding itself, but the false, inverted public portrayal of what happened in the 2014 email exchange. I also have a problem with something else: despite my explicit and repeated private and public requests for him to do so, as far as I know Carhart-Harris never rectified his mistaken media communications. As I write this, for instance, his original 2014 The Conversation essay remains unchanged.

Be that as it may, I hope this post sets the record straight once and for all.

The fix is worse than the problem: A reply to psychedelic researchers

(This rejoinder has been followed by a relevant disclosure and commentary, as well as a follow up essay written by Prof. Kelly).

Several weeks ago, Prof. Edward Kelly (University of Virginia, Department of Psychiatry and Neurobehavioral Sciences) and myself wrote an essay on Scientific American criticizing how recent research on psychedelics has been misinterpreted and misrepresented. Now, six researchers have written a reply to our criticisms, on that same forum. This post is my personal rejoinder: a commentary on, and answer to, their reply.

1. Clearing the semantic fog

First, let us get a semantic point out of the way so we can focus on substance. The researchers state that
neither we [i.e. the researchers] nor others claim that “brain activity randomness” explains psychedelic experiences. Our finding of increased signal diversity is part of a larger mission to account for aspects of conscious experience in terms of physiological processes. (emphasis added)
How is ‘accounting for’ consciousness ‘in terms of physiological processes’ different from ‘explaining’ consciousness in terms of these same physiological processes? Isn’t this just semantic obfuscation masquerading as argument? An attempt to eat the cake and have it too? Be it as it may, let’s just say that what Prof. Kelly and I meant by ‘explaining’ psychedelic experiences is what the researchers mean here by ‘accounting for’ them. This way, we get this word game out of the way quickly.

2. Metaphysical claims

The researchers continue the quote above with the following passage:
In our view, higher signal diversity indicates a larger repertoire of physical brain states that very plausibly underpin specific aspects of psychedelic experience (emphasis added)
Okay. So their work aims at underpinning aspects of the psychedelic experience in terms of brain states. Very well. They then—correctly—define the materialist metaphysics as follows:
… “materialist” views, held by most neuroscientists, according to which conscious experiences—and mental states in general—are underpinned by brain states. (emphasis added)
Right. So the inescapable logical implication of these two passages taken together is clear: according to the researchers themselves, their work supports the metaphysical view of materialism. Yet, they continue:
Our study, like all other studies that explore relations between experiential states and brain states (whether about psychedelics or not), is entirely irrelevant to this metaphysical question. (emphasis added)
What? They go on to say that Prof. Kelly and I espouse
an anti-materialistic view of consciousness that has nothing to do with the details of the experimental studies—ours or others. (emphasis added)
What is one to make of this? Are the researchers again trying to eat the cake and have it too? Either they claim credit for allegedly making progress in explaining—err, accounting for—the mind-body problem in terms of physical brain states, or they acknowledge that they aren’t accounting for it at all, but just charting correlations. They cannot claim the metaphysical credit when they can get away with it—for instance, by systematically allowing the press to do just that in their name, or by directly suggesting it in their own talks and presentations—and then turn around and disclaim it when they need to circumvent criticism. One cannot have it both ways.

But I don’t want to make too much of a meal out of what may be just loose and inconsistent use of words by the researchers. Maybe the point they are trying to make is simply that scientific results do not necessarily entail or imply a metaphysical position; a point with which I wholeheartedly agree. But to say that their observations are “entirely irrelevant” to the mind-body problem—which is a metaphysical problem through and through—is just wrong, betraying a painful degree of naiveté regarding philosophy of mind.

Although scientific observations don’t necessarily imply a metaphysical position, they surely inform metaphysical hypotheses. Metaphysics is not done in a vacuum. While science tries to model the behavior of nature, metaphysics attempts to interpret this behavior so to make educated guesses about what nature essentially is. So scientific observations are very relevant for metaphysics. That there are correlations between brain states and experience reflects a behavior of nature demanding a metaphysical interpretation. That the internal consistency of these correlations sometimes breaks is perhaps even more relevant, insofar as it creates a significant problem for the particular metaphysics of materialism.

3. What the researchers fail to address

In their reply, the researchers discuss, at some length, some of the more detailed technical issues in contention. But they fail, rather conspicuously, to even touch on the elephant in the room. Indeed, a key point of my essay with Prof. Kelly was this:
The problem is that modern brain imaging techniques do detect clear spikes in raw brain activity when sleeping subjects dream even of dull things such as staring at a statue or clenching a hand. So why are only decreases in brain activity conclusively seen when subjects undergo psychedelic experiences, instead of dreams? Given how difficult it is to find one biological basis for consciousness, how plausible is it that two fundamentally different mechanisms underlie conscious experience in the otherwise analogous psychedelic and dreaming states?
Why is this—the opening point of our criticism—not even mentioned by the researchers? Why no commentary at all on the seeming inconsistency between the dream and the psychedelic state? Another important point Prof. Kelly and I made was this:
To suggest that brain activity randomness explains psychedelic experiences seems inconsistent with the fact that these experiences can be highly structured and meaningful.
The researchers even quote this passage of our article in their reply, raising the immediate expectation that they are about to address it substantively. But then their shot is a dud: they simply say that they weren’t trying to ‘explain’ anything anyway (“neither we nor others claim that ‘brain activity randomness’ explains psychedelic experiences”), in a passage I already commented on in Section 1 above. They dismiss the point merely on account of a word they don’t seem to like.

Well, fine, I can change the word. If I re-phrase our original charge—quoted above—by replacing ‘explains’ with ‘accounts for,’ what is their reply? We don’t know, for they don’t provide it. So our criticism stands: How can one account for the highly structured, meaningful experiences of a psychedelic trance in terms of ‘signal diversity,’ which is largely equivalent to randomness? Why don't the researchers address this glaring point, so central to our original criticism?

The researchers also do not counter our charge that they—in ways discussed in our original article and, even more extensively, in two earlier posts in this blog (here and here)—have contributed, either actively or by omission, to the scandalous media misreporting of their findings.

4. A surprising claim

The most surprising passages in the researchers’ reply were these:
These are not the only inaccuracies in the piece that deserve redress. For example, [Kastrup’s and Kelly’s] suggestion that decreased “brain activity” is one of the more reliable findings of psychedelic research is incorrect.
Well, the facts say otherwise. Here is a list—already provided in our original article—of four studies that replicated the salient aspects of the original 2012 findings for multiple psychedelic agents and measurement strategies:
  1. Broadband Cortical Desynchronization Underlies the Human Psychedelic State.
  2. The Psychedelic State Induced by Ayahuasca Modulates the Activity and Connectivity of the Default Mode Network.
  3. Neural correlates of the LSD experience revealed by multimodal neuroimaging.
  4. Two dose investigation of the 5-HT-agonist psilocybin on relative and global cerebral blood flow.
Two of these replications were done by some of the very researchers I am now replying to, so it’s confusing to me that they don’t seem to want to highlight their own successful replications. Moreover, no study I am aware of has contradicted those original findings since their publication in 2012. I believe this is sufficient basis to claim that the findings are now quite reliable. They were certainly “replicated across studies and study teams,” as the researchers seem to demand.

Now the researchers get more specific and claim something that gave me pause:
early reports of decreased brain blood flow under psilocybin have not been well replicated: a subsequent study by the same team using a different protocol and drug kinetics (intravenous LSD) found only modest increases in brain blood flow confined to the visual cortex. (emphasis added)
This is remarkably misleading. That a claim like this is made by some of the co-authors of the very paper in question is even more remarkable. But okay, let’s stick to the facts. I have discussed the paper in question extensively here. I reproduce below the figure in the paper that shows—through direct measurements done with magnetoencephalography (MEG)—whether and where brain activity has increased (red) or decreased (blue) upon intravenous administration of LSD:

No, I am not kidding. Blue represents decreased brain activity. I didn’t create this figure; I downloaded it from the paper in question. Here is the direct link if you want to check it. Contrary to what the researchers claim in their reply, the findings in this paper weren’t “only modest increases in brain blood flow confined to the visual cortex”; they were of widespread decreases in activity throughout the brain.

So what about the “modest increases in brain blood flow”? Next to the direct measurements of brain activity done with MEG, cerebral blood flow (CBF)—an indirect measurement of brain activity—was also measured. Modest increases in CBF confined to a small area in the visual cortex were then indeed found; a small local discrepancy in view of the broad decreases in activity directly measured with MEG. So what did the authors of the paper make of this small discrepancy? Here are their own words, lifted verbatim off their paper:
One must be cautious of proxy measures of neural activity (that lack temporal resolution), such as CBF or glucose metabolism, lest the relationship between these measures, and the underlying neural activity they are assumed to index, be confounded by extraneous factors, such as a direct vascular action of the drug. For this reason, more direct measures of neural activity (e.g., EEG and MEG) … should be considered more reliable indices of the functional brain effects of psychedelics, and it is notable in this regard that our previous MEG and RSFC findings with psilocybin are highly consistent with those observed here with LSD. Thus, rather than speculate on the above-mentioned discrepancy, it may be more progressive to highlight the advantages of EEG/MEG and dynamic fMRI... (emphasis added)
So the authors themselves dismiss these increases in CBF as possible artifacts, expressing confidence only in the decreases in neural activity directly measured with MEG.

What is one to make of this?

5. The issue of statistics

The researchers summarize their main point—on which they base the bulk of their reply—thus:
[Kastrup and Kelly] suggest that the changes in signal diversity we found are “small,” when it is not magnitude but statistical significance and effect size that matters.
They proceed to make a meal of it while ignoring the elephants in the room (see Section 3 above). Nonetheless, let us bite this bullet anyway: statistical significance shows merely that the effect is real, in the sense of not being explainable by experimental artifacts. But we never claimed that the effect isn’t real; that wasn’t our point. Our point was that, insofar as the researchers aspire to explain—err… account for—psychedelic experiences in terms of a change in a measurable physiological parameter, the magnitude of the change measured is indeed relevant. Why? Because the magnitude of the corresponding change in subjective experience is colossal.

You see, from a first-person point of view a psychedelic trance represents a huge—what an understatement—alteration of consciousness, which only those who have undergone it can fathom. So it becomes at least cumbersome to try to account for this colossal subjective effect in terms of relatively small measurable changes in brain physiology, even if these are statistically significant. The researchers don’t address this point. Instead, they create a straw man and proudly burn it down.

6. A non sequitur

The researchers also did not like our claim that there is a formidable chasm between the magnitude of the subjective effects of a psychedelic trance and the accompanying physiological changes. In reply to it, they say:
To claim a “formidable chasm” is to misunderstand the incremental nature of consciousness research (and experimental research generally), to sideline the constraints and subtleties of the relevant analyses and to ignore the insights into psychedelic experience that such analyses provide.
This is a complete non sequitur. There is absolutely no contradiction between (a) acknowledging that incremental progress is being made, with accompanying insights and subtleties, despite constraints, and (b) pointing out that there is still a formidable chasm to be overcome.

7. Final thoughts

Our original criticism wasn’t against the psychedelic research itself. I applaud it and believe such research should continue to be funded and even prioritized. It has important applications, as well as important philosophical implications. Our criticism was against the way the research is routinely and repeatedly misinterpreted and misrepresented. The researchers’ reply, in my view, did not meaningfully address our criticisms in this regard. It left the important points unaddressed, created and burned straw men, got lost in semantic games, and even misled its readership by further misrepresenting the experimental results in question (see Section 4 above). If anything, it has made the situation worse. We, as a community, have missed another opportunity to get the facts straight. Instead, we’ve invested time, effort and media space in becoming more entrenched in earlier errors.