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A Beautiful, Social Mind

When Susie woke up that morning, she didn’t expect that she’d be sitting with a paramedic at 10 pm. The incredible feeling of energy, sociability and freedom during the day that she had put down to her morning coffee had, by the evening, tipped over into confusion and terror as she concluded that the whole room was plotting to assassinate her. Susie had developed a persecutory delusion. This might be a one-off experience, or it may be the beginning of a lifelong challenge to manage her experiences. At the moment, we can’t fully explain why it happened, or how best to treat it.

Sadly, Susie’s experience isn’t unique. The core of a persecutory delusion, paranoia – the unwarranted belief that others want to intentionally harm you – occurs frequently in a clinical setting. It’s most often associated with the psychiatric disorder schizophrenia but shows itself in epilepsy, Parkinson’s disease, insomnia, encephalitis and drug abuse. Paranoia increases the chance of suicide fivefold in the general population and can hinder the therapeutic process in any healthcare setting. After all, you wouldn’t want to see your nurse for a vaccine if you thought it was part of a plot to control you. Worse still, developing strong paranoid beliefs at a young age can damage the foundations of forming and maintaining relationships – the lifeblood of being human. In turn, this stunts the ability to secure a job, a family, and all the other opportunities in life we take for granted.

Current mainstay treatment and management of paranoia still rely on the original observations made by physician Henri Laborit in 1952. Laborit noticed that chlorpromazine – a drug often used for its tranquillizing properties – also reduced the distress his patients suffered around their persecutory beliefs. Since then, a series of innovative studies have identified that drugs like chlorpromazine work by blocking dopamine – a neurotransmitter in the body – and that experiences such as Susie’s might be in-part explained by changes to how dopamine shapes the way information is communicated in the brain. However, this type of treatment only works in around a third of people and predicting when and for whom it will work is extremely difficult.

While newer drugs have taken the edge off some of the awful side effects of earlier treatments – such as agitation, muscle spasms, and sleep problems – making treatment more clinically acceptable doesn’t alone solve the core scientific problem of why strong paranoid beliefs occur. Despite extensive research into dopamine transmission as it relates to paranoia in illness, how these brain changes might relate to the normal social, psychological, relational changes in all of us remains largely unexplored. This blind spot means that we don’t have a fundamental explanation of human behaviour to help us understand what might go awry in illness. Part of the reason we haven’t yet got to this point may be that, until fairly recently, we viewed experiences like paranoia as an aberrant, abnormal human trait, separate from the seemingly otherwise rational mind.

Paranoia may be wholly understandable, intuitive and reasonable, especially when we consider our evolutionary roots. New evidence in behavioural and evolutionary science is uncovering that our minds are far more social than previously thought. All of us have distinct neural functions that strengthen and maintain relationships to our friends, family and strangers, and these fundamental interpersonal processes shape the way we learn about other, more prosaic aspects of life like following a map or learning mathematics. This isn’t even unique to humans, as we find similar conserved social brain function across all manner of species that have any semblance of social structure. This has raised the important question as to whether experiences like Susie’s might be explained by changes to similar core brain processes that regulate and manage our social environment: coalitional cognition.

In fact, while we’ve used Susie’s distressing and relatively extreme experience as an example, paranoia isn’t something limited to illness at all. Our pre-existing ideas about others based on our genetic and developmental history interact with our current social context to shape our sensitivity to experiences in the moment. But they most likely won’t force us to seek clinical support. We have all had experiences where we’ve been a bit wary that others might be trying to take advantage of us with little evidence to back up our intuitions, but maybe it wasn’t something we thought too much about. While we can think about this on an individual level, we can actually see this play out on a wider scale. Conspiracy theories demonstrate how an unwarranted belief about an unseen, intentionally harmful organisation might be shared by entire communities. Science suggests that strong, gravitational paranoid beliefs like the one that Susie had can be found at different intensities throughout the general population. Further, research has shown that, regardless of our preconceived ideas of others, interaction with someone who has differing political beliefs or higher social status increases the probability that we think others are being intentionally harmful. Lending support to this idea, we’ve shown that the neurotransmitter involved in paranoia in illness, dopamine, is also involved in our interpretations of how intentionally harmful we think others generally are.

Anthropological, cultural and archaeological research shows clear evidence that being a social animal is at the core of being human, and this is reflected in our brain function. This is because our social, psychological and behavioural expressions are inseparable from how our brain works – our body is a community, and together we form ecosystems. To discuss the social, psychological and biological as separate entities is to ignore years of scientific evidence, but sometimes when we wish to explain different aspects of a phenomenon it’s helpful to break explanations down into the separate factors to understand how different levels of the ecosystem interact. Paranoia is no different; it’s a change to the interpretation and management of human relationships. Social changes shape our brain, and our brain can shape how we perceive social changes.

Testing how our social world is reflected in the mind may be the crucial step forward to help understand what Susie might be going through, and what we can do to stop life being so distressing for people in her shoes. This has implications for our understanding of paranoia in illness and health, but also perfectly illustrates how attuned our brain is to social relationships, and might be a better, more complete explanation of the mind. 

The science of the social brain matters. This is for Susie, and this is for you.

Solipsis – exploring the phenomenology of psychosis in art and science.

Solipsis_V3.1

Originally submitted as an artefact for a KCL Experience Award as part of the A Beautiful Mind: Art, Science, and Mental Health module.

 Materials: Acrylic on canvas (A1)

Post-production: Photoshop

Solipsism, to be solipsistic, is the concept that the self is all that can be known to exist. Clara Humpston (2018), building upon work from Louis Sass, Barnaby Nelson, and Josef Parnas (2001; 2009; 2014), suggests that the experience of psychosis is fundamentally that of a disturbance to a sense of self – a disruption to the bedrock of ‘I’. The disruption produces a meld of subject/object awareness, shifting focus of an individual to their moment to moment inner experience in a chaotic, unanchored manner – unable to differentiate fact from fiction. The experiencer becomes solipsistic in their being, but not out of choice.

The artefact “Solipsis” is simultaneously a depiction of fusion between subject and object awareness, and also an exploration of my personal experience that accompanied being drowned by my own inner world. Using techniques of art psychotherapy, content inspired out of the work of contemporary phenomenologists, and from my own reflective practice in therapy, the painting is an external representation of internal dynamics. It has been a process of making the invisible and intangible something that is visible and understandable.

The painting depicts two solar or star-like objects in a dance, with one consuming the other to become an assimilated state. The inspiration for the visual dynamics came from observations of black holes or stars swallowing another small, less stable entity. Analogously, the internal dynamics of psychosis as suggested by Sass, Parnas, Nelson, and Humpston is that of a consumption of the boundary between internal and external worlds – the internal world becoming so engorged that it draws in and annihilates the external. Without differentiation of subject and object, moment to moment experiences can be that of pure clarity or utter chaos outside of our apparent volitional control.

This artefact is a work of interdisciplinarity through its use of scientific literature, art psychotherapy, and personal experience. In this piece, much like it’s subject, prominent thought in phenomenological psychiatry is merged with artistic representation. Through this coalition the conceptual experience of psychosis is visually depicted, as well as using the opportunity to reflect upon personal experience in psychotherapy.

Ultimately the process of exploring the self, introspection, research into mental health, and indeed the scientific process requires some degree of solipsism. To progress and generate new ideas we must, even if fleetingly, fuse our internal and external world in moments of clear, and sometimes chaotic reflection to move laterally between trails of thought. This can be a tumultuous process, even if we’re just going by reflections from researchers in their PhD training, and in the best cases leads to new understanding about the boundaries of the self and our potential as human beings – both for clarity and chaos.

I hope this piece to not just be a conceptual fusion of subject/object when our experience of self can be compromised, but also a disintegration of the boundary between those with psychosis and those without – recognising that there is a common humanity in us all. I hope this is a process of developing compassion for those who cannot escape themselves alone – for whom the experience becomes a black hole without any ground of being to fall back on.

 References

Humpston, C. S. (2017). The paradoxical self: Awareness, solipsism and first-rank symptoms in schizophrenia. Philosophical Psychology, 1-22.

Nelson, B., Fornito, A., Harrison, B. J., Yücel, M., Sass, L. A., Yung, A. R., … & McGorry, P. D. (2009). A disturbed sense of self in the psychosis prodrome: linking phenomenology and neurobiology. Neuroscience & Biobehavioral Reviews, 33(6), 807-817.

Nelson, B., Parnas, J., & Sass, L. A. (2014). Disturbance of minimal self (ipseity) in schizophrenia: clarification and current status.

Parnas, J., & Sass, L. A. (2001). Self, solipsism, and schizophrenic delusions. Philosophy, Psychiatry, & Psychology, 8(2), 101-120.

Beyond Expectation – review of “Beyond My Control” for The Psychologist

URL: https://thepsychologist.bps.org.uk/volume-31/march-2018/beyond-expectations

There seem to be fewer and fewer occasions where subjectivity and neural disorder are married together without causing controversy; thankfully, Beyond My Control is raising the numbers. The public engagement initiative IMPACT – a collaboration between the University of Exeter and Exeter Northcott – communicates in equal measures the science, maths, and complex humanness of experiencing recurrent seizures.

Beyond My Control incorporates improvised acting to demonstrate the intricate relationship of neural networks, and what might happen when a seizure strikes. The show introduces us to a family, the Brains – a dad, mum, daughter, and her boyfriend – as they work their way through plausible social dilemmas. This helps explore what happens when communication goes awry, relating this to excessive synchronous activity in the brain. Not only is this a great analogy, but involving the audience to suggest ways forward for the family to work through an issue is actually pretty therapeutic (and entertaining!).

The main takeaway from the show was the recorded lived experiences of those with epilepsy and their relatives – the embarrassment, guilt, confusion, and sometimes pleasure, that a seizure can bring. This really helps drive home the human behind the diagnosis, and the show makes no bones about making this explicit. Diagnosis is treated as practical and sometimes helpful labelling, but by no means thought to be fully encompassing those labelled with it.

While the show emphasises how complex – socially and psychologically – experiences can be for those with recurrent seizures, no one ever disregards the neural basis of the experience. This non-mutual exclusivity is really something special, which we need to see more often. Too frequently there appears to be a split between those who want to treat neural syndromes as a biological or psychological and social phenomena, and Beyond My Control shows that is can be all three at once: saying someone has a brain disorder does not mean their psychological and social experience is meaningless.

Public engagement is rarely something that is put at the forefront of scientific research – it can be clunky and underinvested. Beyond My Control goes above what is often expected from a science and art collaboration – more like this please.

What are psychedelics actually doing? Some thoughts about future research challenges.

A fascinating recent article posted in Science Reports drew a lot of attention over the evidence that a higher state of consciousness had now been captured on MEG through the use of psychedelics.

The team on the paper – a collaboration between researchers at Sussex, Imperial, and Auckland – collected Magnetoencephalography (MEG) data from participants using Ketamine, LSD, and Psilocybin, and aimed to take a look at how a change in spontaneous signal diversity corresponded with the psychedelic subjective experience.

The essential conclusion was that Psilocybin, Ketamine, and LSD reflect an opposite pattern of neural diversity to anesthetics, such as propofol, and a greater level of spontaneous neural activity in comparison to normal waking consciousness – such as you’re using to read this – and so this might be called a more ‘signal rich’ mode of perceiving your conscious experience.

On top of being pretty novel in terms of its findings, the paper was a genuinely interesting way of looking at neural data, and works toward trying to pair phenomenological experience to brain activity in aid of understanding how our underlying perceptual machinery can produce such a strange experience – especially as consciousness has typically been studied through the loss of experience (such as anesthesia), and not often, if at all, through the increased complexity of experience compared to our every-day perceptions.

This paper has definitely got me thinking about the complex role of our brain to filter and define our incoming information moment to moment so that we can perform day-to-day tasks we take for granted, and how changes to this filtering might give us some fascinating insight into what’s actually going on under the hood.

It might also represent a different mode of signal detection, where otherwise ‘silent’ experiences and perceptions which would be otherwise ignored are now pushed up into our subjective platform.

Cognitive Neuropsychiatry takes a similar approach to this paper by studying the neural activity of individuals who have a very different experience of the world – such as in delusions – and using these findings to give us a clue as to the dynamics of related neural function e.g. belief formation.

This study adds to the field by demonstrating that instead of using individuals with a mental illness or neurological difficulty to peek behind the veil, we might be able to use psychedelics to transiently produce very different modes of subjectivity. This has huge potential, and I look forward to seeing where it progresses.


Image result for MEG machine

Magnetoencephalography (MEG) records the firing rhythms of the cortex. These different frequencies are given names like theta, delta, and alpha.
Image taken from MIT News

 

However – I do have some thoughts about challenges the field might face moving forward and some healthy criticism of the data – I hope this only helps to develop our interpretations.

Essentially, I think we need to be careful with getting carried away with the term ‘higher consciousness’ at this point, especially when trying to be true to the data, and the authors do indeed mention that the use of the phrase ‘higher state of consciousness’ is to be cautiously interpreted.

I see this as an issue on two related fronts.

First, as with anything, the media like to make a lot of hype around this finding, and it can be useful to be honest about some of the assumptions that we might attribute to what is actually being said.

For instance – when we hear the word ‘higher’, we might immediately associate this with being synonymous with ‘better’, or even more exotically, ‘enlightened’, as the suggestive image heading this blog post might portray.

But this is a tricky situation, as this plays into some potential assumptions about the quality of our conscious experience, for example, the idea that we need to somehow escape our ‘regular’ or everyday state of mind.

We could equally interpret our brain in its everyday state as an optimal and balanced organ working to reduce incoming information into digestible and manageable pieces which can be used to navigate the environment – much like that theorised in a new paper here.

Now, this isn’t to say that having interesting and rich experiences outside of our every-day can give us a whole new perspective on ourselves and insight into our malleable perceptions, or even that our ‘everyday’ mind can always be a good thing (e.g. outdated beliefs or overbearing self-criticism), but I fear associating this increased ‘free energy’ form with a more desirable function to be can lead to a ‘grass is greener’ type situation which ultimately gives our more everyday, and perhaps more mundane, experiences lesser value. But we need to remember that it’s these more typical experiences that give us the ability to do all the small things we take for granted (cue Blink 182).

Now I might be jumping the gun a little here as to how far most might take the idea of a ‘higher’ consciousness, or even over exaggerating the interpretations, but I think keeping on top of our exoticism over the experience can mean we don’t fetishise it and instead try to fully understand what this altered state actually is doing, and what this might mean for our understanding of the mind.

This leads into my next point, which is that the over exposure of the media may actually begin to bias the subjective experiences of future participants, and may greater amplify the placebo effect.

Neuroskeptic recently wrote an article addressing this issue with the recent APA consensus statement around the medicinal use of ketamine for depression.

Because of psychedelic research permeating most news outlets with tales of fascinating and powerful subjective experiences, we may all now be automatically biased toward what we expect from taking something like LSD.

Future experimentation aiming to further understand the correlation between subjective experience and symptom reduction will possibly find it increasingly harder to parse out expectation and the placebo effect from ‘drug related’ causal effects.

This isn’t to undermine the placebo experience as a useful and effective therapeutic tool, but if we are to get to the bottom of the causal neural mechanisms surrounding the use of psychedelics, massive expectations only work to muddy these results.

Questions might be being raised at this point between what we might consider ‘causal’ mechanisms, and whether we should make a distinction between ‘non-placebo’ neural changes as a hallmark of ‘genuine’ change as this might start bringing up a lot of false separations between our brain and subjective states, as each are one in the same, and doing so undermines the powerful effect of environment, social dynamics, and community belief.

My main question here is: is it the drug that is doing the driving of the experience, or is our expectation and our submission to the ritual process of taking it? If it’s the former, then it matters which drug we are administering, if its the latter, then psychedelics may not be as special as is often touted.

Of course, as with anything, it’s probably a mix of the two. However, if prior belief and expectation are found in future research to play a massive role in the changes in symptom changes, taking psychedelics in a modern medicinal setting with guidance may be conceptually on par with rituals we might not consider relevant in modernity anymore, like the Catholic mass or Sufi twirling – this is simply our modern take with lots of perceptual fireworks.

This might be quite a humbling piece of information, and serve to illustrate a) how powerful community consensus can be for therapeutic means, and b) how much we have in common with our previous generations.

Tyler-Perry-TD-Jakes

This might appear antiquated to modern day 20- somethings, but is the key to a powerful psychological change belief, subjective prowess, and communal agreement?

 

My final point I hope illustrates my previous two, and it’s regarding the data presented in this study when looking deeper at the association made in the paper between the use of all three psychedelics, their effect of increased cortical signal complexity, and a large change in subjective experience.

Authors use a mathematical algorithm to analyse the MEG data called the ‘Lempel-Ziv complexity‘. This algorithm is essentially telling us how ‘random’ the neural signal generated from the brain is across 90 different sites – the assumption here is that the larger the value, the more complex, chaotic or ‘entropic’ the cortex is at that particular time – this is what the authors’ call a ‘richer’ or ‘higher state’ of consciousness because less filtering of our sensory experience is theorised to be occurring, and this is therefore suggested to accompany a vast change in subjective experience, such as the onset of hallucinations, ego-dissolution, and distortions in time and space.


Increased spontaneous signal diversity for PSIL, KET and LSD.
Figure 2(a) Mean scores across participants for the signal diversity measures LZsN, LZcN and ACEN are higher for each of the three drug conditions (white discs) than for the corresponding placebo conditions (black discs). A solid line across conditions indicates p < 0.001 and a dotted line 0.001 < p < 0.05, uncorrected, obtained from a two-sided t-test. (b) Difference in single channel Lempel-Ziv complexity, LZsN, between respectively PSIL, KET, LSD and placebo at the single participant level. The error bars indicate standard error across trials.
Image taken from : Schartner, M. M. et al. Increased spontaneous MEG signal diversity for psychoactive doses of ketamine, LSD and psilocybin. Sci. Rep. 7, 46421; doi: 10.1038/srep46421 (2017).

 

The above figure shows the difference in neural communication complexity using the algorithm I mentioned before. Notice that LSD and Ketamine both demonstrate significant differences between the drug condition (white discs under ‘a)’) and placebo condition (black discs under ‘a)’), but psilocybin doesn’t at all. This insignificance is compounded by the fact that individuals were actually scanned during their peak when you would expect the largest changes to be occurring.

This would suggest that for ketamine and LSD, changes in neural activity using this algorithm may reflect vastly different subjective experiences if we find a significant difference in participants phenomenological reports using the same drugs.

This would support the argument that the different compounds are having a different and meaningful neural impact.


Correlations across measures and questionnaire answers.

Figure 4

(a) For each drug, a matrix indicates in colour the Pearson correlation, r, of the score difference between drug and placebo condition (averaged across trials) of each measure pair across participants. The upper triangular entries and entries with |r| < 0.5 are omitted (and set white) to highlight strong correlations only. These correlations should be considered somewhat exploratory and are not controlled for multiple comparisons as each experiment had a limited sample size. Across drugs, signal diversity measures show high correlation with each other, yet inconsistently, as they capture different flavours of signal diversity. (b) Correlations between the changes in the measures ACEN, LZcN and LZsN and the questionnaire scores (same scale as above). No consistent correlation across drugs was found for any combination of the measure’s scores and scores for a particular question. (c) The changes in subjective ratings under each drug condition are shown as averages with standard error bars across subjects. The average of all changes across these 14 questions (except “InScanner”) is denoted as “total” and shown normalised by factor 20 in order to fit the scale. No consistent differences are apparent across drugs.
Image taken from : Schartner, M. M. et al. Increased spontaneous MEG signal diversity for psychoactive doses of ketamine, LSD and psilocybin. Sci. Rep. 7, 46421; doi: 10.1038/srep46421 (2017).

 

While all drugs showed an increase in signal diversity after drug administration, this hasn’t been established with significance at all for all drugs.

Now, the above figure suggests that psilocybin has the greatest total change in subjective experience compared to LSD and Ketamine, especially on experiences of seeing strange shapes, geometric patterns, and having vivid mental experiences.

As there was no significant difference between using psilocybin and placebo in terms of signal diversity, the fact that psilocybin expressed the greatest difference in subjective experience leaves me with alot of questions.

There still seems to be many questions regarding whether different compounds produce markedly different subjective experiences, and how this relates to symptoms reduction and neural activity.

The study however takes great steps to get the ball rolling in answering this question, and I look forward to seeing how these results develop, with different analyses, replications, and richer phenomenological reports being drawn upon to test these different hypotheses.