Critique of "A Critical Appraisal of a BPS Model and Shifting the Paradigm" (Podcast)

Hi,

I recently listened to parts 1 and 2 of “A Critical Appraisal of a BPS Model and Shifting the Paradigm with Michael Ray” on the Level Up podcast, and read the accompanying articles— Quinter and Cohen’s “Pain Medicine and Its Models: Helping or Hindering?” and Engle’s “The Need for a New Medical Model: A Challenge for Biomedicine”. In the podcast, it was discussed how the transition from the biomedicine to the biopsychosocial model represented a shift to a model that was “less wrong”. However, it was noted that the biopsychosocial model still has its limitations—perhaps pain should be treated as an “aporia” unique to each individual, as suggested by Quinter & Cohen. I have a couple counterarguments to transitioning the paradigm of pain to an “aporia” model that I was hoping I could hear your thoughts on, @Michael_Ray .

Introduction
Our current way of reasoning in medicine involves using the scientific method, which involves making hypotheses that must be falsifiable. For something to be falsifiable, it must be able to be measured. Pain as an “aporia” in medicine is neither 1) falsifiable nor 2) able to be measured, and, as such, perhaps the paradigm should not be shifted.

Counterargument #1: Pain as an “aporia” and the principle of “self-referential systems” are not falsifiable
In “Pain Medicine and Its Models”, the authors argue that the biomedical model is too reductionist, and that the switch from biomedical to BPS was better, but even BPS is too reductionist. To them, pain constitutes a unique individual experience that we cannot measure due to the nature of humans as self-referential systems. As they note in their paper:

The epistemological and ontological constraints of the aporia that is pain are underpinned by our inability to access the secrets of the self-referential brain and by our difficulty in using our languaging systems to express such complex phenomena.

This is somewhat of a catch-22. The backbone of the scientific method involves collecting data and performing experiments. If we are unable to access and measure the “secrets of the self-referential brain” and collect empirical data, then it cannot be falsifiable. As such, this “aporia” they are proposing is incompatible with the scientific method.

Furthermore, the authors attribute the “aporia” of pain due to humans as “self-referential systems”. Specifically, the authors defined self-referential systems as having three qualities: autopoiesis (capable of regenerating inner components), noncentrality (decentralized structure), and negentropy (energy input into the system does not equal its output). The problem with this definition of self-referential systems is that these are not falsifiable statements, and, as such, are not valid hypotheses. For a statement to be falsifiable (and thus be a valid hypothesis to be used in the scientific method) it must be testable. Yet these tenants of self-referential system cannot be tested—i.e. we cannot just go around and try and change the properties of basic human biology to try and violate or confirm those properties. As such, these statements are also not compatible with the scientific method.

Lastly, Quinter & Cohen’s close the piece with a suggestion that we need to pay attention to language to describe the phenomenon of the “aporia” of pain:

We need to play close attention not only to the new language that is used to cope with this expansion of our neurophenomenal world, but also to the lack of language that is currently available to cope with this new phenomenal context…this article is a call to move forward to explore the engagement of self-referential beings through the creative frame of language, in which the narrative of neither the clinician nor the patient is dominant but the way they touch and grow in understanding, empathy, and shared outcomes is paramount

The paradox here is that this “phenomenon [of the aporia of pain]”cannot be directly proven via the scientific method as stated earlier. As such, why should one pay special attention towards language in the context of “pain as an aporia” when the idea of “pain as an aporia” is not able to be proven? This is an inherent contradiction of Quinter & Cohen’s call for action.

Counterargument #2: Models cannot be compared if they are unable to be measured
In Engle’s 1977 work, he notes a critique of the reductionist biomedical model:

In the biomedical model, demonstration of the specific biochemical deviation is generally regarded as a specific diagnostic criterion for the disease. Yet in terms of the human experience of illness, laboratory documentation may only indicate disease potential, not the actuality of the disease at the time. The abnormality may be present, yet the patient not be ill. Thus the presence of the biochemical defect of diabetes or schizophrenia at best defines a necessary but not a sufficient condition for the occurrence of the human experience of the disease, the illness.

A biomedicist may counterargue with the following: if someone has pain or disease and “perturbations” aren’t being detected at the biomedical level, it may not be because the perturbations aren’t there but rather because we haven’t discovered them yet or don’t have the equipment to measure them yet. Essentially, it is a question of whether there is more to be discovered in the current biomedical model of thinking, or if it requires a switch in our thinking to a “less wrong” model altogether. And how could one answer this question with some certainty? By trying new mental models, running experiments, and comparing the results, we can test if different models of thinking are better than each other. For instance, in schizophrenia the switch from a biochemical to biopsychosocial thinking has been able to occur because we are able to measure the “psychosocial” part of the equation—i.e. the patients support system, family trauma, cognition in terms of thought patterns and mindsets, etc—and compare the two models. We have noticed that treating schizophrenia in a biopsychosocial perspective has yielded a “less wrong” view of it. Yet, if the different model of thinking that is being proposed cannot be measured—i.e. pain as an “aporia”—than it cannot be tested and thus cannot be falsified and is incompatible with the scientific method.

Final Thoughts
Proposing new models of thinking in medicine that are abstract and cannot be measured, such as pain as an “aporia”, is not compatible with the scientific method due to the fact that things that cannot be measured cannot be falsified. This means that we need to:

a) stick with current models of thinking since they can be measured and thus are compatible with the scientific method.
b) figure out how to measure new models of thinking so they can be compatible with the scientific method (which becomes harder the more abstract a model is, e.g. an “aporia” model of pain).
c) scrap the scientific method altogether.

A) is the easiest thing to do; B) and C) are hard sells. Thus, I am not sure transitioning to a model of pain as an “aporia” is the right thing to do.

Is a model a hypothesis such that one might expect it to be falsifiable?

It seems to me a model, especially in an applied science, is understood to be a simplification of a complex phenomenon for the purpose of guiding research and in the case of medicine treatment.

The question of whether one model produces more useful results, in this case better treatments, is one that can be addressed with the scientific rigor you desire.

I did just skim your post so sorry if I have misunderstood you.

1 Like

Hey @doxycycline - thanks for the post and for taking the time to read and ponder the articles as well as listen to the podcast. By nature a podcast is a bit limiting in our ability to fully encompass an individual’s thoughts on a topic as the audience losing attention span is a concern of ours.

I can say that much of your counter points appear hinged to the idea of pain as an aporia, also known as quala, and not the BPS model proposed by Engel. To help with this issue I can say I no longer believe pain is an aporia or quala, one of the reasons being related to the social constructs of learning about pain as a word attached to an experience, but I believe a forum will inevitably limit my ability to adequately convey why I’ve changed my mind on this stance simply due to the inherent need to write multiple pages on this topic.

Broadly speaking, this discussion will likely lead to epistemology or “how do we know what we think we know”. indeed science as a method is inclusive of falsifiability, but there is more to this discussion of science as a method and what science can and cannot tell us about the world as well as hierarchy of evidence. There are hints of scientism ongoing here that should be brought to the discussion. As it relates to the human pain experience, phenomenology is one method attempting to overcome the limitations of understanding the human experience of pain addressed in the clinical setting. You would likely enjoy Hartman and Stilwell’s article here but this will inevitably lead to a larger rabbit hole within the philosophical and cognitive science realm: https://link.springer.com/article/10…97-019-09624-7

Additionally, I sense a strong anchor to science as a method equating to quantitative research and not inclusive of qualitative. I think this approach tends to make sense when we are discussing interventions and treatment efficacy vs effectiveness to try and control for the flaws of unsystematic observations and subsequent decision making from the individual level - hence the championing of evidence based medicine that’s been ongoing since the early 90s. However, the major flaw here within the lens of biomedicine is the belief that symptoms are only driven by an underlying biological/physiological problem necessitating an intervention to fix the “problem”. Engel’s premise for proposing the BPS model was the desire to expand beyond just merely biology for viewing the patient and their lived experiences, this wasn’t isolated to just pain. There is an epistemological rationale to Engel’s proposal that can be read about here: https://www.researchgate.net/publica…nical_Practice

In essence, he wished us to overcome the over objectification of the physical human body and our incessant attempts to gain access to their body instead realizing we are helping humans not just tissue.This isn’t to say we cease such attempts in all scenarios but rather we expand our search beyond diving deeper and deeper into the physical body - we’ve seen the detriment of such attempts in the context of low back pain (See Lutz 2003). I have little doubt we will cease trying to objectify the physical body and this is certainly one avenue of questioning that will likely lead to some new information but that information must then be weighted and considered in the context of human experience…we will, dare I say always, be generalizing scientific findings to the individual in the clinical setting. It should also be stated that although Engel’s proposals were ground breaking within the medical community, they were far from novel. Philosophy has been pondering these questions prior to Engel’s proposals. Regarding the human experience of pain, Stilwell makes a great case for expanding beyond BPS with a 5E approach outlined in the paper linked above.

I appreciate the discussion.

Hey @Michael_Ray ,

Thanks for the well thought out, detailed response. You’re awesome, and I apologize for my slow response.

I did enjoy Hartman and Stilwell’s article, and it did lead me down to a larger rabbit hole within the philosophical and cognitive realm, so thank you for that ;)[IMG2=JSON]{“data-align”:“none”,“data-size”:“full”,“src”:“https://forum.barbellmedicine.com/core/image/gif;base64,R0lGODlhAQABAPABAP///wAAACH5BAEKAAAALAAAAAABAAEAAAICRAEAOw==”}[/IMG2]​ The epistemological piece was quite interesting too; I never really though much about the premise that many clinicians operate from of trying to separate the pathological body from the person and trying to treat “just the body”.

I know you guys recommend the “Explain Pain” book by Moseley and Butler. Some of the ideas in Hartman and Stilwell’s paper seem to contradict the ideas presented in the book. In the paper, the following was noted:

Some have challenged the notion that pain is in the brain, arguing that pain is emergent and that the brain is necessary, but not sufficient for pain (Thacker 2015). If this view of pain is correct (the perspective taken in this paper) then its properties cannot be explained or produced only by the brain. As Manzotti explained…“there is no definitive proof that neural activity is sufficient to generate pain. In all known cases, neural structures are involved, but so are bodies, the environment, stimuli, tissue damage, past and future behavior, and social interactions. We have no reason to discard all of that in favor of the neural underpinnings alone” (Manzotti 2016, p. 2).

and later on:

Further, when we look closely, biopsychosocial proponents take a brain-centric approach and suggest that pain is ultimately in the brain (Moseley and Butler 2017).

This sentence above is essentially what is stated in the Explain Pain book:

We believe that all pain experiences are normal and are an excellent, though unpleasant, response to what your brain judges to be a threatening situation. We believe that even if problems do exist in your joints, muscles, ligaments, nerves, immune system or anywhere else, it won’t hurt you if your brain thinks you are not in danger (pg.1, first edition).

My understanding is that BBM views pain as all components (bio, psycho, social) contributing, but that the relative proportions change depending on the person (basically that graphic you posted on your instagram story titled “Sliding Scale of Pain Emergence”. BTW, big fan of your instagram, keep it up :)). How do you reconcile this “sliding scale” view with Moseley’s “brain centric” view–aren’t these contrasting views?

I’m not sure how you could remove the brain from the system to test whether it is necessary to experience pain. Phantom limb pain may be an example of “brain-only” pain, however, where the tissues experienced as in pain are verifiably absent (Of course there is a whole proximal network intact). The rubber hand illusion may be another example. These both rely on social cues, memory, etc, but surely there are neural correlates for those things.

My view is that pain is an output of the brain, and that the biopsychosocial factors are the inputs. I don’t know where that puts me in the brain-centric vs BPS vs other spectrum of pain theory.

Thanks for the questions. Glad the discussion and those papers were helpful.

I have not actually read Explain Pain. I have read many citations put out by Moseley and his group. With that said, I have some complaints with NOI/Moseley messaging or what folks may be misinterpreting from their messaging. I do feel as though their prior messaging was far too neurocentric and further committing overly reductionist missteps by citing pain is “an output of the brain”. To Moseley’s credit, he has started backpedaling on this messaging. I’m presenting at this year’s Virtual San Diego Pain Summit and am going to do my best to articulate my current stance on the human pain experience, our models for examining the experience, and how this effects clinical practice…no promises.

“We believe that all pain experiences are normal and are an excellent, though unpleasant, response to what your brain judges to be a threatening situation. We believe that even if problems do exist in your joints, muscles, ligaments, nerves, immune system or anywhere else, it won’t hurt you if your brain thinks you are not in danger (pg.1, first edition).” This is obviously out of context given it’s an excerpt from a book I’ve not read but I would disagree with much of this statement. Perhaps a pain experience is related to threat some of the time and perhaps not, similarly to danger. Admittedly, my complete response would necessitate a great deal of explanation. I can say I wouldn’t currently cite the scale you are referencing for fear of trichotomizing the BPS framework. Overall, neurology is involved in our experiences, but this is not the entire story. We are not brains in vats. Unfortunately I think the best I can do for now is leave more citations:

On the relation of injury to pain the John J. Bonica Lecture
Beecher 1946
Carlen 1978
Melzack 1982
Pain in language: From sentience to sapience
Pains and Pain Sensations
Why Pains are Not Mental Objects