he theory specifies two functionally distinct branches of the vagus, or tenth cranial nerve. The branches of the vagal nerve serve different evolutionary stress responses in mammals: the more primitive branch elicits immobilization behaviors

Dear Wejdan, it seems we agree on one of the major message of the polyvagal theory. In this project where I asked this question (https://www.researchgate.net/project/Examining-Porges-polyvagal-suppositions?_esc=topicPostRelatedProject), Paul Grossmann initiated a dialogue on the current results in connection with the theory. If you find papers that shed light on the relationship between social engagement and the neovagus and the respiratory sinus arrhytmia, please share. 

Bests,

Benedek

Dear  Wejdan and Benedek, 

To the best of my understanding of the evolutionary biology of the autonomic nervous system, it is a mistake to say that one of these brainstem centers (i.e. the dorsal motor nucleus, DMN) is more primitive.  Different fish and reptile species have evolved different areas of  brainstem centers of parasympathetic control, some more dorsal (precursors of the  mammalian DMN), some more ventral (precursors of the nucleus Ambiguus) that innervate heart rate.  That is the take-home message of a major section of  my  2007 paper ( available over ResearchGate) with E.W. Taylor, certainly acknowledged in biology as one of the very top,experts in the evolution of parasympathetic control. Porges is a psychologist and psychophysiologist, not an evolutionary expert. He has misinterpreted the evidence, This seems utterly clear to Taylor, Tobias Wang (another prominent evolutionary biologist) and other evolutionary experts I have discussed the matter with over the last 12 years; no one in that field has expressed to me a position in fundamental support of Porges' hypothesis here.  Because these Polyvagal speculations are so far afield of their own discipline, they have not directly addressed this issue in a major piece, other than our 2007 paper, but a reading of any of their review papers will completely substantiate what I am writing here.  And Porges has  not dealt with these apparent facts in his recent book or other writings. So the universe of polyvagal ideas and the universe of evolutionary EVIDENCE seem to be operating almost completely independently of each other.  

  By the way the 2007 paper seems to refute the polyvagal premises in a number of additional ways, as well.

thanks for the very helpful Information. As body psychotherapist I of course face this.

Literally no direct evidence is available, but there is a great deal of evidence against all 3 primary first premises of the polyvagal suppositions. Various evidences in contradiction to Premise 1 provided earlier in my own project  and question comments on ResearchGate.

Clear evidence that premise 2 and 3 of the Polyvagal suppositions, stated by SW Porges, are incorrect according to evolutionary biological data of the last two decades:

http://pubmedcentralcanada.ca/pmcc/articles/PMC1626384/pdf/rsbl20050365.pdf

P 486: "These data from fish can be compared with data from other non-mammalian vertebrates. Recent experiments demonstrated increases in heart rate and pulmonary blood flow during bouts of fictive breathing in decerebrate, paralysed and ventilated toads (Wang et al. 1999) and, in conscious Xenopus, denervation of pulmonary stretch receptors did not abolish the increase in heart rate associated with lung inflation (Evans & Shelton 1984). Both results indicate central control of cardio-respiratory interactions. In reptiles, complete vagotomy in the rattlesnake caused heart rate to rise and abolished a respiration-related variability. The breathing rhythm slowed, accompanied by large lung volumes (Wang et al. 2001). These data can be interpreted as loss of vagal tone on the heart, which seems to be responsible for HRV as well as setting the overall fH, plus denervation of lung stretch receptors. Recent experimentation that used power spectral analysis of HRV in the rattle-snake revealed clear respiration-related components, that can be characterized as RSA (Campbell et al., unpublished data). We therefore reject the hypothesis that centrally controlled cardio-respiratory coupling is restricted to mammals, as propounded by the poly-vagal theory of Porges (1995)."

https://www.researchgate.net/profile/Hamish_Campbell2/publication/6976184_Evidence_for_a_respiratory_component_similar_to_mammalian_respiratory_sinus_arrhythmia_in_the_heart_rate_variability_signal_from_the_rattlesnake_Crotalus_durissus_terrificus/links/5457ff570cf2bccc49111add/Evidence-for-a-respiratory-component-similar-to-mammalian-respiratory-sinus-arrhythmia-in-the-heart-rate-variability-signal-from-the-rattlesnake-Crotalus-durissus-terrificus.pdf

P 2635: "Few studies exist documenting the use of power spectral analysis on the fH of reptiles and, in contrast to this study, these authors report no association of the spectral component in fH with ventilation (Gonzalez and De Vera, 1988; Porges et al., 2003). This has led to the conclusion that RSA does not exist in non-mammalian vertebrates, and forms the basis of the polyvagal theory (Porges, 2003). However, recent observations in fish showed that small quantitative differences between fH and fV can lead to erroneous spectral components when undertaking PSA (Campbell et al., 2006). This occurs because in calculating power spectra from fH, it is the time differences in the consecutive heart-beat intervals that are used to measure the underlying (possibly ventilation-induced) oscillations. Consequently, the Nyquist criterion states that ‘a continuous analogue signal can only be accurately identified if it is sampled at least twice the highest frequency contained within the signal' (Denbeigh, 1998). In the lizards Galloti galloti (Gonzalez and De Vera, 1988) and G. major (Porges et al., 2003), fH was not twice that of fV, and therefore in calculating PSA the Nyquist limit was exceeded, and conclusions relating to the presence or absence of ventilatory components within the fH cannot be made. In the rattlesnakes, fH was three to four times greater than fV, and the spectral peak at the frequency of ventilation can be observed......

For decades it has been known that in reptiles vagal activity progressively decreases as fH increases with the onset of lung ventilation (White and Ross, 1966; Pough, 1969; Burggren, 1972; Shelton and Burggren, 1976; Burggren, 1972). We show here, using modern technologies and mathematical techniques, that in the rattlesnake C. durissus, oscillations in heart beat interval are in fact in synchrony with ventilation, and the fV-induced oscillations in fH appear as components in the power spectrum. This is similar to the situation in respiratory sinus arrhythmia (RSA) in mammals (Akselrod et al., 1981). Additionally, whereas previous investigations have hypothesised that activity occurs between the respiratory and cardiac centres of the medulla, this study has identified a dual location for VPN in the rattlesnake, and we propose that there is likely to be a causal relationship between this and RSA. This data refutes the proposition that centrally controlled cardio-respiratory coupling is restricted to mammals, as propounded by the polyvagal theory of Porges (Porges, 1995; Porges, 2003)."

http://www.scielo.br/scielo.php?pid=S0100-879X2010000700001&script=sci_arttext&tlng=pt

P 607: "Wang et al. (23) showed that there are slight changes in fH related to lung ventilation in snakes but it is uncertain if these components formed distinct oscillations in fH at the frequency of fR, and therefore could be categorized as RSA. On the basis of power spectral analysis of heart rate, there was no spectral component of the heart rate signal with ventilation in a small lizard Galloti galloti (55). However, the use of fH dataloggers for long-term monitoring in undisturbed rattlesnakes (22) enabled us to determine HRV in settled, recovered animals when sympathetic tonus was low and vagal tonus high. These animals showed oscillatory components in the HRV signal at the frequency of ventilation that were abolished by injection of atropine. Results from this study agreed in part with Gonzalez and De Vera (55), in that two peaks were detected in the fH spectra of the rattlesnake. However, the frequency and amplitude of these peaks was relative to fH, with high fH favoring the lower frequency peaks and low fH the high frequency peaks. The high frequency peaks that were removed by the cholinergic blocker atropine occurred at the frequency of the respiratory cycle. The respiratory cycle of rattlesnakes consists of a prolonged inspiration followed by a relatively short expiration. Heart rate slowed upon expiration and increased during inspiration, which is similar to the changes in heart rate observed in conscious unrestrained mammals and characterized as RSA (16). Thus, this study contrasts with that of Gonzalez and De Vera (55), as we were able to present clear evidence for respiratory modulation of heart rate that closely resembled that recorded from mammals and accordingly may be classed as RSA. Accordingly, the previous data refute the proposition that centrally controlled cardiorespiratory coupling is restricted to mammals, as propounded by the polyvagal theory of Porges (19)."

http://www.repositorio.unifesp.br/bitstream/handle/11600/3746 /WOS000332041600015.pdf?sequence=1

P 692: "It has been suggested that beat-to-beat modulation of fH that generates RSA is necessarily restricted to mammals that have the discrete population of CVPNs in the NA that possess fast conducting, myelinated efferent nerve fibres. This is the basis for the ‘polyvagal theory' propounded by Porges (Porges, 1995). However, the exclusivity of this mechanism has been contested by Grossman and Taylor (Grossman and Taylor, 2007). Many aspects of the brain circuitry of the mammalian system seem to have been highly conserved throughout evolution. Thus the cardio-regulatory mechanisms that operate in the CNS of elasmobranch fishes show a remarkable degree of homology with those that operate in mammals, including humans (Taylor, 1989). This consideration underpins our comparative survey of the other vertebrate groups, considered in turn from fish, through amphibians and reptiles to birds, in relation to the more thorough understanding of the mammalian pattern. The treatment of each group is necessarily uneven because of the limitations on our knowledge and it must be emphasized here that, unlike mammals and birds, the so-called ‘lower vertebrate' groups have a complex phylogeny; that is to say that fish, amphibian or reptile is an umbrella term describing very diverse groups of animals, some relatively little studied....."

Also Taylor, E. W., et al. "Coupling of the respiratory rhythm in fish with activity in hypobranchial nerves and with heartbeat." Physiological and biochemical zoology: PBZ 79.6 (2006): 1000-1009.

The “polyvagal theory” has suggested that the beat-to-beat control of fH that generates RSA is restricted to mammals, whichhave evolved myelinated vagal pathways that originate in the NA (nucleus Ambiguus; Porges 2003; Porges et al. 2003). However, CRS [cardiorespiratory synchrony] has been reported in both resting dogfish (Taylor 1992) and hypoxic trout (Randall and Smith 1967), and both species have CVPN [cardiac vagal preganglionic neurons] located both in the dorsal motor nucleus of the vagus (DVN) and in a ventrolateral location outside the DVN that may constitute a primitive NA (Taylor 1992).

BASIC PREMISES RECENTLY STATED BY SW PORGES:

Premise 1: Neurogenic bradycardia and RSA are mediated by different branches of the vagus and need not respond in concert.

Premise 2: Neurogenic bradycardia associated with orienting is a phylogenetic vestigial relic of the reptilian brain and is mediated by the dorsal motor nucleus (DMNX).

Premise 3: Withdrawal of cardiac vagal tone through Nucleus Ambiguus (NA) mechanisms is a mammalian adaptation to select novelty in the environment while coping with the need to maintain metabolic output and continuous social communication.

(From Porges SW (2013) Polvagal Theory. NY: Norton)

Article Evidence for a respiratory component, similar to mammalian r...

Dear Paul, I was excited to read your answer, thank you!

So, the polyvagal premise "Dorsal motor nucleus of vagus (DMNX) is more ancient/primitive than the nucleus ambiguus (NA), and respiratory sinus arrhythmia (RSA) appeared only in mammals"  is FALSE, NA and RSA are also apparent in fish.The terms neovagus should be avoided, since it is not newer than the vagal branches coming from DMNX.

Questions:

1.) is it still true, that stress responses are built upon each other evolutionarily in the following order, and are activated in humans in the opposite order due to Jackson's dissolution:

• immobilization
• flight-or-fight
• tend-and-befriend?

The polyvagal theory is the first and only to state this?

2) Do you know a good review on how these stress responses are reflected in physiology, e.g. the connection between RSA, emotions and social engagement? If yes, through which mechanisms and purposes the RSA reflects these higher-order mental processes?

I see that Beauchaine made extensive research and reviewing activity on this topic (2001, 2012 e.g.), showing that higher basal RSA and smaller RSA suppression in demanding situations are linked to emotional stability, emotion regulation, and mental health. But is there a psychoneurological model that explains this connection?

Dear Benedek,

With regards to your second question, you may find this research topic of interest:

https://www.frontiersin.org/research-topics/4767/cant-get-you-out-of-my-head-brain-body-interactions-in-perseverative-cognition

Benedek T. Tihanyi

You ASK some good questions and some I think are immaterial.

Even if there is evidence to say which response is more evolutionarily primative versus "advanced," what does that tell us that we do not already know?

More intelligent creatures (and sometimes people) demonstrate more complex adaptations to stress. The fact that human physical violence is associated with low IQ is indisputable, but does not prevent people with higher intelligence from reaching down, atavistically, and behaving like barbarians.---Evidence "ANTIFA," the Nazis, and the brutal regimes of North Korea and Happy Face China, not to mention Pol Pot, Burma, etc.

Early life (and some would say particularly intense) stress can exert a "wiring" effect due to the neuroplasticy of the juvenile nervous system and brain. The latter's threat and reward circuitry is apparently easy to disrupt and reprogram --- evidence addictions --- through learning, experience, conditioning and the like.

When one considers the amount of perpetual, redundant cyclicity in human behavior (and human life), addiction-compulsion seem to reign supreme and control vast regions of the regulatory brain.

Human beings are necessarily addicted to life because that is what it takes to survive and thrive. Now, as we live lives disconnected from our original neurological life-programming (and wiring), we are "free" to be adicted to non-essential things. That is, the addictive circuitry has open / unused synapses that are just waiting to become connected to something. Arguably, just about anything when you look at all of the crazy things people are into these days.

You asked for an article / model. If there is one, it will inevitably be like climate models --- useful only for claiming knowledge of (and research funding to propound) that which is too complex to model.

https://www.researchgate.net/requests/r59663137

I can appreciate the challenge that is for science to explain the complexity of human experience phenomena. And while science figures out the preferred labels and categories, I submit to consideration the experience of the therapists and clients, like myself, who have and continue to experience permanent resolution of trauma within the polyvagal therapy and associated models. This was previously thought impossible by science, which condemned patients to a lifetime of treatment and medication and living sub-par lives. Perhaps common sense and humanism might have a place back in science research design after all. Is not that its purpose?

Interesting thread. Thanks everyone for sharing your thoughts.

Dear @bernice gonzales ,

Of course, humanism should remain fundamental. It is wonderful that you have been helped by somatic experiencing or some related therapy. Nevertheless, the therapy, itself, may be of huge benefit, although the physiological explanation of its effects are unfortunately wrong. You benefited from the complex lived experience of the treatments, not the supposed physiological changes that occurred. Experience is much more complicated than cascades of (brainstem) vagal activity (how about all those higher-up midbrain and cortical centers, if you need to remain physiological in your explanation). Actually, Peter Levine was doing somatic experiencing well before he came into contact with the polyvagal speculations and only later retro-fitted his explanation for the therapy‘s mechanisms of action. Terms, such as “dorsal vagal shutdown” to explain dissociation or emotional freezing are, according to the very best (and only) evidence, simply wrong. Furthermore, they also reduce complex human experience to a brainstem reaction. In fact, there is zero evidence that the dorsal motor nucleus is involved at all, and substantial evidence to the contrary. That’s just the way it is. Maybe the vagus is partially involved (almost certainly the centrally located nucleus Ambiguus, not dorsal centers), but it’s a lot more complicated than that. If you require some biological metaphor, then one with more scientific substance will probably do you better and will not be so jarring as a false belief that sooner or later will be acknowledged as wrong (all the evidence is already available, but there are too few serious experts interested in taking the time to evaluate it).

So please believe your experience but, at the very least, leave room for some doubt about what caused your improvement. All the best.

Thank you, Paul. I appreciate your vantage point. Yes, Peter Levine's work is a great example. I am familiar with the pioneering work of Peter Levine, and Pat Ogden in somatic approaches to trauma and I concur with your observation: it is the therapy experience itself what yields the results, and it's not limited by the theory behind it. Although, some degree of intellectual understanding might be part of it in some cases. Personally, I think that open acknowledgement of what we know as well as don't know is an important part of psychoeducation in clinical and academic environments.

Unfortunately, our genuine human need to understand/ explain things may sometimes, and many unfortunately so, lead us to simplistic or reductionist "explanations" for complex human experiences.

I appreciate your expressed understanding of the value in therapeutic experiences.

You also mentioned that "all the evidence is already available." This is a topic I'm interested in, and I'd like to ask, if you could share some of those sources. I would really appreciate it.

I enjoyed reading your thoughtful response.

The HPA Cortisol excess due to stress has slightly more evidence compared to polyvagal theory. Also, stress induced autophagy (cells giving themselves a spring clean) might be a benificial effect of stress, promoting longer and healthier lives. So, what dosn't kill you does do you good (maybe).

I am still looking for the supporting evidence that Grossman mentions but so far have not seen it...is it in Non-English papers?

Gary Groesbeck, Hi Gary, could you please be more specific in what you are looking for. I have attempted to cite, document and reference pretty much all my points, and they all comes from English-language publications. You might want to start with my 2007 paper with EW Taylor (readily accessible in RG or Google Scholar) that already long ago provided rather clear refutations of major assumptions of the polyvagal speculations. However in the various RG questions and projects to which I have contributed there are lots of more clearly cited recent papers and evidence. Hope that helps. However if there is a specific issue, please let me know.

Still perhaps more telling for the polyvagal is that after 5+ years of my questions and project, and more than 60,000 reads combined, there has not been a single piece of evidence from any scientist or reader that provides clear direct evidence regarding any of of the major polyvagal assumptions I contest. Isn’t that curious with the explosion of the polyvagal conjectures?

Hi Paul, thanks for the quick response. As a neurofeedback therapist, we use Polyvagal as an explanatory model, but I was put on notice by a friend and colleague who no longer believes it to be correct and cited your research. I'm just trying to sort this out. I did a quick survey of Google Scholar for the last 4 years. There were over 2600 citations for polyvagal theory and not one, as far as I could tell, dealt with any criticism of the theory. I will review your papers on RG, I could find none on Google other than your 2007 papers. I'm not a researcher so it will take a bit to sort this, as the old saw goes... Absence of evidence is not evidence of absence. Looking forward to your papers. I will search for your name on RG.

Gary Groesbeck , Hi again Gary, I agree the situation is quite remarkable, but there are a number of vagal evolutionary experts that have published clear evidence dismissive of the evolutionary polyvagal assumptions, of course in the biology, not biobhavioral journals (provided in my RG polyvagal questions and project). Also some relevant meta-analytic studies do not show any strong predictive effects, which would be expected based on the model and assumptions. Additionally there are many other areas besides evolutions that are speculated upon in the polyvagal conjecturea, that are complex and tricky and lie outside the usual competence of the vast majority of psychologists and therapists, e.g. 1) structure and function of the parasympathetic (and overall autonomic) nervous system; 2) noninvasive estimation of vagal control to the heart and other organ systems (much trickier than most people think and much more complicated than proposed in the polyvagal literature; 3) established and clear knowledge about how parasympathetic and sympathetic function interacts with activity, behavior and psyche; 4) translation of polyvagal assumptions into clear, unambiguous and testable prediction models). This also makes reading my 2007 paper rather challenging if one either has limited background or is unwilling to take the time to slowly go through the paper. (That’s one reason I started the RG contributions: so I could incrementally an interactively update arguments in dialogue with interested readers) .

Additionally there are a few recent papers besides my 2007 ones in the biobehavioral literature that begin to call into question basic polyvagal speculations. Also a friend very recently alerted me that a whole critical section exists at the end of the wikipedia contribution on “polyvagal theory“ that largely but not exclusively is based on my earlier arguments (I had nothing to do with writing this section, and don’t know who the author(s) are; please reveal yourselves if you read this).

About “Absence of evidence is not evidence of absence”, I can only say that if my therory was being broadly brought into question and I had some concrete positive evidence to counter the critiques, and I saw that 60,000 reads had occurred, I think I would certainly present my data. The point of my original question some 5 years ago was to stimulate debate and to be open to things I may have missed. So I continue to be rather surprised that polyvagal proponents have come up with nothing, apparently preferring to ignore the critiques or to employ ad hominem tactics. It rather reminds me of what is currently happening here in Germany with the Covid deniers in the midst of the current Corona virus now raging here, or perhaps a better example, how some 80% of the US republicans, based upon the claims of a single, weirdly (to some) highly charismatic madman, remain convinced that the presidential election was rigged, despite all the evidence to the contrary from law enforcement, election experts and the courts. In each case, people on the other side are attacked, rather than their arguments. I‘m not saying that the author of the polyvagal notions is a madman, but the general process may bear similarity: All the evidence is available but ignored by a large amount of people. All three are fascinating, if scary, phenomena.

The vagus nerve is a remarkable one: the fact that it shows up as one nerve bundle gives the impression that it serves one purpose. However, the effects of stimulating it are so manyfold, that this idea must soon be put aside: apart from the effects on heart rate (lowering) and the intestinal tract (activating motility, but also implied in microbiota sensing) there are effects on the immune system (anti-inflammatory). Activation of the afferent nerves in the bundle may have widespread central effects, of which the epilepsy-suppression has been used in neurology for quite some time. Looking at it from those aspects, a term like ‘multivagal’ comes to mind. (‘Polyvagal’ is a combination of Greek and Latin, a forbidden barbarism to the classically trained ear).

The evolution of this nerve bundle with all these combined functions has not been fully elucidated: soft tissues are not fossilized and extant ‘evolutionary old’ animals have developed over time as well. So, when a ‘multivagal theory’ puts forward ideas on how this all may have come about, and how our emotions and the autonomic nervous system interact, the imagination of the scientist has freedom to roam. However, the psychotherapist wants to heal, preferably using an underlying theory that may explain combinations of bodily aspects (pounding heart, immobilized body) and strong emotions. If a narrative can do this, and help the patient in the coping process, who cares about the exact science?

Something along those lines I wrote in my recent paper (1). When pushed by one of the reviewers to say something about the polyvagal theory, I came up with this:

In this personal review I will not go into the origins and specifics of the “polyvagal theory” (Porges, 2011) but see Grossman and Taylor (2007). One may take a practical view about this: if it works for psychotherapy to help patients understand and manage their innermost feelings, then the scientific merits of the theory are irrelevant.

In the present RG-comment I tried to be a little less reductive and sketchy, but in the absence of proof of the underlying theory versus the sometimes success of its applications, I would let the issue rest until further evidence to deepen our insight has emerged.

(1) Karemaker JM (2020). Interpretation of heart rate variability: the art of looking through a keyhole. Front. Neurosci. 14:609570. doi: 10.3389/fnins.2020.609570

Gary Groesbeck a scientific hypothesis or theory cannot be approved because thousands of people like it or cite it. It needs robust and consistent evidence and as Paul Grossman has explained in his RG question evidence is lacking for this theory.

https://www.researchgate.net/post/After-20-years-of-polyvagal-hypotheses-is-there-any-direct-evidence-for-the-first-3-premises-that-form-the-foundation-of-the-polyvagal-conjectures

John M Karemaker I would challenge that. If something works and we don't understand why, then it is ethical to say openly that we do not understand why it works.

The PV people don't say that; they state with certainty that the PV theory explains traumatic and post-traumatic reactions. And the theory is now being used everywhere in the trauma healing industry to "prove" that trauma healing modalities are evidence based. I'm sure there are insurance-industry-based reasons for this.

I call this "opening a can of science," and it's one way to identify trouble in a modality. Sadly, many of the practitioners who are following PV do not have the training they need to understand the PV theory and its faulty foundations, and they are repeating things they've heard. These people aren't intending to do harm; they simply don't understand the science, and they're listening to their elders, as it were. But what they're doing is based on faulty and false information, and that doesn't provide true service to anyone.

PV theory is moving like wildfire through the trauma healing community, and now you can see rotten articles that explain depression and everything else using PV as their basis. I'm expecting PV-based diet, beauty routine, and home-renovation processes anytime soon. That's a joke, but it's also not; this thing is taking over and it's being used as an all-purpose explainer of all things.

Traumatized people are vulnerable people, and any modality that attempts to serve and help them must be ethical. Practitioners must learn the truth and tell the truth.

If we accept random and easily disconfirmed theories as "good enough," we do a disservice to these vulnerable people, to the trauma healing profession, to the tradition of ethical research, and to the truth.

Karla McLaren - I do agree and think you've put it really well. Your description of PV-based diets, beautify and home renovations made me laugh, but I know this is a real issue.

Karla McLaren Daniela Sieff , Dear Karla and Daniela, as much as I have the greatest liking, respect and admiration for John Karemaker as a cardiovascular physiologist, I agree with you both about the problem of accepting fallacious biological models as a basis to explain and justify psychotherapeutic methods and effects. Even as metaphor, I think most of us would have great difficulty with a specific psychotherapy approach somehow based upon the idea that the earth were flat, and that all our problems were caused by getting too close to or falling off the edge. A rounder metaphor would seem more fitting.

Likewise, a more accurate autonomic explanation of trauma and its treatments would seem more appropriate and less risky for the belief systems of trauma patients (should they later discover the therapist’s “biological” explanation to be discredited), as well as for psychotherapeutic approaches to be considered as credible in the mainstream scientific world.

No one doubts that the brainstem plays a significant role in autonomic (and vagal, i.e. parasympathetic)—regulation in all behavior. But as John, himself, has recently mentioned elsewhere, the vagus may be more appropriately considered as the messenger (transmitter of information) rather than the message. The message is a lot more complicated and certainly additionally involves not only other higher brain centers but the full range of interaction and enaction of the entire organism with all aspects of the environment. Reducing, for example, emotional freezing or psychological dissociation to a concept like “dorsal vagal shutdown” (as is common in somatic experiencing therapy), which putatively causes a decrease of heart-rate, is not only wrong (the dorsal motor nucleus plays no or a very insignificant role in vagal control of heart-rate) but also ignores all nonvagal contributions to the phenomena of freezing or dissociation. Even if that explanation were true, it would be like shooting the messenger rather than targeting the message.

I also believe it is very important to realize that with our current understandings of both physiology and psychotherapy, we are always operating on a metaphorical level when we try to explain psychotherapy by means of biological mechanisms. Psychotherapeutic benefits are aimed at altering the lived experience of the client (they need to feel better). There may not always be a one-to-one correspondence between that lived experience and the underlying biological changes (between people or maybe even within ourselves over time). Lived experience is always individual, covert and only very indirectly to be measured; physiological processes are directly quantifiable and usually studied normatively (in groups of people, yielding statistics of averages and within-group variation). So trying to explain lived experience from the normative physiological data is very tricky. Maybe the very best we can do is to acknowledge the metaphorical nature of that relationship, while still choosing biological explanations that are currently best supported by scientific data.

Thanks Paul Grossman - that is beautifully articulated. Appreciate the clarity and the humanity. Best, Daniela

Thank you again, Paul Grossman

Hi Ali, Paul, thanks for this very interesting thread. I didn't mean to imply that PV was a popularity contest, only that I had run a quick search of Google Scholar looking for any articles in the last four years that criticized or disconfirmed PV theory. I saw none, but perhaps I needed different keywords for the search.

PV evolutionary biology is outside my purview so I leave that to those actually involved with the research. We use many metaphors we know to be wrong, everything from the telephone switchboards to the triune brain, PV theory is a useful metaphor but really has little to do with our NFB protocols. I have NFB colleagues involved in trauma treatment, which I am not, and they seem to be abandoning the PV theory. I will continue to monitor developments in this field. Thanks again.

Sometimes we scientists and clinicians forget that our nomenclature is not reality, but merely a convenient and yet sometimes knowledge-limiting system of labels.

Is the Vagus nerve an entity entirely separate from all of the things it is connected to? I would assert that it is not. The VN is both entity and system (a "systity," perhaps). The VN is an intelligent nerve as Dr. Karemaker can attest. It communicates with various chemoreceptors (and may itself be a multi-chemoreceptor), for example, to control heart function and breathing, and to send blood clotting agents to the exact location of a hemodynamic injury. The intelligence of the VN lies in is ability to collectivize information from a vast array of sources and apply it when/where it is needed. The VN is an intelligent network, much like the BORG in the TV Show STAR TREK.

I have an article that links a religiously oriented mindfulness intervention and heart rate variability that connects a bit with your question. The link to article is here Article Religiously oriented mindfulness for social workers: effects...

Regina Trammel Hi Regina. Unfortunately, simple changes in HRV to an intervention provide absolutely no direct support of the polyvagal conjectures, nor in fact that any vagal changes, whether cardiac or other, have occurred: Simply slowing down your breathing, voluntarily or not, can produce profound increases in HRV that do not at all reflect alterations in vagal tone. Also even if the intervention should actually alter vagal tone, that result would still not provide any support for the polyvagal speculations: it is already known for over a century, long before the polyvagal was dreamed up, that vagal tone is altered by a range of environmental, physical and behavioral factors. Therefore, such changes have no bearing whatsoever on the validity of polyvagal assumptions.

That the parasympathetic nervous system is important in daily life is certainly not due to the revelations of the author of polyvagal notions. We have known that for a very very long time.

Thank you, Paul. The basic premise of the article was not to prove the polyvagal theory, but to show basic changes of HRV from a mindfulness-based intervention. The HRV variable did theoretically lie within a polyvagal framework, I can see your discussion as being helpful in clarifying that and will send me into a deeper dive into that theory. However, I want to clarify again that HRV was one variable, and that it was to triangulate the data regarding measurement of stress in this particular study on a Religiously Oriented Mindfulness Intervention. I think the whole of the study and its results should be viewed. You're making an important point, I was hoping to just contribute to the question, in general. But, yes, will move away from polyvagal theory until I discover more about its general validity. Thank you. Paul Grossman