Thanks for this thoughtful summary of the lack of direct evidence supporting the polyvagal theory.  I have spent hours reading the related literature in search of direct evidence supporting the theory (and have watched interviews with SP) but there doesn't appear to be direct evidence.  In interviews, SP states that this is only a theory.

Hi Paul,

Thank you for this interesting review of evidence about the polyvagal theory. I am a psychotherapist reasonably well versed in neuroscience literature. I know many dozens of practicing psychologists who are “neuroscience” oriented, meaning they read imaginative fashionings of neuroscience data done usually by arm chair theoreticians or those who capitalize on vogues. Virtually none of the people I know who are clinicians are interested in or prepared to read science literature directly. In my own communications with clinicians I generally try to make clear that such theorizing is akin to metapsychology in the psychological realm, rather than some sort of proven science. I usually offer that such notions are useful to us as metaphors or as probes in the search for heuristic possibilities. I can attest to the fact that I know many clinicians whose interest in their art and their concentration on the human body in the psychotherapeutic space is very wholesomely increased by popular and somewhat imaginative metaphors involving neuroscience findings. I think they have a useful effect on the creativity of the clinicians, especially ones who might be getting stale and need an infusion of enthusiasm that novelty can provide. Unfortunately some take these notions a little literally and become true believers of sorts and I have seen such people explain neuroscience to actual neuroscientists, who are usually impeccably polite, without a hint of eye rolling. If you write a formal critical review of Porges’s theory I would appreciate a copy. When I have informally spoken with Porges on various occasions and have nicely asked for some clarifications about this theory, he is very quick to say that the actual situation is more complex than he presents and his behavior implies that it might be better seen as a schematic of sorts. His work appears to offer notions that give some physiologic theory support to the attachment behavior theoreticians, such as Sue Carter.

If you have gazed in that direction, let me know what you think about Iain McGilchrist’s imaginative productions on hemispheric laterality (the one’s in his book). Robespierre comes to mind there.

Frank

After almost 116,000 views of my question, and more than 20,000 views on associated projects, and no positive replies (and several personal ones highly critical of the polyvagal conjectures), it seems that new or older positive evidence may not be available.  It apeears increasingly unlikely that someone will come up with something to support thr polyvagal suppositions.      

Nevertheless, I would like to point out a few papers (see references) with what seems good evidence that the dorsal motor nucleus (DMX) is not involved in neurogenic bradycardia (Premise 1 repeated below). These papers have not been cited in any publications by authors proposing Polyvagal hypotheses but do seem extremely  important and challenging to the premise: when the DMX was chemically ablated in rats, vagal heart rate responses remained all but unaffected; however, when the nucleus ambiguus (NA) was similarly ablated, vagal heart rate was also abolished. These data seem to indicate that only the NA is responsible for vagally controlled heart rate changes under all normal conditions, which include orienting and other examples of sudden bradycardia  (please remember that all our knowledge from respiratory sinus arrhythmia [i.e. high-frequency heart-rate variability] pertains to vagal influences upon HEART RATE), and the DMX may (just possibly) be involved in vagal heart rate changes only when the respiratory tract is physiologically very irritated by hot red pepper substances or other extreme irritants--certainly not during normal neurogenic cardiac responses to orienting. 

   Also I wonder about the distinction made in Premise 1 of "Polyvagal Theory" (below) between neurogenic bradycardia and RSA: BOTH are neurogenic phenomena, and RSA is distinguished from the former only to the extent that it manifests a respiratory rhythm (i.e. the neurogenic bradycardia usually occurring during expiration). Of course changes in breathing during orienting, like breathholding, that sometimes occurs, might alter somewhat the pattern of RSA, or alternatively, the normal vagal discharge pattern in the NA may just temporarily override the usual RSA found under other circumstances (one sees the latter quite commonly when examining breath-to-breath RSA variations under a range of conditions). I don't understand the need to posit another vagal pathway as responsible, especially if there is no evidence . 

Since this premise is at the base of Polyvagal ideas, it would seem that if incorrect, the entire theory collapses. Indeed, this likely fallacious hypothesis is often treated as if it were a fact in the polyvagal lectures and literature. Is there really no scientific interest to clarify this point? A comprehensible dialogue would be enormously useful!

Once again, I am only interested in a serious discussion of these issues, because they form the basis of a number of different lines of research and thinking about psychopathology. 

Studies apparently inconsistent with

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

Cheng Z, Powley TL, Schwaber JS, Doyle III FJ. Projections of the dorsal motor nucleus of the vagus to cardiac ganglia of rat atria: an anterograde tracing study. J Comp Neurol 410:320-341, 1999.

Cheng Z, Powley TL. Nucleus ambiguus projections to cardiac ganglia of rat atria: an

anterograde tracing study. J Comp Neurol 424:588-606, 2000.

Cheng Z, Guo SZ, Lipton AJ, Gozal D. Domoic acid lesions in nucleus of the solitary tract: time-dependent recovery of hypoxic ventilatory response and peripheral afferent axonal plasticity. J Neurosci 22:3215-26, 2002.

Cheng Z, Zhang H, Yu J, Wurster RD, Gozal D. Attenuation of baroreflex sensitivity after domoic acid lesion of the nucleus ambiguus of rats. J Appl Physiol 96:1137-45, 2004.

Cheng Z, Zhang H, Guo SZ, Wurster R, Gozal D.Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence. Am J Physiol Regul Integr Comp Physiol 286:R625-33, 2004.

Article Differential cardiac parasympathetic innervation - What is t...

Article Attenuation of baroreflex sensitivity after domoic acid lesi...

Article Domoic Acid Lesions in Nucleus of the Solitary Tract: Time-D...

This is extremely helpful.  I've always wondered what evidence there is for the polyvagal theory, but don't have the neurobioloigcal grounding to look for it or assess it.  Do you know how one could reference this Researchgate post of yours?

Dear Daniela,

Thanks for your note on ResearchGate. Judging from your professional background and competencies, the "polyvagal" speculations may be of interest. Together with a very prominent evolutionary biologist of the autonomic nervous system, Edwin (Ted) Taylor from University of Birmingham, I published a paper in 2007, which we consider a refutation of Porges' ideas on a great number of grounds, including the evolutionary ones (Grossman & Taylor, Biological Psychology [2007]: it is uploaded on here on ResearchGate).  Although relatively frequently cited for points peripheral to our critique, the paper (plus an another critical commentary in the same issue by Berntson, Cacioppo and myself--alos upoladed to ResearchGate) has had little impact upon the broad embrace of the polyvagal notions among psychologists and psychotherapists. It may well be that the level of discourse was too complex or assumed too much background expertise of the  audience Biological Psychology primarily addresses. I thought a  question-generating dialogue (which--unlike journal comments--could go back and forth) might be more fruitful, hence the question posed here. After a couple of months and almost 700 reads, I find it curious that those carrying out research with polyvagal rationales haven't at least chimed in to defend their ideas and research (they have surely been made aware of the existence this question by now). However, at this stage of my career, I watch with some fascination how post-postmodern science appears to operate. Any dialogue with you or others would be welcome. However, if you wish to cite my comments, those two papers just mentioned would work.

More evidence that runs counter to the polyvagal speculations: In addition to the literature mentioned earlier,  there are both newer and older studies that indicate that the dorsal motor nucleus (DMN) is not seriously involved in vagal control of heart rate (see Gourine et al, in press and Geis & Wurster, 1980, below). These are not the only additional studies to be found that are contrary to Premises 1 and  2 stipulated in the polyvagal propositions.

Geis & Furster (1980) found no effects of direct electrical stimulation of the DMN upon heart rate (HR) , as illustrated by the figures I have appended: note that only stimulation of the nucleus Ambiguus (NA) under conditions in which the vagus was intact (not vagotomized) exerted effects upon heart rate (in the pacing condition, the heart rate was electrically paced at the heart itself, so that vagal effects upon HR were excluded as well);  in Figs 1 & 3 (the first graphic), the changes in HR (right panel) in individual cats demonstrate  the obvious changes of the ongoing rhythms of the various measures only during NA stimulation with the vagus intact. In Figs 2 & 4 (second graphic), mean effects are shown: note that in Fig 2 (left panel), HR is completely unaffected by electrical stimulation of the DMN, whereas in Fig 4 (right panel), similar stimulation of the NA results in massive HR decrease.

The group of Gourine and colleagues have performed a number of recent studies that conclude the same (see attached paper for references and then their supplemental material that show no DMN effects on HR). Interestingly, on the other hand, they find substantial evidence that excitability and contractility of the heart (left ventricular) is affected by the DMN. However this has no bearing on the polyvagal conjectures, which completely rely upon heart rate. 

All in all, it would appear after 900 views and no evidence to the contrary that Premises 1 & 2 are very likely to be false: direct electrical stimulation or specific ablation of the DMN appears to have negligible or no effect upon HR.

Regarding Premise 2,  the evoutionary basis of the polyvagal notions also seem to be extremely questionable, but this is stuff for another time.

https://www.google.de/search?q=Geis%2C+G.S.%2C+Wurster%2C+R.D.%2C+1980.+Cardiac+responses+during+stimulation+of+the+dorsal+motor+nucleus+and+nucleus+ambiguus+in+the+cat.+Circ.+Res.+46%2C+606%E2%80%93611.&ie=utf-8&oe=utf-8&client=firefox-b&gfe_rd=cr&ei=GUCbV7GdC6OF8QfT5om4CA

Article Cardiac vagal preganglionic neurones: An update

Dear Dr. Grossman,

Thank you so much for such an interesting and detailed post. I am a Cognitive-Behavior Therapist from Argentina, just beginning my neuroscientific training. Following this endeavor, I had recently bought Dr. Porges book about the Polyvagal theory. Since Dr. Porges' statements seemed so strong, I googled about his theory's empirical support and, by chance (or not), I found your post. I haven't yet read the papers you suggest, but in case they are too technical for me, can you specify if -based on current evidences- there it is anything salvageable and clinically useful about the Polyvagal theory? For example, is the notion of neuroception (our brain reacting to stimulus without our conscious awareness in a bottom-up fashion) still valid?

Thanks in advance, Ignacio

Dear Ignacio, 

Thanks for your note. As my completely (and, from my perspective, undesirably) one-sided dialogue indicates, there appears to be no empirical basis for the speculations referred to as "polyvagal." After 3000 views, no one from the "polyvagal" camp has come forward with even a single strand of direct evidence to support their beliefs, nor even attempted to discount--to my mind, rather convincing--an evidence base that is clearly inconsistent with the basic premises stated by Porges in his books and papers, not to mention my paper together  with the very eminent evolutionary physiologist of the autonomic nervous system (of course, including the vagus), E.W. Taylor, in which we believe we refuted polyvagal notions on at least 4 different levels of argumentation. The only attempt to counter our arguments was done in the same journal issue by Porges himself, but in a manner that made no sense either to Taylor or to me, nor directly addressed any of our major arguments. Actually, in preparation to write that paper, I first queried 5 evolutionary autonomic physiology experts and asked what they thought of Dr. Porges ideas. I received quick and very dismissive replies from 4 about those ideas (the 5th never wrote back). Since publication in 2007, our paper has been cited over 500 times, bu there has not been a single serious attempt to discredit what we wrote, so far as I am aware. To the contrary, in personal exchanges with top evolutionary biologists, they have termed the ideas as "polyvagal polly wally doodle" or  "ridiculous," and have claimed that they just can't be bothered to take these notions seriously.  So I think it seems very unlikely that these speculations will weather the test of time, despite their apparently broad popularity among clinicians and researchers. 

  On the other hand, if I understand your last question correctly, the idea that our behavior and emotion can be influenced, unconsciously or consciously, by physiological processes has been well established for many decades before Porges or I were born (see arguments regarding the James-Lange theory of emotion). It is certainly not unique to Porges' neuroception thinking.

Friendly greetings, Paul

With almost 4000 readers of this question, and not a single reply--neither from "polyvagal" proposition proponents nor other--offering the slightest of positive support  during over  a year's time, it seems reasonable that these ideas be put in rest (or at least hibernation until clear evidence may emerge). In any case, it seems so far that polyvagal notions  currently merely represent a belief system among a rather sizeable group of investigators particularly in the psychological domain. Any comments to the contrary would be welcome, but there does not seem to be much enthusiasm from the polyvagal camp for genuine dialogue in a public scientific forum. I've tried again and again, and will continue. It's a curious, interesting and sometime even amusing process that has been going on for a quarter of a decade.  I'll  keep attempting to provoke discussion and am very happy that ResearchGate, PubMed Commons and many journal websites offer the possibility for open exchange that the staid publication process of delayed comment and last-word author reply do not allow for. I'm very curious to see (over the long term) whether this new possibility may have any corrective influence on cardiac vagal tone conceptions or other contentious areas of  research and investigation . Obviously the possible obfuscation inherent in old-fashioned authors' counter-responses to critical commentary in journals can be reduced by open exchange in which opinions are backed up with empirical citations (and even downloads)--as I have been attempting. Let's see what happens in this domain? 

Yet another careful and convincing investigation (via Vladimir Kulchitsky) showing that the dorsal motor nucleus (DMN) has nothing to do with vagal control of heart rate: 

https://www.researchgate.net/messages/attachment/1027265_2279.full.pdf

Gray et al. (2004). Parasympathetic control of the heart. III. Neuropeptide Y-immunoreactive nerve terminals synapse on three populations of negative chronotropic vagal preganglionic neurons. J Appl Physiol 96: 2279–2287, 2004.

• As I mentioned previously, I know of not one single study that finds evidence that the DMN  is significantly involved in vagal control of heart rate.  The studies I cite here and above seem more than sufficient to refute a very major tenet of polyvagal supposition: if all vagal heart rate variation is via the nucleus Ambiguus, as very strongly appears to be the case (lots of evidence with none to the contrary), then the DMN cannot be responsible for profound or less than profound bradycardia evoked by any variety of stimuli. 
• When the other arguments of Taylor's and my 2007 paper, are considered, Porges' ideas fail on another few sets of false assumptions, as well: For example, we show that the evolution of the parasympathetic nervous system does not correspond to Porges' contentions (and Porges actually wrongly relies upon Taylor's research as an inaccurate justification, later reeearch indicating that rattlesnakes show respiratory sinus arrhythmi--completely inconsistent with Polyvagal evolutionary interpretations. 
• Thirdly, the polyvagal speculations completely ignore the often confounding influence of respiration when using respiratory sinus arrhythmia (RSA), or high-frequency heart-rate variability, as a marker of  within-individual variation of cardiac vagal tone. 
• Perhaps even more serious, Porges conflates cardiac vagal tone and RSA, when the latter is, at best, merely an index of the former (and it seems clear from our previous research [Grossman & Kollai,1993] , as well as others  [https://www.researchgate.net/messages/attachment/1027264_155.full.pdf] that resting heart rate may be a better index of individual differences in cardiac vagal tone than RSA alone!

All this evidence has been documented by us  already 10 years ago, although several newer studies above provide additional support. I can only guess that the silence of the polyvagal is due to their having no meaningful rebuttal and, therefore, prefer silence to open debate where arguments can be dissected and thrown back and forth. 

In any case, supporting psychophysiological suppositions that seem baseless and  are contradicted by all available evidence does not bear well for my general field, nor for my specific area of  relationships between autonomic control and psychological phenomena. It makes what we do seem silly and ignorant to those who are knowledgeable in the physiological domain. I think that is a shame, and will therefore remain persistent. 

To make it very easy for anyone to present evidence refuting  premise 2 above:

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 breath-ing 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 indi-cate 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/11600/37466/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.

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

Very important in-press paper in top-ranked Journal of Physiology:

From Introduction (bold mine): "The main cardiac function of dorsal motor nucleus DMNV neurons appears to be to exert inhibitory control of the excitability and inotropic state of the ventricles (Geis & Wurster, 1980). In line with this, selective pharmacogenetic inhibition of dorsal motor nucleus (DMN) neurons in vivo was found to alter ventricular function but not heart rate (Machhada et al., 2015, 2016), indicating that the DMN does not provide tone to the cardiac pacemaker."

Last paragraph, Discussion (bold, mine): "In the clinical setting, cardiac vagal tone is measured non-invasively by beat-to-beat or ‘high frequency' heart rate variability. This essentially measures RSA. Although RSA has been found to correlate with vagal tone, it is worth bearing in mind that the two measures are not identical and, as reported here, are of distinct origin."

Farmer DG, Dutschmann M, Paton JF, Pickering AE, McAllen RM. Brainstem sources of cardiac vagal tone and respiratory sinus arrhythmia. J Physiol. 2016 Dec 15;594(24):7249-7265. doi: 10.1113/JP273164. PubMed PMID: 27654879; PubMed Central PMCID: PMC5157093.

https://www.researchgate.net/profile/David_Farmer4/publication/308576470_Brainstem_sources_of_cardiac_vagal_tone_and_respiratory_sinus_arrhythmia/links/57eb178908ae91a0c8d3f6fa/Brainstem-sources-of-cardiac-vagal-tone-and-respiratory-sinus-arrhythmia.pdf?origin=publication_list&ev=srch_pub_xdl

Article Brainstem sources of cardiac vagal tone and respiratory sinu...

Given there are, by now, over 4500 "reads" to my question/blog and only evidence presented that appears forcefully to  discount all three of the first and very primary premises stated by S. Porges regarding  his polyvagal suppositions, does not anyone from the "polyvagal camp," including Porges himself (who has been following this discussion) not want to provide whatever evidence base they may be able in order to support their hypotheses?  This lack of response seems very curious to me for scientists who are curious to explore and expand knowledge, and this open forum provides an excellent opportunity to do so, especially when positions are reinforced with citations and links to papers that back up points (as I have largely tried to do).  What happened to scientific dialogue In this area in the 21st century? A question within a question.

Also added to the project, https://www.researchgate.net/project/Examining-Porges-Polyvagal-suppositions

Still no evidence for the polyvagal speculations and only very substantial evidence against

In this time of "fake news," "alternative facts," "post-truth modernism," "creating one's own reality" (Karl Rove from Suskind, NY Times 2004) and surviving 2017 in Trumplandia, it seems more important than ever to question controversial ideas in "Science" that parade as fact and can have significant impact upon people's lives and pocket books, as well as upon future research directions. Although I have opened up discussion about polyvagal notions a year and a half ago, although probably more than 5000 researchers have viewed the above-mentioned project and/or this question, there has not been a single strand of evidence offered in support of things polyvagal and my colleagues in evolutionary biology and cardiovascular autonomic physiology completely discount the polyvagal suppositions. Evolution of the autonomic nervous system does not seems to work the way the polyvagal assertions claim, nor does the brainstem dorsal motor nucleus appear to play any significant role in regulation of parasympathetic influences upon heart rate. Each of these points is very well substantiated, and each provides--by itself--a source of refutation of the polyvagal speculations. On the other hand, I have personally been at lectures of Steven Porges (the author of things polyvagal) in which he claims the opposite, as though his contentions were fact.

Ten years ago, a very prominent expert on the evolution of the autonomic nervous system (Edwin [Ted] Taylor) and I published a multi-tiered refutation of the polyvagal ideas (attached). Cited almost 600 times (Google Scholar), with not one serious critique of our arguments, its publication has done nothing to stem the tide of enthusiasm for polyvagal suppositions. Two years ago, Ted Taylor asked what can we further do to bring some science into this area: my ResearchGate attempts at dialogue result from his and another well known autonomic evolutionary biologist 's (Tobias Wang) frustration with this business. They wanted to write another paper. However, I thought this ResearchGate avenue might actually reach more researchers--young and old—as well as provide a platform for serious discussion, pro and contra, unhampered by biases of conventional journal publications. I figured that if I could support my ideas with accessible literature documentation (see link above), we could have a lively debate about things.

6000 reads later, only several additionally critical comments about the polyvagal (and most of them in private mails to me), but no dialogue: So what is going on in our "science" and "research"? Has our discipline succumbed to the same sociopolitical and economic forces as the rest of our Western institutions? Are proponents of polyvagal ideas merely keeping quiet in the hope that critical discussion may simply fade away? Are they wary of an open discussion? Are they or the opposite school afraid that funding possibilities may be diminished, should they enter the dialogue? Do researchers feel so profoundly insecure in their knowledge of the issues involved that they fear for entering a discussion? Or has this area of polyvagalness become a place where believers can merely exercise their beliefs and provide a plausible (if untrue) metaphor for relations between mind and body? Or maybe there are other reasons for this state of affairs (please tell)?

Anyhow, I continue to find this a fascinating and curious situation, and I will persist to try to stimulate discussion. We will see what happens.

Dear Emily,

If you mean that myths can affect people's lives, I have no problem with that. I also agree that is probably what has inflated the popularity of the polyvagal speculations. Wampold, in his work, makes a very convincing case that improvements in psychological wellbeing don't rely very much at all upon the method (or, perhaps, ritual would be a better word) chosen: improvement has more to do with having some ritual one believes in, a practitioner of it who seems competent to the client, a joint plan and goals, and maybe most importantly an atmosphere of trust and compassion.

However, my problem is that the ritual becomes conflated with science in this case, and the scientific aspect is used to sell the approach, when all the scientific evidence speaks against the speculations. There are, I hope you will agree, multiple myths that could be invoked to explain the various conditions to which you allude. Why not construct an explanation (myth) more consistent with what we know? That would provide, in my opinion, a much healthier approach for the therapy (i.e. ritual), as well as the societal acceptance of it, in the long run. Right now, what might happen to a client who has gone through a therapy with a polyvagal explanation (and who believes in "science" as the new religion) when they eventually read that in the New York Times that the polyvagal ideas have been thoroughly debunked? What happens to the credibility among scientists of a potentially helpful therapy (ritual) when the underlying scientific premises are thoroughly falsified, as seems to be happening. I don't think that is good for anyone. And I strongly believe one could adjust the vagal myth, employing autonomic explanations that have been around for at least a century before the polyvagal speculations were suggested. That is all I am trying to get at.

Thank you for this discussion. I am learning a lot, and have been at the receiving end of therapists who push this theory, which I have always been skeptical about. The funny thing is, that their approaches are working on my chronic whiplash, opening up greater avenues of self-regulation and deep relaxation of muscle tension. However, these are expensive treatments that seem to have no end, and I am more interested in scientific truth that builds lasting theories under which the body will appropriately heal itself. The idea that "you can't tell the body what to do" is a favourite line for therapists to use when you talk about exercises or seeing a kinesiologist for more active treatments, like stretching the psoas muscle. That makes you the passive recipient of their theories worked out on your body. If I hadn't been in so much pain, I would never have given in so easily. Thank you again.

Thank you, Dr Grossman. This discussion is a relief.

In searching for more information on Porges model, I found Megan Barnsley's 2012 PhD (attached), which addresses some of the issues. It's polyvargal explained for the rest of us, by way of a couple of very nice experiments.

As an aside, I'm doing my Honours thesis in 2019. I can't find contact info for Megan anywhere on the web. If anyone reading this should happen to know Megan, could you possibly ask her to message me on ResearchGate. I'd love to follow up in some small way on her research.

https://core.ac.uk/download/pdf/12826597.pdf

Thank you Paul. Indeed this discussion is a relief!

I fully agree with you!

I guess we should more focus on the understanding of the central autonomic network instead of, which is not a theory but a functional integrative model!

After a long pause, even more clear evidence that the very evolutionary bases of the polyvagal speculations are fallacious, this from a recent paper in Science Advances”, with two of the authors among the most respected evolutionary biologists of the vagus. The very foundation of the polyvagal notions is clearly false, and this is just one level of evidence among many others that I have already reported. It should also be telling that there has not be a single attempt to counter any of these lines of evidence after almost 3 years of a one-sided conversation. If polyvagal proponents have evidence in defense of their ideas, it is really time to present it.

I quote some of the most salient passages:

S C I E N C E A D V A N C E S | R E S E A R C H A R T I C L E

E V O L U T I O N A R Y B I O L O G Y

Cardiorespiratory interactions previously identified as mammalian are present in the primitive lungfish.

Diana A. Monteiro, Edwin W. Taylor, Marina R. Sartori, André L. Cruz,

Francisco T. Rantin, Cleo A. C. Leite

Monteiro et al., Sci. Adv. 2018; 4: eaaq0800

“The existence of dual locations for VPN [vagal preganglionic neurons] outside of the DVN and, in particular, the location of CVPN [cardiac vagal preganglionic neurons] in the ventrolateral NA [nucleus Ambiguus], having myelinated efferent axons, have been considered uniquely mammalian, constituting their smart vagus and providing the physiological basis for the polyvagal theory recently reviewed by Porges (13).

However, these central interactions are not unique to mammals. In an elasmobranch fish, the dogfish, or catshark (Scyliorhinus canicula), CVPNs in the DVN [dorsal motor nucleus of the vagus] show respiration-related activity that is driven rather than inhibited by activity in neighboring respiratory motoneurons (1, 11, 12, 19, 41, 42). The resultant respiration-related efferent activity in the cardiac vagi is able to influence instantaneous fH [heart rate], generating cardiorespiratory synchrony. In L. paradoxa, each air breath is accompanied by an increase in heart rate, induced by a reduction in vagal tone, implying that activity in CVPN is inhibited during “inspiration,” as described in mammals. So, this primitive air-breathing fish has a control system generating CRI that is mammalian-like rather than piscine..........

This representative of a primitive vertebrate group, with its origins located close to those of the tetrapods, has the structural and functional equipment that enables it to exert instantaneous, beat-to-beat control of the heart, which could be considered reasonably “smart.”

There is plenty of evidence for fine and rapidly exerted control of the heart in other nonmammalian vertebrates. Those with discontinuous breathing patterns, such as air-breathing fish or diving tetrapods, typically display bradycardia during apnea and a pronounced cardiac acceleration immediately upon the first air breath, implying overriding central nervous integration of their cardiorespiratory systems (10, 11). The increased heart rate immediately at the onset of periodic air breathing results mainly from withdrawal of vagal activity to the heart due to central interactions between motor neurons driving both systems (1, 11). The rapid response with a marked tachycardia often developing between two heartbeats implies a B-fiber response dependent on myelinated efferent fibers.......

Myelination of the vagal branches has been described in fish, mammals, and birds (5, 40–43).....

Porges (44) has promoted the polyvagal theory, ascribing to it many behavioral and even social functions in humans such as “love.” We do not wish to intervene in the debate around these extensions of the polyvagal theory; however, we do contest its physiological basis and evolutionary assumptions. According to Porges (13), CVPN originating in the NA and supplying the heart with myelinated efferent axons, having high conduction velocities, constitutes the smart vagus restricted to mammals, whereas the “lower” vertebrates retain the ancient vagus, restricted to the DVN [dorsal motor nucleus of the vagus] and supplying unmyelinated, slow fibers that generate slowly developing, defensive changes in heart rate. He identifies a phylogenetic progression from the regulation of the heart by endocrine communication, to unmyelinated nerves, and finally to myelinated nerves found exclusively in mammals (13) and persists in stating that “only mammals have a myelinated vagus,” linking this to the evolution of the NA (13). The present study reveals that the mechanisms he identifies as solely mammalian are undeniably present in the lungfish that sits at the evolutionary base of the air-breathing vertebrates. These include (i) a predominant role for vagal control of heart rate, as described for many other vertebrates, including mammals; (ii) close coupling between respiration and heart rate recorded as instantaneous changes in heart rate due to changes in vagal control at the onset of each air breath, detected by using PSA to characterize HRV; (iii) efferent vagal fibers with fast conduction rates (similar to mammalian B-fibers) conferred upon them by myelination; and (iv) CVPN, responsible for controlling heart rate via the parasympathetic vagus nerve having multiple locations within the dorsal vagal motor nucleus, plus scattered cells in a more ventrolateral location that could conceivably be a primordial NA......

A closer examination of the available literature reveals that other groups of vertebrates also presage the mechanisms required for fine control of heart rate (1, 11). Several authors have shown that HRV related to respiration is present in spe-cies of amphibians (2), reptiles [for example, rattlesnakes (45)], and birds [ducks (10, 11) and shearwaters (43)]. Thus, the repeated contention, central to the polyvagal theory, that the structural and functional bases of RSA are solely mammalian is clearly fallacious.

Fabulous information. Thanks for posting Paul.

Polyvagal speculations about psychopathology are not supported

Porges repeatedly attempts in his book to tie RSA responses to dimensions of psychopathology. His Premise 5 also states that “emotion...will produce changes in RSA.....” A number of research studies have evaluated RSA responses across a range of dimensions of psychopathology. Very recently a very comprehensive meta-analysis** of those investigations, however, has shown that no clinically meaningful relation can be found between psychopathology and RSA reactivity. Average effect sizes were very small  over different dimensions of pathology (d=0.06) and within each dimension (d’s = 0.04 to 0.11), indicating at least 95% overlap between groups with and without psychopathology (see attached distribution plots I derived from the data). This means that the chance one might accurately identify an individual suffering from psychopathology is almost 50-50! When I examined subgroups of studies of participants with traumatic disorders or borderline disorder (the latter often associated with trauma), results were very similar (d’s =0.035 and 0.16; see attached

This study and earlier meta-analyses, as well, provide no support for relations between psychopathology and mechanisms suggested by polyvagal speculations. In fact, the weakness of evidence—at this time several decades after the polyvagal propositions were first uttered—strongly suggests  either no relationships between cardiac vagal reactivity and psychopathology, or such small effects that are completely without clinical significance.  If there were a strong evolutionarily meaningful relationship between psychopathological responses and cardiac vagal reactivity, the numbers would be very different. 

**Beauchaine TP, Bell Z, Knapton E, McDonough‐Caplan H, Shader T, Zisner A. Respiratory sinus arrhythmia reactivity across empirically based structural dimensions of psychopathology: A meta‐analysis. Psychophysiology. 2019;e13329. https://doi.org/10.1111/psyp.13329

Thanks Paul, for continuing to provide clarity regarding the empirical status of polyvagal theory. I very much appreciate your analysis. Best, John SF

Dear Paul - I'm wondering if you could point me in the direction of anything published that summarises some of the critical approaches to Polyvagal theory that you bring together here. In looking at the literature it is easy to come across multiples explanations of the theory but less so (though I might be missing it) published pieces taking a more critical approach - thank you for any pointers. Ed

Dear Ed Freeman , I would suggest that you systematically track the 3 years of comments, references and downloads of the current question and the 35 updates of my RG project https://www.researchgate.net/project/Examining-Porges-Polyvagal-suppositions.

However, the pre-eminent evolutionary biologist of the autonomic nervous system EW Taylor and I wrote a multi-faceted critique and refutation of the polyvagal speculations in 2007, and two other highly respected cardiovascular autonomic physiologists and I wrote another complementary critique in the same journal issue (Porges attempted a rebuttal in this issue, which neither addressed any of our central issues nor made any sense to me, but see what you think for yourself). I paste our links below, plus some other stuff. But do check out the voluminous newer purely contrary evidence in my RG project. Also, of course, I am open to dialogue and further explication.

Toward understanding respiratory sinus arrhythmia: Relations to cardiac vagal tone, evolution and biobehavioral functions

Whither vagal tone

Studies apparently inconsistent with

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

Cheng Z, Powley TL, Schwaber JS, Doyle III FJ. Projections of the dorsal motor nucleus of the vagus to cardiac ganglia of rat atria: an anterograde tracing study. J Comp Neurol 410:320-341, 1999.

Cheng Z, Powley TL. Nucleus ambiguus projections to cardiac ganglia of rat atria: an

anterograde tracing study. J Comp Neurol 424:588-606, 2000.

Cheng Z, Guo SZ, Lipton AJ, Gozal D. Domoic acid lesions in nucleus of the solitary tract: time-dependent recovery of hypoxic ventilatory response and peripheral afferent axonal plasticity. J Neurosci 22:3215-26, 2002.

Cheng Z, Zhang H, Yu J, Wurster RD, Gozal D. Attenuation of baroreflex sensitivity after domoic acid lesion of the nucleus ambiguus of rats. J Appl Physiol 96:1137-45, 2004.

Cheng Z, Zhang H, Guo SZ, Wurster R, Gozal D.Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence. Am J Physiol Regul Integr Comp Physiol 286:R625-33, 2004.

Article Differential cardiac parasympathetic innervation - What is t...

Article Attenuation of baroreflex sensitivity after domoic acid lesi...

Article Domoic Acid Lesions in Nucleus of the Solitary Tract: Time-D...

TOWARD A BETTER UNDERSTANDING OF THE VAGUS IN PSYCHOLOGICAL AND BEHAVIORAL SCIENCES

(a copy of a rcent update to the RG project “Examining Porges’ polyvagal suppositions”

John Karemaker, one of the world’s most recognized experts on cardiovascular autonomic physiology and heart-rate (as well as other measures of cardiovascular ) variability, recently wrote a comment to this project I think is very important, with which I almost fully agree (see his quote below). Whereas he acknowledges that based upon numerous sources of evidence, the polyvagal theory is dead, its popularity rests with the fact that the parasympathetic nervous system plays a large role in physiological and behavioral functioning. The latter is a point that I have continually maintained in my own comments and research over the last 35 years. It seems that may be the main message that researchers are receiving from the high visibility of the polyvagal speculation over the last decade. So although the basic polyvagal premises are clearly false, most researchers equate and/or conflate “polyvagal“ with “vagal”, assuming long established tenets of parasympathetic function are inherently tied up with the erroneous polyvagal propositions. So perhaps we should thank Stephen Porges for bringing increased attention to parasympathetic roles, then dispel most of his primary suppositions (and even labeling of the ”polyvagal”) and get on with further serious investigation of vagal influences upon behavioral and psychological functioning. In my opinion, It is time we align what has genuinely been established about the vagus and parasympathetic physiology (very long before the proposals of the “polyvagal“ notions) together with our behavioral and psychological data, which employ indirect and imperfect (yet often still meaningful) measures of vagal activity (e.g. HRV and RSA). This will require investigators and readers of the literature to develop a better understanding of that which is actually known about the vagus, as well as how to measure the effects of vagal activity on different organ systems (e.g. the heart, the gut, the lungs).

Karemaker writes:

“Dear Paul,

There is a problem in the polyvagal theory, or actually a series of problems. You, very eloquently and convincingly, dismantled the basic assumptions it is supposed to rest on. However, to no avail, the theory has many followers and they are not listening and will not listen either. Why not? Well, not because the theory is correct, but because, indeed, there are there are good reasons to look for vagal effects as they are measured most easily, i.e. in heart rate (but not only there). That is not to say that heart rate (or its variability) is a reliable indicator of health be it physical or psychological or both. But we know that the vagus nerve is involved in not only in heart rate control, but also in efferent and afferent control of the gastro-intestinal tract and other organs (liver, lungs, etc). On top of that it is probably the link between the brain and the immune system. I became aware of that when I got involved in a study where heart rate and HRV were tested in patients who were on their way to develop rheumatoid arthritis (*). Since then, I read many reports on wider aspects of vagal function. In particular the electroceutical use of vagus nerve stimulation is finding more and more applications, not only for its peripheral effect on the heart but also for central effects, where it had already been in use for suppression of epileptic seizures.

In short, I think that this discussion on Porges’ Polyvagal theory should be put to rest. Paul, you are right in your criticism, but let us now look at the broader picture of what the vagus nerve might be capable to do, the functions that have escaped us while we were looking in the other direction.

(*) EBioMedicine. 2016 Apr;6:231-237. Koopman FA, Tang MW, Vermeij J, de Hair MJ, Choi IY, Vervoordeldonk MJ, Gerlag DM, Karemaker JM, Tak PP. Autonomic Dysfunction Precedes Development of Rheumatoid Arthritis: A Prospective Cohort Study. doi: 10.1016/j.ebiom.2016.02.029.”

Longtime reader, first-time commenter. Thank you, Paul Grossman, for your work on this sticky issue. I've been interested in the somatic approach to trauma, and while I find it valuable, the neurononsense is thick. Triune brain, PV theory, and other iffy suppositions are everywhere within the field, and are taught with absolute sincerity.

Yet I have not found any other trauma modality that can touch the somatic approach in terms of its efficacy (I do not include EMDR in this, because I find it silly). My feeling is that they found a good approach, which is to trust that the responses to trauma were functional, and that not learning to down-regulate or resolve the trauma is at issue. For me, those ideas helped me resolve numerous serious traumas pretty handily -- after decades of cognitive or intellectual approaches did nothing.

But I think the wrong turn they made was to try to describe what they were doing in terms of ever more complex theories of brain functioning, many of which are now far out of date, or demonstrably wrong.

As a trainer and educator, I work with traumatized people a great deal, and often refer out to the Somatic Experiencing approach of Peter Levine, a colleague of Porges'. I tell people right out to take the brain information with a grain of salt, and that the process doesn't actually need it. But that's nowhere near ideal, and without responsible information to support them, people are often led down a primrose path of what amounts to neuro-agnotology.

I keep hoping that someone within the field will bring a current understanding of neurology forward and help to right the many wrongs that exist in the approach. But the level at which the incorrect ideas about the brain are woven into most somatic approaches makes me think that this may not be allowed to occur.

Well, Karla, but there is some basic brain knowledge "for dummies" that is helpful for us clinicians, isn't it? Even if it is quite simple, I for instance found very useful the idea of the so-called emotional brain being poorly connected with the cortex in complex trauma cases—when I firstly met it. (And if I got it right ...). That confirmed my clinical impressions about emotional dysregulation, and helped me being more cautious and at the same time more precise in targeting areas of intervention with clients (that, like in your case, are more and more somatically oriented). I find the notion of first and foremost addressing and soothing hyperarousal very useful clinically, and I think that the brain internal disconnection is a good idea to support that kind of interventions.

If it's true, then it's fine to use it. But as clinicians and educators, it is up to us to make sure that the information we ingest and disseminate is -- to the best of our ability -- correct, updated, and responsible.

And of course, if we later find that there have been updates or even reversals of earlier knowledge, we should willingly update our work, even if it shifts the foundations of our approach. For me, this is a part of the excitement of education, though it is sometimes painful. Especially if you've got books or studies out in the world that need updating.

That makes perfect sense Karla, in particular the part about pain.

For perfection effort , faith and surrender mind is also important in any type of treatment then only we will achieved a desired result.

I have recently added to updates to my project that readers may find helpful:

https://www.researchgate.net/project/Examining-Porges-Polyvagal-suppositions

STILL MORE DEATH THROES FOR “POLYVAGAL” EVOLUTIONARY ASSUMPTIONS

In yet another study in Journal of Experimental Biology, evolutionary and comparative biologists clearly demonstrate that respiratory sinus arrhythmia (RSA; also called high-frequency heart variability, and in many earlier papers, erroneously ‘vagal tone’) is evolutionarily very old and definitely not a mammalian development, as falsely posited in many of Porges‘ papers on his “polyvagal“ speculations. In fact, this paper presents evidence that RSA may be a primitive relic of earlier cardiorespiratory functioning during which pulmonary and systemic blood circulation were not completely separated, as they are with mammals. Thus instead providing some advanced function related to such aspects as ‘social engagement’, RSA may be largely or purely vestigial. I have highlighted the relevant passages for readers’ convenience. Also by pointing out highly relevant and highly expert papers from disciplines far removed from psychology, psychophysiology and psychiatry, I hope to expose the RG audience to publications with which they ordinarily will not come in contact. This is one of the true benefits and advances that RG offers.

After 2 years of using the SSP and 60+ participants, it is hard to imagine that such gains can come from a myth. When you multiply this across the large number of clinicians using it worldwide, it seems even more improbable that this is a belief system at work.

Samar Singh, I know very little about SSP (am genuinely curious whether there are studies documenting benefits??), but I do have some expertise about the science related to the polyvagal suppositions: There is no evidence to support several of the most fundamental premises posited by Stephen Porges, and there is a great deal of counter-evidence, as I have presented here, in my associated ResearchGate project on the polyvagal, and in two papers back in 2007 with top expert coauthor colleagues in areas of biological evolution of the autonomic nervous system (EW Taylor) and autonomic psychophysiology (J Cacioppo & G Berntson) , not to mention earlier papers together with several of the most well recognized cardiovascular autonomic specialists (e.g. M Kollai, J Karemaker, W Wieling, JA Taylor) that contradict crucial underpinnings  of Porges’ beliefs (e.g. regarding estimation of vagal tone) . All of these other scientists, highly recognized leaders in their own fields (even if their names are unfamiliar to behavioral scientists), agree that the basic assumptions of the polyvagal suppositions are contradicted by the available evidence, and have often published their critique in their own journals (e.g.check out the morst recent paper I updated in ResearchGate).

I agree with you that the acceptance of the polyvagal notions is broad. But my ResearchGate projects were initiated in order to stimulate dialogue and discussion about this matter. With about 20,000 reads by now, there has not been a single comment containing any support for polyvagal notions. Surely, one should have been inundated with evidence if there were plausible bases for those ideas. Therefore I find it highly improbable that a belief system is not at work.  And there are numerous enough examples from the “scientific” past  (and certainly present) where very wrong ideas have been broadly accepted for very long times. Although I can’t be certain, I attribute the popularity to two main things: 1) psychologists and psychotherapists today are often very eager to employ physiological mechanisms, feel the need to have a biological justification for what they are doing, but ordinarily lack anywhere near sufficient expertise to evaluate the physiology and physiological relations to psychological functioning, and  therefore maybe quite gullible to speculations that are presented not as hypotheses but as fact. 2) The particular areas involved in polyvagal speculations include (a) biologically evolution of the autonomic nervous system, (b) autonomic physiology, itself, (c) often relatively complex issues related to estimation of autonomic activity (e.g. cardiac vagal tone), and (d) the existing evidence linking autonomic processes to psychological functioning; there are very few people that possess expertise in all these areas, so it is very difficult for a serious evaluation of polyvagal aspects to be done, and readers just tend to be impressed by the polyvagal author‘s assertions (who, like me, is a psychophysiologist—definitely not an expert in evolution or in autonomic physiology). That is why I have repeatedly chosen to pair up with experts in those other fields, as a possibility to bounce my ideas off, of them.    Anyhow, it is fascinating to me how many people seem to accept the polyvagal ideas, despite the available facts to the contrary.     

One last point: a therapy which employs a false scientific metaphor for mechanism of action may, nonetheless, be effective, but for very different reasons that the false theory.  

The Polyvagal theory is not my field of investigation. I agree on the need for an intellectual discourse and also agree that every theory should be constantly challenged until a new and better theory evolves.

My work is in deploying the SSP to do the maximum good for the largest number in an area where there has probably not been any equivalent solution in the past that was affordable in my country both in terms of time and resources. If you ask whether the SSP works, my answer would be that it does not work equally well for everyone but it would be a rare case where I have not found it to work at all - except for cases where the participants did not comply with the preparatory measures. In the next three weeks I will be working with 15 children in three cities. I will be very surprised if there are no children who do not benefit dramatically and I would be equally surprised if any do not benefit at all.

In that sense the SSP is a major contribution to the ASD community as well as other areas of its application. Hence, I have no hesitation in commending it to anyone else in that field of work - even allowing for the possibility of a myth effect. That supports your contention that a therapy can be effective irrespective of an ongoing challenge to the theory which underpins it.

Thank you Samar Singh! I definitely have the feeling that you are doing good and valuable work. Surely, science can never be the final arbiter in matters of the psyche, heart and soul. They can never meaningfully be cast into (scientific) objects. (From someone who values and engages in scientific research but who also sees its serious limits, Paul G)

But, Paul, the basic (scientific) assumptions about layers in the brain/body where some of our emotional set up is "hard-wired" still holds even if Porges is wrong, isn't it? Because this assumption is very useful to therapists, in my opinion. For instance that the cortex can be poorly connected with the lower brain? It confirms the sense that some layers have to be treated carefully and with patience and respect since they involve and challenge the whole personal system and balance, and not just the "mind." Am I wrong?

Thank you Paul Grossman for understanding the wider perspective of the SSP.

Dear Adriano Bugliani , your comment suggests to me that you are employing physiological and brain explanations as metaphors more than as scientific explanations. However, the cortex is anything but poorly connected to the brainstem, and the Triune theory of brain organization and function has also been subjected to serious criticism. As you write, we are dealing with a whole personal system, not just the mind or brain.

It is very difficult to objectify those personal experiences of trauma, grief, shame etc., since they are private, personal, covert and idiosyncratic. The experiences of trauma, grief, depression etc. are uniquely lived experiences for each of us that must be transformed into something measurable in order to empirically investigate them with the methods we commonly employ today. They are, consequently, mere representations, or even caricatures, of those underlying processes of lived experience we are actually primarily interested in when our emphasis is upon reducing suffering. To me, relating these objectified representations even to well-founded physiological knowledge is very tricky business; relating them to clearly false suppositions (like those of the polyvagal premises—especially when those polyvagal speculations are mistakenly treated like facts!!!) is extremely damaging for patients, for therapists and for the therapies that might be genuinely beneficial—but for other reasons than the fallacious, assumed ones). For example, emotional freezing and/or dissociation are often explained as states of brain stem ”dorsal vagal shutdown” when there is not a single thread of evidence suggesting this and lots of evidence indicating that the dorsal vagus is not involved in emotional vagal heart rate changes. Therapists and patients come away with a false and very simple explanation that reduces the lived experience of dissociation to a singular physiological state: the empirical representation of dissociation gets associated with a monocausal and very likely wrong brain explanation.

What that kind of explanation does, in my opinion, is to pull the patient and therapist farther away from the lived experience the patient is suffering from: her/his/their experience gets reduced to an object, a factum. Attention is drawn to the physiological—and a very simple (and wrong) monocausal brain explanation, as well—that orients away from the obvious complex and unique reality of the patient. We are not brains in a vat.

Dear Paul,

thank you so much for your very clear answer, with which I totally resonate. Being not a scientist, I constantly need clarifications, and in my experience that is more easily to get from expert PEOPLE like you, than from books.

This is one of the most amazing resources of ResearchGate: a huge community where you can get every kind of good and useful information.

You're right, I'm using metaphors, quite often with clients themselves. For instance, when "traumatized" clients blame themselves for what they perceive as their inability to change, I might use body metaphors because people are more inclined to have respect for physical suffering and damage than for psychic one. So I might say something like that: "You know, if you've got a wounded knee and your leg muscles are consequently atrophied, it's quite obvious that you will need some physiotherapy and training after surgery, and you would never expect that the day after surgery you will be able to run the 100 meters. Everyone understands that you need to train your muscles and the whole knee and leg, before you are able to run the way you were used to do before your accident. In the same way, that you're not able now to immediately stabilize and manage your dysregulated emotions doesn't mean that you're totally helpless and hopeless. We just need to carefully and gradually 'train' that side of your mind/brain. I'm not a scientist, but maybe some complex neuronal patterns have to gradually build their way, and we cannot expect that this happens immediately as a result of an act of will."

In my opinion, this is a way to make people feel that a) their problem is "hard-wired" and that it doesn't simply depend on their bad will if they're not fast improving, and b) that this is absolutely not to say that there's no hope—on the contrary, their will and self-agency is necessary if they want to train themselves towards improving, because treatment needs some constant effort and commitment and exercise from them.

Do you think that this is a good way of using a body and brain metaphor?

Thank you so much for your attention.

Adriano

Dear Adriano Bugliani

What you are suggesting is that if falsehoods are therapeutically useful, they are OK.

However, the example you give shows WHY falsehoods are not even therapeutically useful, much less OK.

It is not the legitimate province of a therapist to make people believe or "feel that their problem is hard-wired" if the facts are otherwise.

Neither is it legitimate to shape a client's sense of agency with falsehoods regardless of the rationale.

Adriano, the real problem you describe is that because you do not understand the science, you make up fake facts in an effort to make clients (A) feel the way you think they should and (B) feel the way you believe they will feel in response to falsehoods and misrepresenatations.

You're focusing not on real matters on the table but on your own fantasies about what will make people feel better. That is exceeedingly dangerous, even reckless.

You believe that the stories you make up will assist the client in recovery. It is just as likely, actually more likely, that the fake "facts" will only confuse and disempower clients just as they have confused you, as evident in your last paragraph. Making clients feel that something false is true is malpractice regardless of the tortured reasoning and illogical one uses to do so.

A therapist's job is to leave holes/gaps in his/her knowledge unfilled -- not to cram them full of rubbish.

Competent, ethical therapists know how to say "I don 't know" and avoid efforts to manipulate the feelings of their clients.

To tell or suggest to a client that his/her will and effort in recovery are not of much concern because a problem is hardwired is simply crazy.

As my Irish great-grandfather used to ask: "Is this a private fight, or can anybody join?"

Jonathan, this is a model of pugilistic engagement, and I haven't seen this kind of behavior on Research Gate as of yet. But I may have been fortunate in my choice of subjects and communities. It's like we suddenly fell into a Facebook brawl.

What do you hope to gain by treating Adriano with disdain and unkindness? He was writing directly to Paul with politeness and honesty, and Paul has been engaging with empathy and directness that allows others to maintain their dignity as their ideas are being challenged.

That has been the overarching tone here, even if Paul is frustrated as hell with Porges et al.

This was badly played, and as a bystander, I'm not willing to stand by while Adriano is treated dismissively. This is a fellow human being; he's not a punching bag.

Dear Jonathan,

being not a scientist, I can only (have to?) rely on books like Van der Kolk's The Body Keeps the Score, or Allan Schore's Affect Regulation and The Repair of the Self, or Mark Solms' papers, and so on. So my explanations are based on what I got from literature like that, and I might be wrong in what I got from them.

But your point still makes sense, and it is not so distant, in my opinion, from what Paul wrote.

To what extent may I use informations that I am not able to verify?

I just wonder if and how can we therapists really stay away from every form of explanation (that is necessarily based on many assumptions) or contextual meaning in the work with our clients, and just stay with the session's lived experience—what I think I'm trying to do most of the time.

In my opinion, it is not that simple that this experience is simply lived and not imbued of unavoidable thought frames of every kind, frames that therapists and clients share.

The point is the way we use these frames.

Therefore, I never sold metaphors as scientific truths to clients, I'm not that unethical—I always made clear that they were just maybe useful ways of thinking, and that I wasn't an expert. We use many kinds of metaphors at work. As Paul says, the point is not to sell to the clients that these metaphors are particularly "true" or that they have to swallow them because they are "scientific truth".

And I never thought that a client's will and effort in recovery are not of much concern because a problem is hardwired. How could I?! On the contrary, I just meant that if some sides are more gradual and difficult to change, a "body" metaphor could be helpful in decreasing self-loathing and INCREASING self-agency and gradual, effective, targeted efforts. It's a way to foster little, positive steps instead of having people think that if they're not immediately able to change this is because they're basically "wrong".

So I precisely need experts like Paul in order to better grasp the foundations of these widespread metaphors.

But, as said, your point is useful and a healthy shock for me.

Sorry if I'm taking too much space.

Adriano

I agree, Karla, that we should stay friendly and respectful. Actually I would prefer to veer back to the original question of supporting and contradicting evidence to the polyvagal suppositions. These other issues are really something quite different. I fear we may be getting sidetracked from answering the main question.

Hi Adriano,

I appreciate your thoughtful reply. I agree with Dr. Grossman, but the cat is bagless at this point. I certainly did not intend any disrepect to you. However, as a clinical psychologist I found much of what you wrote as practice description simply astonishing. And I believe you are correct about a "shock" being beneficial. Unlike Karla, I believe you can handle a real reaction and won't curl up in a fetal position. You took a risk posting what you did and I honored that by risking my own post-back to you. That there is a viewpoint calling "foul" and characterizing my response to you as "fighting," "pugilistic engagement," a "Facebook brawl," "disdain[ful] and unkind," "badly played," "dismissive," and a "punching" is its own revelation. I'll leave you to handle the assumption that you need protection via political correctness intervention after enduring such a, ahem, supposedly "dismissive punching."

Paul,

What I would be interested in know is whether you've presented your concerns and criticsms to Prof. Porges.

Regarding your concern about post-truth or post-fact therapy relative to Polyvagalism, doesn't this assume there was at some time a fact / truth period in psychotherapy? I wonder if there are any artifacts which establish this. The historical record indicates that psychotherapy skipped a fact-truth stage and went from pre-fact/pre-truth directly to post-fact / post-truth without passing GO once they developed the terminology and pressure tactics to discredit science and the scientific method as "racist," "homophobic," "sexist," etc. etc. Karla appears to be an expert in discrediting methodologies, so you might want to ask her about it.

Jonathan M. Honeycutt Yes Stephen Porges is long aware of my critique of his polyvagal conjectures, which formally goes back 12 years to two papers (with colleagues) I have frequently referred to in this forum. Although, he provided a single written response, also in 2007, his reply did not address or answer any of my arguments back then or later. Since I started my RG question and project dialogues, he has repeatedly looked in (based upon evidence of viewer identification). However, neither he, nor any of his associates or adherents, has ever contributed a written comment or defense to the evidence I raise. My posting of this question and the accompanying project was meant as a opportunity for serious—and civil—dialogue about the evidence base, or lack thereof. Because of the mass of available evidence in contradiction to his major polyvagal premises, I can only assume that there is no real direct supporting evidence for polyvagal Speculations that he or others can come up with. That is why I assume his major assumptions have been refuted (actually since 2007, but there is much new evidence in that refuting direction since, which I have cited and linked in my RG updates).

Also because of ad hominem attacks upon me (of which I have even written evidence, and which I have been warned of by word of mouth, from close colleagues, as well, for decades), I am quite sensitive to lacks of civility and attempts to manipulate scientific discourse. Therefore, I don‘t want arguments here that get personal or hostile.

Finally, the other questions that you and Adriano address don’t really fit in this RG question but in one of the others I have asked.So please let us discuss them there: https://www.researchgate.net/post/Are_the_polyvagal_suppositions_in_the_autonomic_heart-rate_variability_literature_an_example_of_post-truth_in_Science

I agree Paul, and I will post this little reflection also on the link you indicated, and I’ll shift to that forum.

Thanks again for your attention.

Yes, Jonathan, I can handle a real reaction and I’m everything but curled up—and your point is useful to me.

The basic issue is that we clinicians are flooded with scientific information that we cannot ignore, also because it is very fascinating. On the other side, we cannot directly control nor really grasp the meaning of these informations, because we lack the actual research and competence level upon which this information is based.

How may we use that knowledge, and to what extent?

Paul, I would add to this a few thoughts:

1. In late April about a hundred therapists from about 14 countries got together to review the experiences of therapists about the SSP over the last few years. There are I understand more than 9000 therapists using the SSP worldwide.

2. I have worked with just under 100 SSP participants and there were some there who had done more than twice that number. There were a few others whose own children had been impacted by SSP.

3. Whether there is a scientific basis to the Polyvagal theory or not, one would be hard put to refute the experiences of all these people about the positive impact of SSP.

4. I am personally NOT a trained therapist but I work with children with ASD in India because there has never before been a tool that shows impact in months for physiological and psychological states that have troubled their caregivers for years. In my case I have to use objective measurement to measure change so this is hardly my imagination at work.

In conclusion, I would suggest that you may continue to discuss the various issues relating to the Polyvagal theory but let us not extend that to dismiss SSP as mere correlation. One of the attributes of causation via correlation that has been suggested is the belief in a true link. If you had been there you would have also begun to hold that belief.

Dear Samar Singh , please let us stick with the question about proof regarding the scientific evidence about the premises and assumptions of the polyvagal speculations. SSP may be popular and may be effective, but that is a whole other issue: it may, for example, be effective because of mechanisms totally unrelated to polyvagal notions. So please only reply to this question if you can provide concrete directly supporting or refutational empirical evidence bearing upon the major polyvagal premises and assumptions. Thanks.

Dear Paul Grossman. I'm grateful to you for the information you provide us. I'm a psychiatrist interested in somatic ways to treat psycholological trauma and dissociation and I'm very surprised with so much talking about polyvagal theory around me. Though my main point is that we do not need such a theory to work with procedures that do not arise from that theory, people wannts explanations so I read "The polyvagal theory: phylogenetic substrates of a social nervous system" by S.E Porges and I became astonish as I find several false assumptions, for example that there is a specific neurological "social engagement system" in which eyelid opening, facial muscles, head turning muscles... seems to be part of it jointly with myelinated vagal efferents fibers from nucleus ambiguus that now are separated from the vagal fibers from the dorsal vagal nucleus, as these last fibers form part of other kind of vagus nerve. This is an easy to prove false assumption so I don't know why this kind of speculations as got so much attention. Nevertheless I have continued my research and have found mysel reading about the vagus nerve of fishes!

Fortunately for these questions of phisiological nature you have been of great help

Thank you so much for opening this discussion Paul Grossman, particularly so as it has been recently recommended that I add Porge's theory to a paper I'm writing, and I wanted to understand more about his theory, especially that which challenges a theory which seem now to be a "Holy Truth" in the field of "trauma informed" therapies. Could you please point me to any literature that I can access?

Grateful for this dialogue. Polyvagal Theory has become trendy in the vocal pedagogy world, and I have always been skeptical. The hard science is much more convincing than anecdotal evidence. Although I agree, some 'myths can be true' it is important not to conflate it with real science. Correlation is not causation.

Dear Marie-Christina Virago ,

sorry to be so late. However if you go through the comments and answers to this question, as well as the updates to my ResearchGate project on the polyvagal suppositions, you will find a wealth of evidence refuting the major assumptions of the polyvagal speculations. Also check out my 2007 paper on the topic coauthored by one of the most recognized evolutionary biologists of the vagus that counters the speculations on no less than 6 areas.

ss th

I thought somatic sensations go to the Thalamus (the brain relay station), then sent to facial /and eye movement muscles to attend to the stimuli as well as to the limbic system to determine the extent of emotional reactivity needed. So, nothing to do with the vagus nerve. I also thought the classic 'butterflies in the stomach' experience is more to do with vascular shutdown (with blood diverted to muscles) during a feared experience / recollection. This is more linked to the sympathetic nervous system, possibly linked with excess cortisol production (cortisol resistance at hippocampus, then no negative feedback to hypothalamus. Please correct me anyone if I am wrong.

 In this update, I comment upon the main points of my ResearchGate (RG) questions and project, as well as providing some recent history that led me to employ the RG platform as a means of explanation, exchange and documentation. First, however, I attach four very recent relevant biology papers that explicitly refute major evolutionary assumptions of the polyvagal speculations (there is also substantial much earlier evidence [e.g. see Grossman & Taylor, 2007]). Contrary to polyvagal assertions, respiratory sinus arrhythmia (the noninvasive index of cardiac vagal tone) is found in fish, snakes and toads, none of these species particularly advanced in terms of psychological processes associated with attachment, social engagement, love or emotional trauma. Furthermore the origin in the brainstem for control of  respiratory sinus arrhythmia is not consistently located in one area (i.e. not consistently ventrally situated, as in mammals):

https://jeb.biologists.org/content/jexbio/222/9/jeb197954.full.pdf

https://www.researchgate.net/publication/337094395_Heart_rate_variability_in_the_tegu_lizard_Salvator_merianae_its_neuroanatomical_basis_and_role_in_the_assessment_of_recovery_from_experimental_manipulation

https://advances.sciencemag.org/content/advances/4/2/eaaq0800.full.pdf

https://www.researchgate.net/publication/321252999_Analysis_of_the_respiratory_component_of_heart_rate_variability_in_the_Cururu_toad_Rhinella_schneideri/fulltext/5a170288a6fdcc50ade602d8/321252999_Analysis_of_the_respiratory_component_of_heart_rate_variability_in_the_Cururu_toad_Rhinella_schneideri.pdf?origin=publication_detail

Plus one article below from the Porges laboratory that contradicts polyvagal speculations about relations between oxytocin activity and brainstem mechanisms. Namely,  the results appear to disconfirm a hypothesis that there is dissociation of the brainstem dorsal motor nucleus and the nucleus Ambiguus, a point that the authors do not comment upon in the paper or elsewhere, to the best of my knowledge.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5768414/pdf/nihms932085.pdf

A BRIEF COMMENTARY AND HISTORY OF THIS PROJECT The classes of fundamental flaws documented regarding the polyvagal suppositions are numerous. Among others, they include 1) various misattributions regarding neuroautonomical structures and functions of brainstem centers; 2) incorrect assumptions of equivalence between actual vagal tone and its indirect, sometimes unreliable heart-rate-variability estimates; 3) unacknowledged methodological errors when employing such heart-rate-variability indices; 4) category errors equating complex psychosocial behavior with brainstem function;  and 5) disregard for the abundance of autonomic evolutionary evidence that refutes fundamental polyvagal assumptions.

Most of these points have been repeatedly dealt with and empirically supported in the updated RG questions and project to which I have contributed, as well as in two 2007 publications which I coauthored with renowned psychophysiologists and perhaps the premier evolutionary biologist of the vagus and the autonomic nervous system, E.W. Taylor. Above I have focused once more upon the weight of evidence countering the mistaken evolutionary assumptions presented within the polyvagal assumptions. As mentioned above, I have attached links to very recent papers published in biological publications that are usually not read or noticed by psychologists, psychophysiologists, medical practitioners nor psychotherapists. The above articles are authored by the leading experts in the area of the evolution of and the comparative biology of the autonomic nervous system—obviously including the vagus and the parasympathetic nervous system. These new papers merely add to the overwhelming evidence that the polyvagal assertions comprise false speculations that may be harmful for the credibility of psychophysiology.  

To provide a rationale for my insistence in pursuing a critique of the polyvagal speculations, I provide just a bit of historical context. After EW Taylor and I published our 2007 paper and John Cacioppo, Gary Berntson and I published another article in the same year and volume, we felt confident that we had shown that the basic premises of the polyvagal notions were untenable on multiple accounts and that we had provided a brief, more plausible alternative model of relationships between cardiac vagal tone, heart-rate-variability indices and psychological functioning, a model we considerEd to be both more empirically accurate and more adequate, although still very rudimentary. We also found that that Steven Porges’  (the inventor of the polyvagal  suppositions) responses in 2007 to our papers addressed not a single major point we had made, and quite frankly, that his piece was completely tangential and irrelevant to our substantive arguments (please read all three papers and decide for yourself; if you come to a different conclusion regarding the relevance of Porges’ counter-arguments, I would be very grateful for a personal detailed note from you, which I would be happy to discuss personally or on RG).  

In any case, as the years wore on, although Taylor and my paper has been cited many times (840 times since publication, and over 100 times during the last year), the popularity of the polyvagal claims continued to increase, and thus it appeared that our arguments did not seem to be understood by the audience we had primarily attempted to address. So about 4 years ago, my colleague Ted (EW) Taylor contacted me to ask what we were going to do about these polyvagal inaccuracies.  The first idea was that he, another renowned autonomic evolutionary biologist Tobias Wang (https://scholar.google.com/citations?hl=en&user=lIk3KwQAAAAJ&view_op=list_works&sortby=pubdate ) and I would write an additional paper summarizing the earlier ones and adding newer evidence. After querying Wang and others as to why the biologists had never taken up a full critique of the polyvagal, I received several very similar responses to the email exchange I had with Wang, posted just here:

From: Paul Grossman Sent: Tuesday, December 01, 2015 7:07 AM To: Tobias Wang Subject: Re: Ted Taylor Thanks Tobias, By the way, what do you think of the Polyvagal speculations, and, if negatively, why haven't more evolutionary biologists of the autonomic nervous system come together to discredit it after 20 years? Is it just to inconsequential to what you all are doing, or do you see some value in Porges' ideas? I'd be curious for your opinions? Greetings again, Paul 

________________________________________

On Tue, Dec 1, 2015 at 7:22 AM, Tobias Wang wrote: Dear Paul, being very blunt and honest, I think we simply laugh at Porges. It is so obviously wrong, naive and without any bearing to all the data published :-) Perhaps it would be interesting to write another review going specifically towards criticizing his suggestion? I noticed that your review with Ted was cited a lot, but perhaps not so much amongst the evolutionary and comparative biologists? best wishes tobias

After much deliberation, I was afraid that another article would merely, once again, be over the heads of the readership I was particularly interested in reaching psychologists, psychophysiologists, physicians and therapists: this is not to be condescending, but the issues are multiple and very complex. They include some understanding of several difficult areas, including brainstem neuroanatomy and function, the evolution of the autonomic nervous system, the noninvasive and indirect assessment and estimation of autonomic functioning (i.e. vagal and sympathetic activity) and the interactions of psychological processes with each of the above.  I, myself, have been professionally occupied with these areas of investigation for 40 years and have repeatedly needed to rely on the collaboration, cooperation and patient counsel of specialists in each of these areas.  So with hindsight, I came to understand that the scientific veracity of this area would be very difficult for many psychology-oriented scientists to ascertain. I also thought that a more modern internet-based approach would reach a much larger audience than a journal article, and that it would allow readers to gradually familiarize themselves with these complicated issues, as well as to be able to exchange ideas and information, ask questions, and challenge my position. 

Therefore, I started this ResearchGate exploration of the polyvagal conjectures with the intention to have an open, educational and informative exchange.  I thought I could slowly lay out, explicate and discuss the substantial body of evidence that runs completely counter to the polyvagal assertions and that proponents of the polyvagal notions might present any supporting evidence I may have been unaware of or inadvertently neglected. We could then have a serious exchange that might lead to greater understanding of the critical issues for all those interested. I have continued to pursue these aims. However, after more than 40,000 reads of my RG documents, not a single piece of evidence counter to my arguments has appeared in RG or elsewhere, to the best of my knowledge. On the other hand, I have privately been the subject of repeated ad hominem attacks that claim I had already partially withdrawn my critiques (completely untrue), that I had actually plagiarized aspects of the polyvagal assertions (totally ridiculous and unsubstantiated ; I possess a copy of an email sent to someone else to that effect that I amhappy privately to share) and that I am  involved in some kind of personal vendetta against the conjectures and their author (equally untrue).  Nothing, in fact, could be further from the truth: if anyone is able convincingly to empirically demonstrate that any of my arguments are misguided, I would be glad to know and to revise my statements. 

Four years down the line, I am still waiting either for a constructive dialogue or a clear retraction of the polyvagal assertions.  And I will patiently add to my updates whenever my other professional obligations allow. 

Kind regards, Paul G.

Hi Paul,

I write about emotional trauma, healing and wellness, though I have a background in evolutionary anthropology. As you know its practically impossible for somebody within the therapeutic community to talk about trauma without talking about Porges. I'm wondering whether you have ever considered writing an article that would make your critique more accessible, and whether you'd either seek to publish it in one of the 'trauma' journals, or simply have it as a PDF that can be shared (not everybody wants to sign up to ResearchGate.).

These days most therapists in the trauma world have bought into the idea that there are two ventral nerves - a reptilian one that mediates collapse and a mammalian one that mediates social engagement. And because that is as far as their 'understanding' goes, reading about respiratory sinus arrhythmia isn't going to touch them unless they are led though that step by step and shown how that challenges the polyvagal.

I have a background in animal behaviour (which is more than most who explore trauma) and I can't follow much the science you cite. So, a 'counter-arguments to polyvagal for non-scientists who have adopted Porges' would be an incredibly valuable document. And if it could be published as a PDF so easily circulated that would be even better.

Best, Daniela Sieff, PhD

So thanks to your and others' work, it is now quite clear that RSA is not unique to mammals, and that Porges' evolutionary suppositions are incorrect. However I feel that Polyvagal theory has sparked useful discussions and practical therapeutic applications. On an essential level, what I have learned from Dr. Porges' work is that the limbic system can be regulated with feelings of safety and comfort (triggered by soothing visual/audio/touch social safety/love cues). This has a twofold beneficial effect on ameliorating trauma:

1. it allows the autonomic system to come to flexible homeostatic balance, rather than be stuck in sympathetic (fight/flight) or parasympathetic (freeze) dominance.

2. it allows the prefrontal cortex to come back online, thus enabling full cognitive/executive function and capacity to learn and play.

It seems very likely that the vagus nerve is the facilitator of this mechanism, due to its bidirectional functional connectivity between the viscera, brain stem (medulla oblongata), limbic system (amygdalae) and prefrontal cortex.

Similarly to the technically incorrect (as the exact lines between such hierarchies are a bit fuzzy) but useful metaphor of triune brain (mammal/reptile/invertebrate), Porges' hierarchy of arousal makes sense from a high-level evolutionary perspective. (i.e. freeze/digest, fight/flee/hunt/f*ck, shame/fawn/nurture/play)

Hi Paul, like Daniela and others, I too would really like a synthesis "for dummies." What are the basic, practical consequences for therapists if your critique of Porges is correct?

Maybe the practical differences help clarify the theoretical issue too?

Thank you again for your kind availability and for this interesting forum.

Best, Adriano

Dear David Lowenfels

Thanks for your reply and thoughts on the issue: it’s important to have an exchange on these matters. I insert my comments below in italics within your text.  

“So thanks to your and others' work, it is now quite clear that RSA is not unique to mammals, and that Porges' evolutionary suppositions are incorrect.” : 

The fact that RSA is not unique to mammals, of course, runs diametrically opposite to a very major supposition of Porges that runs throughout his polyvagal thinking. He bases his “mammalian system for love and fear” (Porges’ words)  and his derived assertions fundamentally on such a false distinction. So this error is central and not some trivial scientific error, so far as I can see.

“However I feel that Polyvagal theory has sparked useful discussions and practical therapeutic applications. On an essential level, what I have learned from Dr. Porges' work is that the limbic system can be regulated with feelings of safety and comfort (triggered by soothing visual/audio/touch social safety/love cues).”:

I think you may be making a category mistake here about relations between the limbic system and felt experiences of safety and comfort: the mind, or, in this case, the mind’s feelings of safety and comfort, cannot be somehow equated with the limbic system as the primary material substrate, if there is such a thing (which I doubt, even being the psychophysiologists who I am). Sure, I would agree that the limbic system and autonomic functioning are likely to be involved in producing and responding to emotional processes.  However, the limbic system is merely one complex system involved in the processing of emotions like love, sense of safety and comfort, which are pretty complex, and very personal, private and individual lived experiences in themselves.  There is not likely to be a one-to-one correspondence between limbic functioning and such private emotions across all people, and to focus merely upon the limbic system, or even more extremely upon vagal processes in the brainstem, seems problematic. In the end, we are talking about a particular human being’s experience in the world, and even the statistically significant differences in limbic activity to emotional experience between groups of people (e.g. traumatized vs. nontraumatized) represent merely one small part of it all—and that statistical significance typically masks the substantial variation between people in relations between limbic and emotional functioning (there is very likely to be huge overlap between groups in limbic function that simple reporting of p-levels hide). 

Furthermore, in the end, it is not the limbic system that we care about but the person herself.  For example,  I don’t think it helpful to present overly simplistic and fallacious “object”ifications of the suffering person’s experiences as “dorsal vagal shutdown” (as many trauma therapists apparently do), falsely reducing, reifying and gravely oversimplifying a person’s lived experience. Reducing a traumatic person’s experience to a brain event may not always be helpful and may even be sometimes humiliating to people. 

Finally here, when there is additionally a fundamental error within the chosen metaphor, things really can get dangerous: for example, to the best of my knowledge, no evidence exists that the brainstem vagal dorsal motor nucleus is responsible for any parasympathetic shutdown of heart rate during  episodes of emotional freezing or dissociation. However, there is a huge amount of evidence (to be found in my RG citations and older papers) that the dorsal motor nucleus has little or nothing to do with vagal heart rate control under any circumstances, and I can also find little clear support that massive parasympathetic surges even  regularly occur during those states. So very likely, even at best, we are dealing with a very, very flawed metaphor! Providing fictional narratives to therapeutic processes can be damaging for the credibility of a therapy (that may, none the less, be effective for very different reasons) and may turn out to be very harmful for clients or patients once they discover that the physiological explanations of the therapeutic process are wrong.  

“This has a twofold beneficial effect on ameliorating trauma:

1. it allows the autonomic system to come to flexible homeostatic balance, rather than be stuck in sympathetic (fight/flight) or parasympathetic (freeze) dominance.”:

Once again, the autonomic system is merely one part of an intricate system of behavioral response and adaptation. Of course, we couldn’t even get up from our beds in the morning without the sympathetic and parasympathetic adjustments to heart and body supporting the recruitment of energy. Still I would not say that those autonomic changes are central to my lived experience of rising from bed in the morning. The experience of my getting up is conditioned by a whole range of factors (how well I just slept, how much I drank the night before, how hungry I am, what I might have just done with my partner in bed, etc. etc.) that may affect my momentary autonomic responses but cannot be represented as the sum total of my autonomic function, or my autonomic functioning as the sum total of my perceived experience. Those things in parentheses above are the kinds of things that are of meaning for me. Autonomic responses merely facilitate my getting up but do not define it. 

“2. it allows the prefrontal cortex to come back online, thus enabling full cognitive/executive function and capacity to learn and play.”:

To be overly repetitious, cortical responses facilitate cognitive processes, learning and playfulness. They don’t define it, and there is a good deal of evidence that there is no one-to-one correspondence between emotional processes and brain areas or even brain networks (e.g. see Luiz Pessoa’s and colleagues’ papers—available on ResearchGate). 

“It is fairly obvious that the vagus nerve is the facilitator of this mechanism, due to its bidirectional functional connectivity between the viscera, brain stem (medulla oblongata), limbic system (amygdalae) and prefrontal cortex.”:

I think my repeated arguments above also essentially address this point. To pick out the vagus as a central operator seems wrong to me. My take is that the vagus should be considered more as a messager that simply mediates and moderates necessary physiological, typically metabolic, demands upon different systems of the body (like getting up in the morning, then going for a run). That‘s essentially where my model of vagal-psychological processes, briefly mentioned in my 2007 paper, is going. 

“Similarly to the technically incorrect (as the exact lines between such hierarchies are a bit fuzzy) but useful metaphor of mammal brain, reptile brain, worm/jellyfish brain, Porges' hierarchy of arousal makes sense from a high-level evolutionary perspective. (i.e. freeze/digest, fight/flee/hunt/f*ck, shame/fawn/nurture/play)”:

David, thanks again for your reply, which has allowed me to further work out my own thinking a bit more.  I hope I have provided a somewhat coherent and intelligible explanation of why I don’t think the polyvagal speculations provide a helpful metaphor for therapists or psychologists. Of course, any physiological explanation of private, idiosyncratic processes of lived experience (whether trauma, depression, joy or mindfulness, as I recently published) are metaphorical in nature and merely attempts to reify and objectify that lived experience (which can still be useful provided one keeps in mind what one is doing). However there are better and worse metaphors and representations of lived experience. And I find that the polyvagal conjectures are particularly problematic, since they present biological speculation as fact, which have already been disproven, and they ignore all evidence to the contrary. The mistaken evolutionary assumptions are one example, as is the misinterpretation of the specific importance of the vagal dorsal motor nucleus for aspects of social engagement and trauma. The lack of dialogue among polyvagal enthusiasts in this RG platform is another example, as are the repeated ad hominem attacks on my person.

Dear Daniela Sieff and Adriano Bugliani

Thanks for your interest. As I mentioned in my update yesterday, these issues are complex, and it’s not easy to provide simple explanations. That why I chose RG as a platform where I could address aspects of this issue more or less step by step, also providing links, texts and even sometimes graphs to illustrate key points. I also envisioned that there might be particular requests for clarification of specific points that I might try to address, as well as helpful, constructive dialogues like the one David just began with me. Even with some people not wanting to register in RG, I think this platform is a lot more useful than writing another paper that would certainly be read by far fewer people and be much more limited and dummed down than I would be comfortable with. Still let me think if I could eventually write something I could download here and elsewhere. However this is no easy task, and I have lots of other things to do around the whole very different area of mindfulness in science and society (for better and for worse).

Dear Paul, actually in your answer to David Lowenfels (thank you David) there's already something in the direction I hoped. Basically, I guess that a useful consequence of your discussion is that one-to-one, reductionistic brain-mind connections are not allowed by current scientific knowledge. As it seems, on the contrary, in the case of Porges? (I would be curious about what do you think of Van der Kolk's work). These connections are maybe still useful as metaphors (and one has to be transparent about this metaphorical nature with clients), and they were appealing to therapists who were working with "trauma" (which, in turn, is another pragmatically useful label and not an objective essence), given the well-known difficulties with such a clinical population.

Personally, as already said previously, I found sometimes useful to use brain-mind metaphors in order to relief these clients (or even just myself) from the subjective sense of being "stupid" or "crazy" because, for instance, of their "exaggerated" and hard to extinguish reactions. Thinking of it also in brain terms can soothe self-loathing—but this is not intended to diminish self-agency and the sense of working upon the problem: on the contrary, it just gives more gradualness, as in the case of training an atrophied muscle (another metaphor). It gives to clinical work a sense of step-by-step positive and specific work (mindfulness?), that can decrease hopelessness. Something like: the problem is "real" and big, and maybe you cannot solve it immediately, but the good news are that with steady, everyday work you can improve your conditions.

At least, I have this sense of very specific, concrete, everyday work with so called traumatized clients. Like "attach wires one at a time."

But, as you explain, the issue is extremely complex and nuanced, so I guess that this means that clinicians have to be very careful and tactful in using such complex knowledge.

I really welcome your careful and phenomenological approach.

Thank you!

Warmly, Adriano

Dear Paul Grossman Thank you very much for your ongoing work in keeping this RG discussion going and the thoughtful way that you are approaching using an Internet forum such as this. Particularly when this has meant that you have been subject to the ad hominem attacks you refer to and which should be anathema to the scientific community but unfortunately are not.

As a clinician I very much agree with the comments of Adriano Bugliani and David Lowenfels We need ‘simple’ metaphors (both for ourselves and) for the clients that we work with. But given that the functioning of the human mind and anatomy is anything but simple it is important that these do not ‘throw the baby out with the bathwater’ and defend into descriptions that are simply incorrect, as seems to have happened with the polyvagal work. While these incorrect metaphors can still be useful in clinical work as David says their longer term effects are likely to stifle development, potentially undermine clinical work when their incorrectness becomes more widely known (as it will in the end) and obviously feel ’wrong’ to those of us who wish to be as truthful in our clinical work as we can.

The popularity and spread of the polyvagal theory is no doubt strongly related to its simplification of something of something very complex in a way that can be helpfully applied to clinical work (and, I think, the amplification of this through the complex interactions of the financial, clinical, and popular worlds - but that is a whole other thesis in its own right!). In danger of stating the obvious, what we need are ways to present simply something extremely complex but that does not go over the line into incorrectness (as it seems polyvagal theory has done). Doing this is obviously not straightforward but might helpfully happen through collaboration between those on the strong science side (probably more represented on RG) and clinicians (most likely much less represented on RG).

Paul, I realise it is a big ask, if you you were able to write something summarising and as dumbed down as you are comfortable with that might help us (already dumbed down) clinicians take it the next stage in simplifying in a way that still manages to keep more of a hold on the truth than the polyvagal theory does... I guess one of the difficulties will be that to simplify in a clinically useful way we will need to make positive statements about how things work (“it is likely that...”; ”xxx is linked to yyy although the exact nature of the link is not yet clear”) and it may be that the science is not yet at that stage. While science may work (to some level anyway) through falsification of hypotheses, the everyday functioning of human minds tends to work on positive confirmation of hypotheses (with all the biases that we know this introduces).

Anyway thank you again for the excellent work on keeping this discussion going and I look forward to seeing, and maybe participating in, how things develop.

Thanks for this dialogue Paul Grossman. I have no contention with your evidence-based physiologic perspective, and the potential harm of reductionism. I also appreciate the synthesis of contrasting different viewpoints e.g. the four quadrants of Wilber's Integral perspective, ontology vs. phenomenology, etc.

One question I am left wondering about: is it possible to effect one branch of the vagus nerve and not have an impact on other branches? Is it not all connected bidirectionally? (Taking it even further, can we ever effect one part of a human being and not the rest?). I have also really enjoyed studying Thayer and Lane's Neurovisceral Integration Model which seems to be well-backed by heaps of neuro-imaging data (and lacking in evolutionary suppositions). As I understand the Model it illustrates how top-down and bottom-up vagal information flows work in synergy. It also informs how/why HRV biofeedback can have such positive and diverse clinical impacts across body/mind/emotion regulation, a topic of great personal interest to me.

Dear (Paul Grossman) Paul!

You're right, this discussion is like, or maybe better than, an excellent paper. I would like to quote it in three papers I'm working about at very different stages of publication (I also quoted your beautiful papers Daniela Daniela Sieff), one about "Psychotherapy and Ideology" (...), and two other contributions about two very difficult "complex trauma" clients of mine—clients who are dear to me now.

Does anyone know what is the best form to quote this discussion?

Thanks!

Dear Paul,

Your detailed response to David Lowenfels and then his futher response are very helpful. As research now finds the vagus nerve directly involved in transcripting cytokines in locations too many to enumerate, it is clear that the complexity of the design has given rise to something quite beyond the sum of its constituent neurological components and processes. Nonetheless, one thing is clear. Man is a highly stimulated animal. No other life form possesses the refined and peerless complexity of the human brain and its nervous system communication-control network. Man is designed for stimulation and our stimulation capacity defines everything from our intelligence to our creativity, industry and ingenuity.

Dear Paul

Thank you for your research and sharing it on ResearchGate - and particularly the several discussion threads on this and similar topics.

I have much to say but will hold fire for now.

However I think it would be good to be aware and perhaps connect up with the group of psychology researchers who are particularly focused on "outing" the myths in the psychotherapy field - and the dangers of mis-suing psychotherapy.

Notably Steven Jay Lynn and Scott Lilienfield.

Steven Jay Lynn (Scott is not on RG)

They are serious debunkers and have huge stature in the field.

And I could really see a chapter from yourself in perhaps the 3rd Edition of Science and Pseudoscience in Clinical Psychology?

https://www.amazon.co.uk/Science-Pseudoscience-Clinical-Psychology-Second/dp/1462517897/ref=sr_1_8?crid=1WBG2KM60NID4&keywords=scott+o.+lilienfeld&qid=1583852033&sprefix=scott+lil%2Caps%2C160&sr=8-8

Or in a new edition of 50 Great Myths of Popular Psychology.

- or perhaps we need 50 Great Myths of PsychoPhysiology?

My point being there are serious efforts to address the nonsense and non-science in clinical psychology, and publish to the wider public and the clinical psychology and psychotherapy field.

Your work would be a very valuable and needed contribution.

The other team that it might be worth connecting with is Richard McNally, Director of Clinical Training at Harvard University.

Richard J. McNally

He and his team do excellent research on memory and trauma.

(Although I can't persuade him to publish a 2nd edition of his excellent Remembering Trauma).

And are also debunkers of pseudoscience (his critique of the theory behind EMDR, has been consistent and rigorous for many years).

He has been very critical of both the diagnostic category of PTSD and the even more problematic "repressed memory trauma" psychotherapy - which is still very much in evidence.

This short paper by Richard is an excellent summary of the critique of many trauma based models (including Van Der Kolk):

Article Debunking Myths about Trauma and Memory

(I have yet to find a better, short, clear article on the issues - and we use this in our training courses).

McNally fleshes the argument in much more depth in Remembering Trauma - and I think connecting with him and his team on the issues around "freeze and amnesia" would be very fruitful - and they would much appreciate your work in this area - and vice-versa.

There is a lot more to say - but this is enough for now.

Please do consider publishing something in collaboration with others.

Very best regards

Mark R. Davis

Hi all,

I have been following this discussion with interest.

Edgar Comfort and I have prepared a set of three articles, the first just recently published, about a body/mind/emotion regulation technique known as Calatonia, created in WWII by Petho Sandor, a Hungarian physician who worked for the Red Cross in refugee camps at the time. His work is quite impressive in its results, and was born right from war trauma to treat the traumatize population. However, there are few quantitative studies (many qualitative all in Portuguese) and the articles we are writing serve the purpose of identifying some hypotheses about its neurobiological and neuro cognitive bases. The first one is about its relationship to the orienting reflex and the cascade of events from there that contribute to the autonomic regulation achieved with Calatonia. At the end of the article, we introduce the other hypotheses that will be discussed in the other articles, about 1) brain self-regulation and mentation produced in DMN, and 2) skin neurons and touch receptors as facilitators of homeostatic regulation. Article here: https://www.mdpi.com/671052

Stay well!

Anita

We need RCTs in cPTSD individuals. For example Human Touch vs Animal stroking. also correction of deficits in micronutrients (Magnesium) and Vitamins (D3). Psychological therapies have all been tried without much success (apart from healing with prayer). Prof Alan Guile has a case series of 45 using this procedure.

I‘m trying to maintain the main topic of this question. So please let us stick to scientific evidence about how the parasympathetic nervous system interacts with behavior and what evidence there is pro-and-counter the polyvagal speculations.

OK, use vagal nerve stimulation to see if it works in cPTSD.

This is a recognised treatment for depression as you know. Just stop the speculation, more action as Elvis said.

Article Cardiac Effects of Vagus Nerve Stimulation in Patients with ...

There are more studies similar to this.

I guess Polyvagal theory is aimed at people with anxiety +/- cPTSD (complex PTSD associated with Adverse Childhood Experiences).

My 35 year clinical experience is that cPTSD individuals can present with a label of 'chronic depression' (with shame / guilt / pervasive anxiety), largely resistant to traditional psychiatric treatments. I don't know of VNS being used in this group specifically, as the diagnosis is very recent in ICD11.

Not sure if VNS backs up or contradicts the polyvagal theory (which appears to be linked with a the theory of evolution). I never believe a theory built on another theory.

Paul Grossman thank you for this fascinating thread. It is a strange mix because you address the psychological field that has taken up the polyvagal theory without enough critical assessment, yet your answers are in terms of neurophysiology well beyond our training and comprehension. But of course we all want an accurate understanding of the cascade of responses to threat and how best to help our clients based on this.

I was in the process of writing an article on how the polyvagal theory relates to the aetiology and treatment of nightmares, and came across this thread. It was a relief in a way, because I was having trouble fitting some of the polyvagal assertions to my actual clinical experience of working with PTSD and nightmares. Like many of the therapists who have chimed in on this thread, I found the polyvagal theory to be a helpful metaphor, and my first impulse was a desire to retain it as such. However, reading further, I find that even as a metaphor it is not accurate and I am left wondering what can be salvaged from all of this because the world of trauma treatment has become steeped in the polyvagal theory. I wonder, what about this theory has made it so compelling? Some ideas:

We have a strong desire, as therapists working with the complex responses to abuse and suffering, to have a simple map that proposes a solution, a way of understanding what we are seeing that brings hope and humanity.

The theory also suggests that responses to trauma are, for the most part, beyond our control, so it is a theory that removes the stigma and shame from the entire range of reactions to trauma.

As well, it has indirectly educated an entire generation of therapists about the basic workings of the nervous system. It has brought the body into trauma therapy in a way that I think is very needed. It has stressed the importance of interoception, of including and privileging information from the body about states of response to cues of safety or threat, and an understanding that many of the resulting thoughts and behaviors are state-dependent. So many cognitive approaches treat trauma patients from the neck up, and this one focuses completely (maybe too completely) on what is happening from the neck down.

The theory speaks to all of us because we can relate to the physiological states described in the theory -- although of course the information about the nervous system response to threat predates the polyvagal theory.

Many people in this thread are asking what is salvageable from the polyvagal theory, and there are many good things that have come from it. However, if it is inaccurate, even as a metaphor, we need a new one. Our clients could grasp the polyvagal theory, see themselves reflected in it, and gain some relief. In seeking alternatives, I am drawn to the work of Bruce Perry, whose neurosequential model may provide a more accurate map of how trauma affects nervous system and brain development. But I am looking for other ideas and suggestions as well.

Oh, thank you, Leslie. This is such a good example of professional ethics and awareness.

I've studied Bruce Perry's model, and I'll have to look again, because I thought it was primarily developmental/child-focused, and might not apply to people who were traumatized in adolescence or adulthood.

Something that I have noticed, as a survivor of extended childhood trauma that left me dissociated and destabilized for many years, is the concrete essentialism that many of the polyvagal-associated trauma modalities promote about the brain and the nervous system.

It's why I was drawn to this thread. Something was very "off," but I didn't know enough about PV theory to know what it was.

This is a simplification, but the concept seems to be that once a trauma happens, a cascade of reliable and nearly identical effects occur and destabilize the brain and the nervous system forever: trauma as destiny.

I haven't found this to be true, and I know the brain to be far more elastic, self-correcting, and crafty than most trauma modalities give it credit for.

I am grateful that I didn't experience the bulk of my trauma healing in this modern ideology, because it's likely that I would become not well, but "trauma-informed," incorrectly locating all of my issues in some area of the mythological triune brain, or learning to track my polyvagal whatever, and essentially throwing a lot of neurononsense at myself.

I have many friends and colleagues (fellow trauma survivors) who are startlingly unwell, yet they can track and locate their behaviors in terms of their tragic traumatic residues, brain structures, and nervous system tics.

I know it's an important stage in healing, but it is painful to watch because I haven't seen it lead to wholeness or wellness. I am glad that you're looking elsewhere.

I am also grateful to Paul Grossman for continuing the lonely work of challenging a theory that has so many proponents (witting or unwitting), and has entered into the zeitgeist because it speaks -- not to what is actually occurring in trauma survivors -- but to a group of theories that are fashionable right now for many reasons.

We need to get away from this brain / neurocircuitry mush.

Evidence suggests that PTSD (and probably cPTSD) is due to perturbations of the immune system, specifically Chemokines and Cytokines.

See Zhang, L., Xian-Zhang, H, Xiaoxia, L. et.al. Potential chemokine biomarkers associated with PTSD onset, risk and resilience as well as stress responses in US military service members. Translational Psychiatry. 2020; Vol 10 (3) https://doi.org/10.1038/s41398-020-0693-1

I am a clinical psychologist who actually treats people with relationship problems. I do not use Polyvagal theory to help patients with emotional issues of attachment and bonding for reasons Dr. Grossman so clearly specifies. But I find it useful to mention Polyvagal theory to patients in terms of levels of arousal when giving some quasi-science rationale for meditation exercises. It is interesting that for some patients a science-sounding explanation motivates meditation.

Yes, we psychiatrists do the same with medical students; chemical imbalance in the brain leading to depression and psychosis, where as the truth is there is no evidence for this; more likely linked with immunology (microglial activation).

Interesting post, thank you for your expert knowledge and input to learn from.

In reference to PTSD, extreme stressors and long term release imbalances within the Immuno/endocrine responses this article may serve as a starter as to how long term release of cortisol within the body may suppress but also helps to balance IL-6 levels, the results are still inconclusive and further testing should be done. If psychologically the conclusion does not pertain to neurotransmitter imbalances that serve to override or deaden receptors further blocking normal synaptic response, than this article may be of interest to you. Article Relationships between inflammatory cytokine and cortisol res...

Thank you.

Presanna de Silve

Do you think that our explanations objectify the patient's problem, so they are more open to our suggestiions?

Anna Kun Hall Brant Lichner Prasanna de Silva Karla McLaren

I agree with your last answers that physiological explanations can sometimes be helpful for clients in psychotherapy, even when such explanations are simplified. However, they can and should be plausible and based upon real state-of-th–art evidence. The parasympathetic nervous system (i.e. the vagus) has been clearly implicated in behavior and psychological responses for greater than a century (the sympathetic system as well): for instance, increases in cardiac vagal activity slow down heart rate, whereas decreases speed heart rate up; gut vagal responses contribute to digestive processes; bronchial vagal activity will constrict the bronchial making it more difficult to breath, etc.). These are well known and established phenomena that can be built into narratives of physiological activation related to behavioral reactions to psychological changes. However fanciful stories contradicted by existing evidence (e.g. about “dorsal vagal shutdown” or reptilian vs. mammalian vagal responses) are not helpful because they simply don’t tell the truth. It’s like willfully importing fake news into how our own mind/bodies function. That can only throw patients off and make them wonder about the effectiveness of their possibly very beneficial therapy when they discover that the physiological explanation offered by their clinician is highly controversial or even plain wrong. So I would always go with physiological simplifications that have real hands and feet and not try to explain (in this case) why there is a ”poly” in the polyvagal speculations (which genuinely seems to be a misnomer). Just talk about how the vagus has been known to work for at least 150 years and maybe add in a few sympathetic ingredients, which have also been long established as absolutely vital in the psychophysiological literature. (And to the neurotransmitter issue in depression, it’s also probably better to say we don’t really understand how depression is expressed in the brain, but neurotransmitter substances are likely to contribute: modesty may be the best policy when one doesn’t have the answer).

Dr. Grossman. Thank you for your highly informative comments. I do not mention the Vagus nerve or any of Porges's home-spun concepts, except for one. Namely, that Social Engagement occurs within a moderate level of arousal, not too high and not too low. Is this real science? I certainly do not want to feed my patients with scientific myths, there is already far too much of that going around.

Interesting. So, PVT is debunked? Is anybody aware of an actual article reviewing Porges' work, to which he might respond? Thank you!

Apparently the efferent parasympathetic (cholinergic) action of the vagus only relates to 20% of its neural traffic. Is the remaining 80% afferent traffic considered parasympathetic, or something else? Vagal afferents are clearly involved with processing of emotions and environmental safety, though these functions recruit both sympathetic and parasympathetic networks. The Central Autonomic Network is apparently not so polarized. The phylogenetic nature of this seems to be irrelevant to psychotherapy (and as Paul Grossman points out, incorrect).

I came across this recent work I think is relevant to the present discourse: Article Uncovering complex central autonomic networks at rest: a fun...

I appreciate the continued conversation.

No matter how one looks at the physiology of the vagus nerve, we are still just scratching the surface.

Putting forward models in biology or physiology is hard because the statistical evidence is more difficult to secure than in, say, physics and causal relationships are even more difficult to ascertain. So much seems left to personal perceptions about which data to trust.

I do think we need models that we can test and refute. A refuted model is the best model when it leads to a better one.

It seems that several of you are looking for a rationale to teach affect regulation (emotional regulation/autonomic regulation) skills to the client. But I really do not think you need PVT to do this.

You probably want to be looking for research on arousal and threat monitoring, arousal and threat focus, arousal and threat interpretation/appraisal, as well as arousal and problem solving.

i.e. we can't "solve" (figure out) how to handle a social situation if our arousal is too high, we react with aggression or avoidance.

There's lots of work on this that was used for the basis for of designing new CBT interventions for anxiety etc.

So also research on habit and high arousal vs creative problem solving and lower arousal.

If I have time I'll try to dig some out. (It is common sense that we are more reactive when tense and nervous and more able to choose/select a response when less tense.)

Tone/tension in skeletal musculature is related to reflexes.

High muscle tone = strong reflexes.

The original source material for this is Edmund Jacobson's 1929 text on Progressive Muscle Relaxation.

But I will bet Paul has more recent research on this?

Patellar reflex and startle reflex are well known as measures of skeletal muscle tone.

(Hence the isometric tensing that your doctor has you do when your patellar reflex seems not present)

So we can build a strong solid rationale (that has "hands and feet"!) for both affect regulation and muscle relaxation (these are different, usually in synchrony, but not always) for social engagement (collaboration with others, learning with and from others and problem solving how to handle difficult interactions with others).

It seems to me that PVT has become a way for explaining the need for clients to learn emotional self-regulation skills.

But we simply do not need it. That rationale is there already.

Indeed emotional self-regulation is the very first step on the ladder of self-efficacy (Bandura).

And I would offer that Bandura's steps for the development of self-efficacy provide the most cogent rationale for client's acquiring emotional self-regulation.

Self-efficacy and socio-cognitive theory is right up there with classical and operant conditioning in terms of empirically based learning theories.

Children learn to self-regulate in order not to be "bound by the present moment" - and this is tied in with language development (as in self-talk for self-regulation) and the development of the imagination (the imagined presence of absent things). (see Vygotsky)

Clearly then the basics of self-regulation are even tied into our initial sense of time (else all is just the present moment).

I hope that helps shift the focus onto the relevant research areas.

Perhaps another way to view this clinically is with Paul Gilbert's compassionate mind work. He conceptualises 3 systems - threat, drive (challenge) and soothing which either arouse or calm the SNS and vagal activity. Improved HRV and thus emotional well being, are fostered, at least partly, through regulated breathing.

I am no expert and would suggest that anyone interested has a look at the work by Gilbert or books by him, Chris Irons and others

Can be the vagal activity only a compensatory phenomenon?

I’m starting to understand why do experts measure increased sympathetic and/or decreased parasympathetic activity in a hypoarousal state, (e.g. in depression). I have understood it from social defeat experiments. @Charly Brouillard

https://www.researchgate.net/publication/343410370_Social_defeat_Vagal_reduction_and_vulnerability_to_ventricular_arrhythmias

In this case, clinically decreased sympathetic and increased parasympathetic activity prevails (which is hard to doubt) - the hypoarousal is complete. But the researchers measure just the opposite. It should relate to permanent bradypnea/hypercapnia (supposed intracellular acidosis) which occurs during chronic social defeat experiments. @Charly Brouillard

https://kopernio.com/viewer? doi=10.1152%2Fajpregu.00021.2016&token=WzE2ODMwMTYsIjEwLjExNTIvYWpwcmVndS4wMDAyMS4yMDE2Il0.7Ir_kY_BDN0t4gx3fpndIWO5OJk

At the same time, feedback systems will trigger increased adrenergic and decreased vagus answers. (Compensatory mechanism cannot reach their target due to reduced sensitivity. I am convinced that this derivation is close to reality, which would also explain the controversy surrounding polyvagal theory, too. I look forward to your meaningful answers!

Isn't the problem one of trying to measure a rose with a ruler? Having applied and adapted PVT for the past 15 years within the context of a bodywork practice and Pat Ogden's Sensorimotor approach, I must admit that I don't use most of the scientific core of PVT. Instead, I find that Neuroception along with a generic division of human behaviour into three zones (1) fight-flight/Sympathetically doninated, (2) normal range, and (3) Parasympathetically dominated - is the most useful part. I agree that it's mythological, and that is a prioblem. I have actually seen people get a lot of benefit, and then abandon what they found experientially useful because some asshole who read an article they only half understood told them that it wasn't scientifically valid. Such is the modern world. So if there is another formulation that is more scientifically valid, I would be very interested, but considering the infinite nuances of human adaptation the likelihood is that it would still be measuring a rose with a ruler, and in practice still have as many holes.

It seems to me, Andrew, that you've highlighted one of the major issues, without identifying it. The necessity for "scientific validation" of almost everything now, without addressing the serious dissonance between "science" (as defined by the material scientists) and the ART of psychotherapy (and what is "normal" and case appropriate). That this is also laboured by those who call themselves experts in Medical Science, when the practice itself relies on at least 40% of its' practice, "Because it works", is a travesty!

Yes, I wish the trauma healing community would just stop trying to open a can of science on what they're doing. It's a mess.

They're still talking about the triune brain, lizard versus neocortex, and all sorts of bollocks for goodness sake, and that's been known to be dead wrong for decades.

These easily disconfirmed theories are really getting in the way of this community creating a functional model of what they're doing and how it works. It's okay if it's an art, and it would be wonderful for people to be able to say that without shame.

Hear, Hear!!! Thank you Karla!

I'd also add that the constant focus on "trauma" is unhelpful. True it must be recognised, and at the same time resilience must also be honoured; the capacity, in the first place, to make it to a therapist's door id barely noted, and "empowerment" is a term which simply feeds therapist's egos and breeds dependence.

Marie-Christina

I agree with you about "trauma". Calling everything "trauma" is an exeggeration that does not promote growth of our understanding of people's emotional problems and tends to reduce most client's difficulties to problems with attachment. This is humbug. I treat teenage girls who are well attached to their mothers yet struggle with a gamut of emotional problems that are existential to the human condition, not a result of "trauma".

Yes, I wonder how much of these "trauma and attachment" issues are just an over-personalization of people's natural responses to the increasingly toxic and unjust world we humans have created for each other.

I would love it if there were such a thing as a practicing clinical sociologist who could help people understand that their seemingly private issues are a response to inequality, environmental degradation, political instability, and injustice.

Without that larger view, I wonder if the individual-focus of psychology tends to support the very structures that oppress people?

It is not “calling everything truama”. Amd it onyl clouds the issue if you are mis informed about the approach. Yes, i ahree that scince often overteaches and peope try to use The idea of “science“ as a sort of validation or justification to procedures. When one begins to understand epistemological foundations of real things, then we find that “science” is just a procedure. It is a series of procedures. It doesn’t say anything about what is true or what actually exists. It “practices” and reveals outcomes to those practices, but the practices are always negotiated all the timeTrauma informed” does not mean that we are disgnosing

... sorry, my stupid phone browser will only allow me to see so much of what I’m commenting. So I have to post it and then continue what I was saying.

Yeah idea that science is giving us truths is just a kind of religious faith. Science is a way of doing things which perpetuates itself for knowledge. But this knowledge is just about practice. It doesn’t give us true things of the universe.

... “Trauma informed” approach to mental health, means that we Are not reducing the individual to a manifestation of problem. As though somethings wrong with the person. There is nothing wrong with anyone. Trauma informed means that the issues that the people are dealing with is due to a trauma. There is no absolute formulation of what this trauma means across humanity, rather, it is what the individual has experienced that, for themselves, for their unique individuality, amounted to a trauma that is informing them to behave in a certain way