Dear Paul,

I am not aware of published studies but you may want to contact Martin Bohus at ZI Mannheim. His group has investigated dissociation in the context of Borderline and PTSD and they have used peripheral as well as central psychophysiological assessments.

Best, Jürgen

Not sure about dissociation as an adaptation, but I am quite sure that the life-threatening event that triggers the initial dissociation would be associated with a significant bradycardia as the body goes into death preparation mode.  Also, in continuously monitored preterm babies and babies in the ICU, bradycardias are a common response, and indeed in people with severe enough sleep apnea to have significant oxygen desaturation (and really most don't despite what people assume) the response to the desat is a bradycardia.  And thanks Jurgen for the referral, I did not know about them.

Thanks all 3 so far.  Johannes, the paper you refer to shows an increase in heart rate, NOT DECREASE AS WOULD BE EXPECTED by polyvagal ideas!  Also Phyllis, of course vagal activation does occur under certain circumstances tied to metabolic demands, but you provide no evidence that dissociation with life-threatening events produces bradycardia. Your certainty needs, for me, to be backed up with evidence. The assumption that trauma can cause potent vagally mediated bradycardia is what I would like to examine. That particular physiological events can produce vagally mediated bradycardia in infants or others is well known, but that isn't the issue. If you have clear evidence, I would be grateful if you would share it. Jurgen, thanks also. I'll ask Martin if he has published relevant data or has unpublished findings that are pertinent. I also hope others will chime in. Greetings, Paul

Actually after taking a closer look at the paper Johannes mentioned, even the High-frequency heart-rate variability (HRV) changes (I.e. respiratory sinus arrhythmia, (RSA) or as also so often erroneously named "cardiac vagal tone") do not correspond to the assumptions of the polyvagal propositions: according to them, there should be sudden decreases in heart rate unaccompanied by changes in RSA, since the "reptilian"dorsal motor nucleus ought to be responsible for heart rate reductions but without increases in RSA; otherwise it is the "smart"  mammalian nucleus Ambiguus that is in charge. This does not occur.  

And it seems rather clear that the very assumptions about how the Dorsal motor nucleus (DMN) functions is at odds with the rather substantial available scientific evidence, that finds 1) the DMN has little or nothing to do with heart rate control& 2) it may also show rhythmicity

I wonder if this reference would be relevant to your interests:

Griffin, M. G., Resick, P. A., & Mechanic, M. B. (1997). Objective assessment of peritraumatic dissociation: Psychophysiological indicators. American Journal of Psychiatry, 154(8), 1081–1088.

and possibly this one:

Williams, C. L., Haines, J., & Sale, I. M. (2003). Psychophysiological and psychological correlates of dissociation in a case of dissociative identity disorder. Journal of Trauma & Dissociation, 4, 101–118.

There is a bit of evidence that dissociative experiences are associated with reduced heart rate, but aside from these two articles, I don't know of any others.  Perhaps more recent articles have cited these two?

Check this out.  There's a section on HRV.  :-)

Thanks Rose and Mimi, so far the papers you cite don't seem to provide any clear evidence of vagal heart-rate decrease during or around dissociation. If at all, there is an mildly attenuated heart rate response, and in Griffin et al. study that attenuated response might be more do to sympathetic reduction, as suggested by the skin conductance decrease than anything necessarily vagal.  But maybe someone else knows something?

That's a awesome and useful article that you posted above Leonhard Kratzer!

Maggie Schauer (the citation posted above by Leonhard Kratzer) seemed incorrectly cite Sierra et al.,2002 as a study that had showed "decrease in heart rate when [patients] became depersonalized". The same seem true for Kelly & Walter, 1968. I found an interesting proposal in Sierra et al.,2002's study that people high in alexithymia may have the same autonomic mechanism as patients with depersonalization. I was going to suggest the same because people with high EOT factor of alexithymia (with mind and attention withdrawn from affective stimuli processing, Wiebe et al., 2017) did not show higher HR decrease or other vagal activation in response to affective stimuli (films) compared to  people with low alexithymia in my study (Davydov et al., 2013).

Thanks Leonard, Tina and Dmitry,  Dmitry is correct that the Schauer & Elbert paper, cited by Leonard, is wrongly cited. Thanks Leonard: The Sierra et al. paper measures sympathetic skin responses and find attenuated SYMPATHETIC, NOT VAGAL, EFFECTS! The Kelly & Walter paper focus on forearm blood flow response in various groups of clinical diagnoses and also do not directly address dissocative responses. I haven't read the Lader papers, also cited,  in a long time and do not have them available. However, I  am familiar with his 70's work and can't recall him coming to the recent paper's conclusions either.  I would also not know why we should be focused so specifically on the parasympathetic, since sympathetic activation and withdrawal seems every bit as significant in the literature (as suggested by both the Sierra and the Kelly&Walter investigations. 

 The Schauer & Elbert paper is, indeed, an interesting theoretical piece, but without any apparent direct empirical support (e.g.fainting as an example of cardiac vagal exaggerations not that paper  is not the same as dissociation). I, however, am looking for data here, not other theoretical models that merely PROPOSE  huge vagally mediated heart-rate declines during psychological dissociation. AND NONE of the papers that article cite provide any direct evidence of profound vagally mediated heart rate decrease. 

Also small decreases in heart rate or small attenuated heart rate reductions do not fit the assumptions of the trauma specialists (like Schauer) who assume really very huge vagally mediated heart rate dives as a late phase of trauma , which they assume is dissociative. 

It would be interesting if anyone has any reliable data, but so far, not. Any relations to polyvagal speculations in trauma therapy and research are predicated upon this assumption.  Of course, even if there might be such a real phenomenon, it seems very unlikely that it occurs via the dorsal motor nucleus (a primary further assumption of polyvagal notions), since the DMN has never been demonstrated to play any significant role in parasympathetic heart rate control in humans (or rats, for that matter).

I find it fascinating that these ideas have such a broad audience of believers, and no one (so far) can come up with any evidence at all after several decades. Still maybe  this will yet happen. I remain open to be wrong (certainly would not be the first time). 

Anyhow many thanks so far, and I hope the discussion continues. 

Mimi, sorry I meant you, not a "Tina". My apologies. 

Paul, I think, it should be another central mechanism associated with autonomic (re)activity explaining dissociation as a coping mechanism with trauma. In my study I found the same attenuated sympathetic reactivity (SCR and PTT) as in Sierra et al. paper, but associated with alexithymia as a protection (mind and body decoupling) mechanism. Different terms (dissociation and alexithymia) might describe the same phenomenon. High heart rate changes (both higher decrease or higher increase) from baseline detected the same higher level of involvement, but in processing of different affective stimuli.

Paul, maybe this is one of the articles you already found that shows small decreases in a subset of the study participants who were assessed to be more dissociative.  I came across the article today.

No literature I'm afraid but let's step out of Porges' cerebral logic and into the real world of survival, and that of our ancestors in whom 'fight/flight' became our hardwired response to mortal danger. The same threat that would trigger dissociation would presumably trigger fighting and fleeing. Porges would have to explain how a mechanism that produced large decreases in heart rates helped our ancestors to escape.

Mimi: In dr. Chou et al.'s study (you cited) a 'regression to the mean' effect was not controlled for while their groups differed in baseline HRs (higher in LSG).

Thank you Dr. Davydov,  your comments are very helpful.  I'm struggling to contextualize my dissertation research, which included HRV measures....So it's very helpful to hear how reported results are interpreted/viewed/what would have made them more clear... etc.

Thanks Mimi and Dmitry. I think there are several problems in this context relating the Chou et al. paper Mimi sent. First of all, the paper does not examine how dissociating persons respond in heart rate to various challenges, but how people rather arbitrarily divided into 3 groups, based on startle responses, may differ in psychological measures and heart rate to a film task. This is not the question above. Secondly, the number of dependent measures is much too large for any reliability of results with just some 60+ participants: there were at least 13 scales or subscales assessed among the psychological measures, and the likelihood of spurious results and somewhat of a fishing expedition is great. Thirdly, although the peak increases to startle were different, the decelerative phase from peak to trough were pretty similar (Fig. 2), certainly not evidence of a profound cardiac vagal burst in any group, and the LARGE startle group showed the greatest heart rate drop. Finally, of course, startle is not dissociation. 

Thank you Dr. Grossman.  Your detailed answer is so very helpful to me in developing an understanding of this area!  I appreciate your taking the time to craft it. I shall thinking about it and revisit it many times.

• With the large number of  relevant  scientists ssubscribed to ResearchGate and the lack of any supporting evidence, can we assume that there is no available evidence for assumptions that trauma and psychological dissociation produce profound decreases in heart rate? It seems that this assumption at this time  is merely a belief, rather than a hypothesis based upon empirical physiological evidence. 

Paul, how about distinguishing between the actual trauma event where there is a response to something that is overwhelming and lifet hreatening, and the triggered response later where the dissociation is a way to manage the trauma memory?

Hi Phyllis, If you could provide evidence of profound heart-rate drops to either condition in humans, it would be helpful toward answering my question. Also showing that such drops were not accompanied by increases in respiratory-sinus-arrhythmia amplitude (i.e. high-frequency heart-rate variability) would provide further much needed support for the so-far non-existent evidence for so-called "polyvagal" speculations.

However, merely posing the distinctions, above, that you do, does not provide an answer to my question. Rather it creates a new corollary hypothesis that  waits to be tested. From the sparse literature, cited and reviewed in this rather meager exchange, there does not seem to be any concrete evidence that large heart rate drops occur during later triggered dissociative responses to traumatic memories, which seems to be the idea at the base of trauma therapy assumptions regarding relations between trauma and cardiac parasympathetic responses. 

If you are aware of such evidence, please share it with me and the other readers of this exchange. Of course, anecdotal perceptions don't really satisfy. 

I am genuinely open to be proven wrong about my own deep skepticism about things termed "polyvagal" (I often put quotations around the term, since I think it is an unfortunate and misleading choice, even were there some truth to its underlying suppositions: poly means many, not just two, as in the two main brainstem nuclei of parasympathetic control [with only one having been demonstrated, over and over, to influence heart-rate phenomena, like cardiac vagal tone]). 

However, the longer it takes for ANYONE, including proponents of these notions, to come forward even with the very slightest of directly supporting evidence--after more than 20 years to begin to gather some, and no positive response to any of my questions among 4000+ readers--the more I wonder how anyone can take these ideas seriously, unless they are prone to being true believers or to religion.  

Often in books and journals authored by proponents of things polyvagal, the topic is treated as established fact. My evolutionary biologist colleagues find this laughable, and I think they are the most knowledgeable group to know. I have encouraged them to debunk the errors in evolutionary thinking they find so  blatant, and which actually EW Taylor and I already actually did in 2007 (if psychologists might take the time  to deepen their understanding of  relations between autonomic evolutionary biology, heart-rate variability, caricature vagal tone and psychological phenomena [e.g. traumatic responses] in order to understand what we wrote: I don't mean to be disrespectful nor arrogant here, but genuinely feel our treatment of the topics in that paper assumed a greater underlying knowledge of the areas than psychologists generally have the time and training to have developed--and I am sorry we did not try to make things simpler to comprehend). Unfortunately, these evolutionary physiologists specialists are apparently too busy to get involved in the psychological literature that they are, anyway, unable to take seriously. At least that has been my honest experience with perhaps the top physiologists in this rather small field.  

So, Phyllis, thanks for your comments, and I hope we can keep the exchange going. I wouldn't know why proponents of the "polyvagal" would not be interested in publicly debating ideas that they hold dear to them, if there are truly interested in scientific investigation and inquiry. Actually such open platforms as ResearchGate and PubMed Commons really opens things up much more, and offers more timely point -and-counterpoint than the limited and staid journal exchanges of the past--provided opinions are clear and backed up by available and sound published research. That is what I am after here. 

Warm greetings, Paul  

Dear Paul,

I’m chilled by your project, and feel thankful to inspire this dialogue.

A) I see that you with the other commenters processed many papers (I noticed here works from van der Kruijs, Bohus, Griffin, Williams, Lader, Sierra, Kelly, Schauer, Chou). I would like to discuss with you some further papers, from the book edited by an other column of Polyvagal Theory, Frank Corrigan, https://books.google.hu/books?id=RziDAwAAQBAJ. Here they mentioned bradycardia several times, linked it to parasympathetic activity, and I try to summarize to work cited:

1.       Pereira, 2010: deep-brain stimulation of ventral PAG in humans elicited increased HF-HRV component, which might refer rather to parasympathetic than sympathetic activations, right? http://www.sciencedirect.com/science/article/pii/S0014488610000464

2.       but Bandler, 2000: no mention of vagus or parasympathetic tone (rather sympathetic).

3.       Richter, 1957: sudden death in hopeless situations (’voodoo death’) is linked to parasympathetic and not sympathetic overactivation in rats: https://scholar.google.hu/scholar?cluster=10698908573364346084&hl=hu&as_sdt=0,5

4.       Hofer, 1970: the arrhytmias observed in rodents in immobilization or feigned death state can be elicited by the stimulation of the vagus. https://www.researchgate.net/profile/Myron_Hofer/publication/17653931_Cardiac_and_Respiratory_Function_During_Sudden_Prolonged_Immobility_in_Wild_Rodents/links/54f888970cf2ccffe9df5444.pdf

5.       McNally, 2005: Meeting with an autobiographic trauma script showed rather nonsignificant increase in heart rate (examples are collected in the book, https://books.google.hu/books?hl=hu&lr=&id=88Axi0huzYwC&oi=).

6.       Schore, 2001: cited many works that linked traumatic dissociation, the conservation-withdrawal strategy to the parasympathetic system. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.130.917&rep=rep1&type=pdf. In fact, in one of his earliest works (1994), he already mentioned this https://books.google.hu/books?id=1IT4CgAAQBAJ&lpg, and referred to the postulates of Engel and Schmale (1972).

Are we heading to create thorough critical review of the literature regarding this topic ;)?

I added further questions on your project wall (which aspects of the Polyvagal is proved?), and my related projects wall (what are the polyvagal implications regarding health, placebo, non-violent communication, self-awareness and compassion?) https://www.researchgate.net/post/What_are_the_theoretical_implications_of_Porgess_Polyvagal_Theory_for_health_body-mind_connection_communication_Were_these_implications_tested please check and comment.

Article Cardiac and Respiratory Function During Sudden Prolonged Imm...

Dear Benedek,

Thanks honestly so much for entering this exchange and providing the links to the various papers and books. First, a comment about the polyvagal speculations, in general: Porges bases his ideas upon the assumptions that 1) the dorsal motor nucleus (DMN) is an evolutionarily more primitive center of brainstem parasympathetic control than the nucleus Ambiguus (NA); and 2) bradycardia elicited by extreme emotional circumstances (like trauma-related dissociation) is due to DMN efferent activity to the heart. Neither of these assumptions appears to be correct: There is consensus among evolutionary biologists that there are huge species differences among fishes, reptiles (and birds) with respect to whether dorsal brainstorm centers (corresponding to DMN) or ventral centers (corresponding to NA) are responsible for parasympathetic control of heart rate. Even the results of Porges own study on 2 species of lizard was flawed due to inappropriate measurement of heart rate variability (see Grossman & Taylor, 2007, as substantiation of all the above points; available from ResearchGate; also a host of more recent evolutionary papers by EW Taylor or T Wang, among others; also a number of recent papers further documenting that human parasympathetic control of heart rate is only or at least almost exclusively under NA control, with no existing evidence that the DMN plays any role at all in humans (see documentation at https://www.researchgate.net/post/After_20_years_of_polyvagal_hypotheses_is_there_any_direct_evidence_for_the_first_3_premises_that_form_the_foundation_of_the_polyvagal_conjectures

Hi Benedek again,

Regarding the issue of trauma-related bradycardia, we have to keep in mind a few things:

1) If this actually occurs in humans, it need not at all be support to the polyvagal notions: This may and strongly appears to occur via the NA (since the DMN has not been implicated I vagal heart rate control in humans or other mammals). As Schore writes this may simply be a hypometabolic cardiac response to immobilization, since the parasympathetic system is largely responsible for quick-acting changes in metabolic activity (from sitting to walking to running). So it is possible that there is bradycardia without providing the least support for polyvagal ideas.

2. I am of course curious whether we even see this bradycardia among humans during dissociation. So far, also from the literature you provide that I could gain access to, even with animals (e.g. the Hofer paper), it seems inconclusive from the Table 2: with species pooled,there was no significant effect with 17 animals. There actually appear to be substantial in only a very few animals, maybe 5, and at least 8-10 animals showed almost no change or increased heart rate during immobility--not very convincing!

If you come up with clear evidence of this phenomenon of severe bradycardia, particularly among humans during emotional stress of some sort, I remain open to thev idea (although it had no direct bearing upon Porges' speculations). What you have cited seems--at least so far--based on indirect inferences regarding bradycardia. But please correct me if I am wrong.

Dear Paul, to sum up, the polyvagal premise "Neurogenic bradycardia is mediated through the DMNX in humans" seems to be FALSE, since the parasympathetic innervation of the mammal heart is from NA almost exclusively. Moreover, such bradycardia was not consequently reported in very stressful situations or dissociation.

Question: even if decrease in heartrate is not obvious, what about decrease in RSA e.g. during dissociation (which would be also suggested by the polyvagal)? Do you know about papers where the connection between RSA and fear, anxiety, dissociation vs. safety, social support was analyzed?

Thanks Leonard! This paper provides no evidence for freezing and bradycardia among people with borderline personality, a group far more likely to engage in dissocative responses than healthy controls. Quite the opposite is stated: "This study investigated automatic fear bradycardia (indicative for freezing) and emotion avoidance in BPD patients and healthy controls. As expected, BPD patients did not display bradycardia in response to unpleasant pictures compared to neutral or pleasant pictures, regardless of emotion avoidance tendencies." 

Given that no one has come up with a single example of confirmatory evidence,  should we not assume there is no research that documents large heart-rate decrease during episodes of psychological dissociation? What does this imply for biological hypotheses which relate trauma-related freeze-like responses to cardiac vagal activity? 

Most recently, Hagenaars and colleague have been conducting a number of studies that bear upon this issue. They find evidence of reduced movement (which they suggest may be "freezing" is associated with a gradual 7 beart-pe-minute decrease in heart rate over a 30-s period of viewing unpleasant pictures. However, this affect was only found for healthy controls, NOT for traumatized individuals, who showed no differences to pleasant, unpleasant or neural pictures. 1) This certainly doesn't fit the assumptions of much of trauma theory, I believe; 2) the heart rate changes are very quite gradual and more in line with the slowness of sympathetic effects upon heart rate, rather than the very rapid vagal effects; 3) the 7-bpm effect with healthy controls could have been merely an effect of normal cardiac decreases due to reduced metabolic activity as physical activity lowered; and 4) a 7 bpm decrease in heart rate Is stilll rather small and is not, by definition, bradycardia (which is a profound decrease). All these findings, however, further call into question the strong influence of the vagus in heart rate reduction inane freezing among trauma patients.

https://www.researchgate.net/publication/315060449_Reduced_Freezing_in_Posttraumatic_Stress_Disorder_Patients_while_Watching_Affective_Pictures/fulltext/58c9460792851cdbae9c803a/315060449_Reduced_Freezing_in_Posttraumatic_Stress_Disorder_Patients_while_Watching_Affective_Pictures.pdf?origin=publication_detail&ev=pub_int_prw_xdl&msrp=UfePzsHY1Nigk3uuRkp0ovItkDzcu6_yVgEK-6osyd5sQjo4VtpbvSrObWgJxs8pQZkc0uoP9RFx7_OMzOQGf75bbaP8Rbm_T9h6VaVJKEhHV9g5J7Os-F8I.US73wjZOZhCGD1cu8n4qw6aZWN8Mj0eCZJMpeuYp8Nc6jk3nq_fcvllNzaytyVem9dDX9XUQHYaN0zRoI5Lr2omTgU5Zqldx343YmQ.XrJ7W59QbA-DYA0sl5Ie-BKOYZH3CBTxA3I_fwrTDf3NGNKd5Y53hYuJImn6pf3FpyGCuPmC2rNy2yua-aIJ7IWCPRid8j8kO9VOZw.E_bTFnF5H2ae6vTUoshGL3r3xA-CUf-PaQdMqrGSFVq7WbVwOeSSX2OE-FzBHKzpbOzI_3CsIYSaf7xiIIcEcsviu9PHQtH2pt74vw

Article Reduced Freezing in Posttraumatic Stress Disorder Patients w...

Dear Mr Grossman,

First of all, I would like to thank you for initiating this discussion. As a medical doctor with specialization in anaesthesiology, a psychophysiologist and a trauma therapist, I am extremely interested in gaining a full insight into the physiological driving forces that trigger bodily reactions in my clients.

Clarifying the mechanism of mentioned bodily reactions would provide a foundation that would help a lot of people suffering unnecessarily due to lack of adequate treatment.

The number of individuals experiencing PTSD is on the rise, and neither current psychotherapeutic methods nor the conventional medicine has proven themselves to be fully effective. This represents one of the burning issues of our time, medically speaking.

Conclusion, based on the review of the available papers on the cognitive and related type of therapies, is that those methods, unfortunately, display only the short-term positive effects. In that light, the need for further research becomes obvious.

The connection between the ANS, the social engagement and the active and passive defense in the situations of stress or “bad memories” is apparent for clinicians, and all that without the paramount being to determine which part of the nervous system is activated in those situations. The exact phylogenetic age of the structure responsible is also not taken into account by practitioners.

Laboratory research studies have come to different, often contradictory findings, and we, the clinicians are grown used to being sceptical to every new piece of information that is being presented.

Different economic factors have managed to diminish the quality of the scientific production in the last 70 years. As an anaesthesiologist, I have encountered multiple practical issues while having to follow the standards imposed by the experimental studies.

Namely, the standard requirement was to use beta- blockers (before the surgery and applying anaesthesia) in patients with variable (unstable) heart rate. I will not go into a more detailed discussion of this matter, as this is of no interest to the readers of this debate, but this practice had some serious repercussions. The protests from practitioners were futile. At that time, as it is today, the research was reserved for the ones “socially correct”, the ones with the access to sufficient financial means and for the projects making a profit for the pharmaceutical industry. A couple of years ago, it was discovered that the 10 key papers in this area of study were forged, so the previously imposed standard was abandoned, the fact that joyed lots of medical practitioners.

That is why I am extremely interested to hear your take on the matter and to examine every relevant fact that needs to be tested. Still, I do not fully understand, the overall effect that is accomplished by creating the “academic storm in a teacup“. I am under the impression that your approach would be served by slight refocusing of the key area of interest. RSA does not represent a perfect index for the cardiac vagal tone and I do not believe that doctor Porges comes to this exact claim anywhere.

Cardiologists, anaesthesiologists and other clinicians monitor every single patient they treat and are fully aware of the fact that the RSA depends on multiple factors. That, in turn, does not mean that two different vagal nuclei do not influence heart rate. Nor does it mean that those nuclei do not activate (perhaps even multiple centres) in situations evoking great fear. You are certainly aware of the existence of studies that refute your claims and that in many of those studies, more than two distinct centres responsible for vagal control of the cardiac rhythm are mentioned. ( [i])iologyr the cardiac vagal tone m učestvujete u ovoj akciji i tako pomognete ovom mladom čoveku da pobedi opaku bolest ali i noThis is especially true in the situations of the social engagement. The newest findings mark a distinction between research performed on animal models and the ones performed on people. It becomes clearer that "It is, therefore, surprising how little modern research has been done to elucidate how this human difference emerged. It appears that we are sometimes so seduced by similarities between species that we neglect the differences."[ii]

What is the significance of these differences? The recent findings have uncovered that for example, “bad memory” is not only located in limbic area but also possesses control regions in the neocortical area.[iii] I interpret this as a urgent need for psychosomatic approach in working with traumatized patients.

You asked a following question: Does anyone know of research documenting large heart-rate decrease during episodes of psychological dissociation?

Firstly, I would like to remind you of the vasovagal reaction, in other words, sudden decreasing of heart rate, and sometimes even full stop of cardiac activity due to intense fear. Working as an anaesthesiologist in the operating room for 32 years, I had the opportunity to witness lots of vasovagal reactions in extremely frighten patients.

In my practical work, I differentiated between two levels of fear: The first one that activates the sympathicus and increases the pulse in patients, and the second one that reduces the pulse. I was always more afraid of the latter. Atropine that is commonly used in these cases, does not always resolve the issue. That very fact is known in literature. (That could imply that the blockages stem from different vagal nuclei.)

I would now share an episode from early stages of my career. As a young doctor, I lost a patient on the operating table. She told me before the surgery that was afraid of dying in the OR. Unfortunately, she did die in that very operating room right in front of me. As a result, I dedicated the rest of my medical career to psychophysiology, defending my PHD thesis on fear of the anaesthesia and the operative intervention. The fear was estimated by measuring the level of cortisol as well as the vital functions in selected patients. I was very surprised to find out that the levels of cortisol in extremely frighten and totally dissociated patients were low. Those findings did not fit in what was known at that time about stress response reactions and the activation of the HPA axis and the releasing of adrenaline and other so called stress hormones. The explanation of the low cortisol levels in extremely frighten patients, I later managed to find in Porges^ theory. It states that in the situations where the extreme fear is experienced, the vagal tone is increased, but not the symphatic one.

I have experienced this personally, and that led me to contact with the clinical psychologist and neurophysiologist that is working with Somatic Experience, Trauma Releasing Exercises and Neuro Afective Relational Model as well as some other methods that search for the explanation of the effectiveness of their practice in the Polyvagal theory. The mentioned methods have been developed independently of doctor Porges, but, with his clinical experience, he contributed a lot to proving the efficiency of these methods. Namely, he introduced the usage of the Body perception Questionnaires and the Integrated Listening Systems for professionals. I currently apply these methods and I use a pulse oximeter in my work in order to monitor the HR (heart rate) in my clients.

Still, I would have to tell you that it is not always the case that the HR decreases during the dissociation of the patient in a therapeutic session. Why? I do not know and I am thinking out loud: The clients have different previous experiences and the traumatic memory in them differs. It is dependent on the reaction of the patient, if he/she attempted fight or flight. That is why some of the patients have high cortisol levels while others do not have it. The treatment of the second group is usually more demanding and complicated.

In addition to that, I have witnessed a lots of vagotomies in my, nearly 4 decades long medical career. Those vagotomies did not lead to full stop of the vagal control of the digestive tract, so this stopped being our method of choice. The discussion here was about the proving of the role of multiple collateral of n. vagus which take over the role of the main one, but also here the role of the dorsal and the ventral vagus could be discussed.

My suggestion is for you to set up a multicentric clinical study and to study this hypothesis in work with clients.

[i] https://www.ncbi.nlm.nih.gov/pubmed/26371169

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure.

[ii] Evolution of the neocortex: Perspective from developmental biology) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913577/

[iii] https://www.sciencedaily.com/releases/2013/08/130827091629.htm

Dear Ms. Sarah Zorica Mitic,

Thanks for your comments. We both agree to the importance of understanding psychophysiological aspects of trauma, as well as the importance of autonomic mechanisms, and the limits of science. However the polyvagal suppositions comprise an attempt toward a coherent scientific theory, so that we are not residing in the world of pure metaphor nor religious belief. In this your dismissal, just below, of my examination of these ideas is completely unjustified:

"Still, I do not fully understand, the overall effect that is accomplished by creating the “academic storm in a teacup“.

First of all, I present substantial evidence, supported fully by other experts in evolutionary biology and cardiovascular physiology, documented in ResearchGate, that the fundamental premises of the polyvagal suppositions, stated by Porges himself in his book, are wrong, period. Please remember that that a premise is defined as "an assertion or proposition which forms the basis for a work or theory" (Oxford English Dictionary). So if one is even vaguely interested in a scientific basis, this is anything but a storm in a teacup. Of course, I do think faith and belief are valid motivations, but we should then recognize the difference to scientific thinking.

Along another related line you state:

"RSA does not represent a perfect index for the cardiac vagal tone and I do not believe that doctor Porges comes to this exact claim anywhere."

In fact, in many publications, Porges claims to measure "cardiac vagal tone." He even has a patent on a machine he called the vagal tone monitor. He also writes about using a measure to construct a concept of cardiac vagal tone:

"This was followed by the introduction of cross-spectral analysis (Porges, 1976) as a strategy to describe the coupling between respiration and heart rate and the application of spectral analysis to define a construct of cardiac vagal tone (Porges, et al., 1981). Porges, Biol Psychol 2007, 4: 116–143."

In his premise 4, he states that the "ability of NA to regulate both special visceral efferents and general visceral efferents may be monitored by the amplitude of RSA. (P. 193)." In doing so, he claims that respiratory sinus arrhythmia is not only a close measure of cardiac vagal tone, but also of vagal influences upon other organ systems (e.g. lungs and gut), which has been proven for many years not to be the case.

I could go on and on with quotes where it is claimed that RSA equates to vagal tone.

With respect to the evidence regarding the influences of the two major brainstem centers upon vagal heart control, you write:

"You are certainly aware of the existence of studies that refute your claims and that in many of those studies, more than two distinct centres responsible for vagal control of the cardiac rhythm are mentioned.."

I don't know whether you were intentionally trying to be offensive, but I certainly take umbrage to your remark that I am hiding studies that would refute my claims. I know of none, only a host of studies, also cited and downloadable in ResearchGate, which refute the polyvagal claims that the dorsal motor nucleus (so-called dumb vagus) can exert anything but very small effects upon heart rate, and others that indicate no effects. Here Porges misleads when he attempts to provide evidence in his book:

"Research supports the importance of the unmyelinated vagal fibers in bradycardia (Daly, 1991) and suggests the possibility that massive bradycardia may be determined by the unmyelinated vagal fibers associated with the DVC [dorsal vagal complex] recruiting myelinated vagal fibers to maximize the final vagal surge on the heart (Jones, Wang and Jordan, 1995)."

In fact, Daly (1991) did not investigate this issue at all. On the other hand, the Jones et al. paper found no to very small effects upon vagal heart rate of different animals (rats, cats and rabbits), definitely nothing in the way of any possibility of being responsible for "massive bradycardia." Take a look yourself, since each paper can be downloaded from the internet.

Also, my ResearchGate contributions have been dedicated to exchange of information in this regard. Despite many thousands of reads over 2 years, there has not been one single offer of evidence contrary to my position. Please explain how this could happen if I was covering up research?

Additionally thanks for the papers, but they had really nothing to do with my critique of the fundamental premises of the polyvagal.

Lastly, and also related, the vasovagal fainting response (which may be quite different in nature than emotional freezing) has never been tied to the dorsal motor nucleus but there is a plethora of studies indicating it is mediated by the nucleus Ambiguus (just check Pubmed or google scholar yourself, if you don't believe me).

But thank you for allowing me to further formulate my position, and I of course welcome any reply, but hopefully one that takes what I am doing in good faith.

Friendly greetings,

Paul Grossman

Dear Mr. Grossman,

thank you for your reply. I am sorry for the misunderstanding that has occurred. Please, allow me to explain myself in more detail. As you already know, I am not a native English speaker, so the meaning could be misinterpreted by the less fortunate non-native phraseology. The cultural differences between us could also contribute to the lack of the precise and complete comprehension. I would kindly ask you to forgive me if I my contribution to this discussion could be viewed as anything else than constructive and well meaning. Here, I apologize if what I wrote came across as offensive in any way. I can assure you that it was never my intention. My goal was to ignite the motivation to reach the common target.

The phrase -Storm in a teacup- was intended to have a light hearted, purely humoristic component. As an anesthesiologists, I have slightly different perspective in my daily work, than one purely scientific. I am actively engaged in saving lives, so the prompt and precise reactions are of vital importance. I am therefore, interested in methods immediately effective in my practical work.

Mr. Grossman, I am not your opponent. I have taken my time to find and read some of your published papers. Had some of these been published some years earlier, I am sure that they would have been referenced to in my own PHD thesis.

Still, I would kindly ask you to consider the matter from my point of view. We, the clinicians have finally got the tool to explain, to some extent, the occurrences we have been witness to, in our daily jobs. Of course, all of our conclusions are tentative ones. I am aware of the fact that there are still none controlled clinical studies that could directly prove the clinical significance of the Polyvagal theory.

Still, the theory is of great practical importance to us, especially while working with the developmental traumas.

This is exactly why I have asked you in my previous letter to set up a clinical (not laboratory) study which would determine what happens to clients that dissociate. Let us seriously monitor what is going on with them through the whole therapeutic process.

There are a lot of institutes around the world that could potentially be interested in that type of study, as well as in connecting the qualified experts with the opposing views on the matter. Well being of the patients is the first and foremost priority for clinicians. Who set up a theory that explained our work is without a doubt, crucial in scientific terms, but quickly becomes obsolete in the practical context.

I find it somewhat peculiar that you and me discuss the Porges’ theory while he stays silent and, as you say, does not make an active effort to communicate with you.

You are critically oriented towards the Porges’ polyvagal theory, so please give your contribution by gathering and explaining your findings in form of a book. Do confront his theory on the adequate level and give us all the opportunity to refocus.

As far as my faith goes; as Jew living in the post Holocaust era ( with relatives suffering from PTSD caused by the Holocaust)as well as my own experiences I had during one war in which I was an active medical volunteer for several years , I could safely say that I am not religious.

Respectfully

Dear Sarah, Thanks for your last mail and clarifications. I suspected that part of the difficulties and misinterpretations might have been caused by language issues and nonetheless admire your ability to communicate in my native English!

About things polyvagal, I haven't written a book about the topic and won't. However, my 2007 paper with perhaps the most eminent and experienced evolutionary biologist of the autonomic nervous system, EW Taylor, goes a long way toward refuting the polyvagal suppositions (on multiple grounds) and is easily available to download and dive into. The fact that Taylor had the desire--or even felt the need--to debunk the polyvagal assumptions about the evolution of the vagus should cause pause to reassess acceptance of Porges' notions regarding the two brainstem vagal nuclei. After all, Taylor--and Tobias Wang and others, who have similarly chimed in--are the real experts who have dedicated their professional lives to studying this area, not Porges who is a psychologist with limited understanding of the topic. So I would ask what could be "the clinical significance of the polyvagal theory" (as you mentioned), if the basic tenets are already considered to be wrong by the leading experts whose studies those experts believe to have been seriously misinterpreted by Dr Porges (that 2007 paper is clear evidence of this particular point)? Wouldn't you think it more appropriate that it should be up to Dr Porges or his followers to come up with some evidence after 20 years that his evolutionary ideas make sense? Shouldn't he and/or Peter Levine come out of their silence to reply to Dr Taylor and myself, rather than suggesting that this is too adversarial (actually the hallmark of scientific progress) or rely on other vague arguments to maintain their silence? The current situation has even come so far that rather than to welcome such dialogue, I was first delighted to have been invited some 2 or 3 months ago to give a talk on this topic at the 2018 Potsdam international conference of somatic experiencing, only to be disinvited just 2 weeks ago.

So in light of this very one-sided conversation with the polyvagal proponents, I welcome exchanges, such as ours, in the hope that this may stimulate dialogue, not hostility or unpleasantnesses. True science includes the willingness (and maybe even satisfaction) of proving oneself wrong, just as much as refuting the ideas of another. Anything else is business as usual: greed, aversion and delusion entering into the supposedly sacred objectivity of science.

My best guess is you could continue to do good therapeutic work without relying on a theory that seems extremely likely to have no foundation. Based on my reviewing his book "Walking the Tiger," Peter Levine appears to have initially developed the major aspects of his therapy, without any awareness of the polyvagal suppositions. My assumption is that the therapy worked fine without this very questionable biological rationale, and that it was added in order to provide a "scientific" physiological justification for Levine's therapy. So that the therapy was not developed as a consequence of intimate prior knowledge of polyvagal speculations. If I am correct, this means that a potentially valuable and effective therapy has had, very likely, an erroneous physiological basis added to it later to enhance the scientific credibility of the therapy. It's too bad if the physiological premises that were chosen appear to be so false (there are certainly more plausible explanations, but that is really another topic). However, that is exactly what I suspect, based upon lots of already existing evidence, which I do cite in my paper and ResearchGate contributions.

Consequently, I think the onus of proof is not upon those critical of the polyvagal theory, but its proponents. And this is anything but a trivial or peripheral matter for trauma therapy. In the end, it may well determine the very credibility of this therapy to the scientific community. Anyhow, that is the way I analyze the situation, but remain open to others' counter-arguments, if they are aired and make sense.

My genuine thanks again for entering into this discussion. And please DO ACCEPT that I hide nothing, that I realize that I am fallible and that I would be very willing to consider new evidence that challenges my reasoning (if it should ever appear, which, to the very best of my knowledge has not yet happened).

Friendly greetings, Paul

I have also tried to understand the "dorsal vagus response", as I understand it from models based on the Polyvagal Theory. While there is a plentitude of research on the RSA, there is very little that I can find on the unmyelinated dorsal vagus response. In theory, you should get bradychardia. But the few studies I find say that bradycardia also depends on the myelineated vagus.

Pure unmyelinated stimuli gives (a short episode of?) bradychardia, followed by quick shallow breathing that in theory should be related to sympathetic activation (and withdrawal of the myelinated vagus). Dorsal vagus activity is also related to "sickness behaviour", but bradychardia is not (as far as I can tell) part of that.

And the fainting reaction, the only research I can find have results of a combination of a withdrawal of the function of the arterial baroreceptor system, followed by a short period of deep breaths which causes the blood flow to the brain to be very instable, followed by fainting or pre-faint symtoms.

I would be more than happy if someone could present a better model on the actions of the dorsal vagus system. I am not testing this, I have only done litterature research on it because it is valuable in my clinical practice, but there is certainly an area that needs more research and scientific confirmation.

With regards

Tomas Waldegren

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Vagus Nerve as Modulator of the Brain–Gut Axis in Psychiatric and Inflammatory Disorders

In order to get an answer to that question, you would need to go from the field of psychology to the field of somatic medicine. In somatic medicine, you could find a sound amount of evidence, mostly from medical practice and not from a laboratory. It is not considered ethical to perform experiments on humans that can lead to a temporary heart stop.  It is virtually impossible to recreate conditions in a laboratory  where the patient fears for his/her life. I worked as a medical doctor, an anesthesiologist for 35 years and I had  witnessed, a lot of occurrences of that type in cases where the patients were extremely frightened. One of my terrified patients died while on the operating table, and that lead me to dedicate my work to psychosomatics and I even wrote a doctoral thesis on the subject: Fear and anesthesia. In addition to that, I am an active trauma therapist and I constantly monitor pulse in my clients. Then you can clearly see when the client dissociates.

Sarah Zorica Mitic

More than a year later . . . I would love to get more information from you if I could. I'm a feline veterinarian, and I'm intrigued by a cluster of puzzles about feline physiology that may all involve different functions of the vagal nerve or its branches. This is far less urgent and imperative than the vital work that you are doing, of course. But given that even rough data are so difficult to obtain, perhaps we could find some information that might help, even if it's to serve ultimately as a contrast between species.

Cats uncommonly have what are presumed to be vagal episodes of collapse while undergoing cystocentesis. This happens routinely enough that we are trained to monitor for it, but not routinely enough for us to study it well. And GP vet clinics usually lack the resources even to write up such cases in detail. Despite numerous reports, only in 2015 were the first two confirmed cases reported of cats collapsing during cysto with the expected bradycardia and hypotension, occurring in hospitals that were able to monitor them with enough detail for publication.

Vets have anecdotally reported similar-appearing collapses in cats after severe vomiting or even constipation episodes, or even manipulating an esophageal tube in a patient with multiple problems.

Cats under anesthesia have had plummeting heart rates and blood pressure apparently triggered by exteriorizing a pancreas, manipulating eyes during ophthalmic surgery, or even neurologic stimulation such as clamping a testicle.

Usually the cats recover uneventfully - not always. And the usual common-sense treatment is atropine, IV fluids, possibly some short-acting corticosteroids. These treatments are just based on what we think is going on, not based on any study results. And we have no good data whether the cats are recovering better/quicker/more often because of them, or regardless of them, or even in spite of them.

The usual explanation is just that some part of the vagal nerve is getting directly tugged on or otherwise activated, out of the usual "rest and digest" context. Yet the fact that cats can collapse and, rarely, die from a side effect of vomiting or straining in litter box would seem to indicate that something remains to be explained.

And the fact that cats seem to be more prone to these than, say, dogs is also slightly baffling, since cats are reputed normally to have a unusually high sympathetic tone, as befits a species with limited social needs and occupying a dual ecological niche as both small predator and prey animal.

There is also the more mundane puzzle (yes, owners ask this!) of why terrified cats (and various other mammals at least) who are cornered sometimes lose bowel or bladder control, since cats in this state are in the highest sympathetic state imaginable, and so shouldn't be suddenly manifesting parasympathetic functions - certainly not these ones, anyway, if scents could lead a predator to follow them easily.

Something like Porges's polyvagal hypothesis could accommodate explanations for these puzzles. His main contribution would be that the some aspect previously categorized as parasympathetic, perhaps the vagal nerve, has complicated and sometimes contradictory functions, and that these may be related to the "freeze" response.

The actual anatomy of different autonomic functions here is less important clinically except to neurosurgeons, and it may well be species-specific. (I want to see research into the vagal nerves of marsupials!) The evolutionary development of them is even less clinically important, and probably very complicated, and no doubt will be fascinating.

But Porges's distinctions between apparently opposing functions of the parasympathetic nervous system seem extraordinarily useful clinically already, and possibly immensely fruitful for future studies. And I haven't seen any criticism of this part of his hypothesis yet that hits the target at all.

Cats, incidentally, seem to go into a mild cat version of a "freeze" response very frequently on a vet exam table. And usually the heart rate and blood pressure will be higher than normal. Then again, with cats, that may be a combination mode of fight-or-flight and freeze, becoming immobile and thus less visible until they can fly up into the nearest air duct.

So far, answers to the puzzles I've mentioned would benefit cat vet med slightly, in perhaps guiding treatment of "vagaling" cats and cats under anesthesia.

But any cat veterinarian deals with feral cats and "problem behavior" cats too, and another goal of mine would be to understand how to prevent these cats from being terrified and how to understand and decrease what seems to be a common feline analogue to human PTSD. And any insights for these could massively improve feline welfare for us cat vets internationally.

Apologies for the length, and best wishes, and thanks for your work.

Barbara Goodrich , Hi Barbara, I think your assessment of the Porges polyvagal Model is not at all justified by the evidence. To the contrary, virtually all the physiological evidence contradicts the main assumptions of the polyvagal speculations. Please see my ResearchGate questions on the polyvagal, and I would be glad to discuss it all afterwards, whether you are supportive or not of the evidence I present. Much of it is also redundantly described in our RG project on things polyvagal. The gist is, though, after 4 years and some 55,000 reads, according to RG stats, there has not been a single scientist who has presented any data that directly supports the polyvagal premises, nor a single challenge to the evidence that contradicts those assumptions. However, we should always remain open.

On the other hand, parasympatheric mediation has for a very long time been known to mediate physiological responses to environmental and internal changes in behavior and activity. So a simpler model of autonomic effects might support your ideas, without employing them highly questionable assumptions suggested by polyvagal conjectures.

Thanks so much, Markus!!

I think the question you are asking here is not recognising the reality of normal situations. The human sensory-motor-ANS-[everything else} does do one thing that's quite simple, in that it usually goes to a high energy/Sympathetic externally oriented response (no matter how brief that response might be) before going to Plan B and trying a vegetative/dissociative/Parasympathetic/internally oriented response. So the Parasympathetic/dissociative response ALMOST ALWAYS ALSO contains an element of sympethetic arousal somewhere inside itself. So yes - if someone does the full hibernation thing and ends up in a coma, they will exhibit bradycardia. But most dissociative responses stop short of full coma/hibernation/organ failure.