Hi Benedek,

You pack a lot of questions into one question, so I have decided to respond by giving you two questions that may help you move towards answering some of the points you are interested in. When looking closely at polyvagal theory. research has mapped out contingencies that explain in more detail how polyvagal development and functioning shape behaviour. My question to you is, what is the relationship between these contingencies (the adaptive system varies across people depending on these contingencies) and the development of adaptive or less adaptive behaviours. Then extend this question by correlating the more person-and small group related contingencies with the broader external conditions that support adaptive functioning versus less-adaptive functioning (I suggest to be precise when defining them). One area of interest that intersects with another question you posted at a different time is resources (such as the work of Hobfoll and Antonovsky). 

Research related to both  my questions is available and may help build a foundation towards answering your questions. My knowledge from clinical psychology is that these variations matter considerably as the macro-level functioning (societal level) is intricately interwoven with the micro-level functioning of people (intrapersonal and interpersonal) and vice versa. I am interested to see  how your project is unfolding,

Angela

Dear Angela,

Your quesions and comments assume that there is support for the most basic premises of the polyvagal hypotheses. That does not appear to be the case (see Grossman & Taylor, 2007). There is no evidence that there is anything such as polyvagal development.  This appears to be a hypothetical construct without empirical basis.  

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

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

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

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

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

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

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

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

http://www.repositorio.unifesp.br/bitstream/handle/11600/37466/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): 1000-1009.

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

BASIC PREMISES RECENTLY STATED BY SW PORGES:

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

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

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

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

Various evidences in contradiction to Premise 1 provided earlier in the project comments.

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

 Dear Paul, thanks for your detailed answer. 

Even if precursors of the ventral vagal complex (VVC), and even if the function of VVC (e.g. respiratory sinus arrhythmia (RSA)) had evolved in fish already, theoretically, later in the mammalian evolution RSA could be associated to social engagement. So I have the following open questions:

My question: is RSA connected to socio-emotional processes? Do you know a detailed review on the connection between social engagement and (cardial) physiology? 

Does social engagement improve the functioning of the immune system, e.g. reducing inflammation, or decrease perceived pain? Through the parasympathetic system? Is it reflected in RSA?

What is the nature of social engagement? Is it nonviolent? Is it activated by lonely self-soothing or self-compassion?

Thanks Benedek for your thoughtful questions. I would like to throw the ball back to you asking you and others carefully to evaluate the literature on RSA and social engagement:

1) From the several meta-analyses and individual studies I have reviewed, it appears that the effect sizes of this relationship are small (Cohen's d approximately 0.3 overall). This means there is an overlap of distributions of those competent vs. less competent in social engagement of about 90% regarding RSA differences. Given the publication bias that positive findings are consistently overreepresentedvin the literature, the author bias of those interested in this relation being disposed to find positive effect sizes, these biases also indicated in some of the meta-analyses by statistical tests, and the weak relations found anyhow, how convincing is the notion that RSA is a highly relevant biological marker of variations in social engagement? If this relationship was so important from an evolutionary standpoint, shouldn't the effects be clearer?

2) Respiration rate and volume are known to confound the relation between RSA and cardiac vagal tone, particularly within individuals between also sometimes in analyses across persons. These respiratory parameters may also be influenced by aspects of social engagement (e.g. We know breathing is very sensitive to variations inemotion and psychological tasks). Very few of the relevant studies have taken these respiratory parameters in account when examining RSA and aspects of social engagement, or have appropriately adjusted for respiration when they have. Is this not a necessary first step before making assumptions about the importance of the vagus for social engagement?

3) Regarding RSA as a marker of individual differences in cardiac vagal tone, can we really assume it is just that? There are multiple indications that at very best, it is a moderate index of cardiac vagal tone and may be worse than resting heart rate (I have cited numerous references in my own ResearchGate question/blogs). At best, RSA is a marker of vagal influences upon heart rate, not even a maker of parasympathetic effects upon other aspects of cardiac function, e.g. how excitable the heart ventricles are or the level of contractility, not to mention that individual differences in RSA do not correlate strongly with individual differences in markers of bronchial or gut vagal activity. So how are we to believe that RSA is a good index of general level of vagal tone that affects the whole organism, when individual organ systems are not correlated? And that is the clear implication of the social-engagement/RSA literature.

4) It has been known a very long time that the parasympathetic nervous system subserves a very broad range of physiological functions--in regard to the cardiovascular system making sure that enough oxygen quickly gets to the necessary parts of the body that are active at different tasks, e.g. physical exertion, eating, lovemaking, speaking, etc. That this extends to biological substrates of psychosocial functioning is nothing at all new. What is new is the fixation upon the vagus as the predominant player. Interesting in the 70's and 80's, it was all about the sympathetic nervous system. Our psychobiological functioning is far more complex than even the workings of these two systems, with lots of local events at the organ levels integrating and interacting with autonomic influences to determine dynamic functioning. So is there sufficient grounds to hypothesize that the vagus is somehow the primary player, especially since the main theoretical assumptions appear false and the applied empirical,evidence is weak at best?

Very frankly, I guess I see psychologists attempting to grasp at biological explanations of behavior and psychological functioning that are far too simplistic. They become confused by varying opinions among different authors because they have not ventured beyond the "psychological vagal tone" literature. They are right to assume that the vagus plays some role in the body and brain's rapid responses to life's vagaries (so do sympathetic processes and more complex interactions with local factors, often giving rise among physiologists to the idea that the heart has its own little brain and the gut too). So shouldn't we rise from this vagal fixation and simultaneously explore more parameters than RSA (even heart rate, by which RSA is determined fails to be reported in most of these RSA/social engagement studies and could have substantial bearing on interpretation of findings)?

Dear Paul, I'm thankful reading your clear and detailed answer again. Since I agree with your answers and points, I guess there is no other step left for me than plan a research where the connection between these variables and RSA can be tested :).

Is there a paper that stated this effect-size of RSA-social engagement statistical connection? Even if the effect-size is small, what is your suggestion, 1) how and why social engagement alters RSA, 2) what kind of social engagement has the strongest connection, 3) why this connection appeared in the evolution? 

Hi Benedek,

I think it might be useful further to test and tease apart relations between RSA and aspects of social engagement. However, particularly because each of those terms represent complex phenomena with diverse underlying processes, it is important to precisely define and operationalize your measurements and hypotheses, e.g. 1) exactly what do we mean by "social engagement"-relations with strangers, friends, intimate partners, under conditions of challenge, relaxation, conflict, neutral conditions, just to mention a few of many dimensions; how generalizable is whatever we are measuring to other aspects? 2) Is RSA a proxy for individual differences in cardiac vagal tone or within-individual change of cardiac vagal tone (CVT)? Particularly in the latter case, are changes in respiration clouding the RSA-CVT relationship? Are you implicitly assuming that CVT, even in this limited indexing by RSA will somehow reflect overall variations in vagal tone (of which the literature already clearly says no!). 3) What are your precise, prestated hypotheses for your study, and upon what evidence do you base these?

These are just a few issues I miss in most of the existing literature I have reviewed that would be valuable to include.

About the meta-analyses of effect sizes, if you just use Polyvagal and meta-analysis together as keywords in google scholar you will get to the relevant studies. And you will see that the effect sizes tend to be modest in most cases, so far as I can see.

Why should CVT be implicated in social engagement? It's involved in all of our activities to help keep activity in balance with metabolic demands (how the vagus affects things other than the heart rate cannot be predicted from RSA, or at least all current evidence strongly suggests that) . In my opinion, it has no special "smarts" for social engagement, just has been around during the various species-specific modifications in social behavior and had adjusted with them over evolution. There appears to be no such thing as a "smart" and a "dumb" vagus, although there could be such a thing as "smart vagal research" which I hope you will perform.

Also Hope these points are useful. I suggest you try to contact emeritus Professor Mark Kollai from your university. He is a leading expert on cardiac vagal tone, although I don't know whether he is available for discussions.

Greetings Paul