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Fundamental challenges and likely refutations of the five basic premises of the polyvagal theory

Reference 38 NG-BIB-038 Polyvagal Theory, Social Connection & Loneliness Physiology
Evidence reader Fundamental challenges and likely refutations of the five basic premises of the polyvagal theory
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Abstract

The polyvagal collection of hypotheses is based upon five essential premises, as stated by its author (Porges, 2011). Polyvagal conjectures rest on a primary assumption that brainstem ventral and dorsal vagal regions in mammals each have their own unique mediating effects upon control of heart rate. The polyvagal hypotheses link these putative dorsal- vs. ventral-vagal differences to socioemotional behavior (e.g. defensive immobilization, and social affiliative behaviors, respectively), as well as to trends in the evolution of the vagus nerve (e.g. Porges, 2011 & 2021a). Additionally, it is essential to note that only one measurable phenomenon—as index of vagal processes—serves as the linchpin for virtually every premise. That phenomenon is respiratory sinus arrhythmia (RSA), heart-rate changes coordinated to phase of respiration (i.e. inspiration vs. expiration), often employed as an index of vagally, or parasympathetically, mediated control of heart rate. The polyvagal hypotheses assume that RSA is a mammalian phenomenon, since Porges (2011) states “RSA has not been observed in reptiles.” I will here briefly document how each of these basic premises have been shown to be either untenable or highly implausible based on the available scientific literature. I will also argue that the polyvagal reliance upon RSA as equivalent to general vagal tone or even cardiac vagal tone is conceptually a category mistake (Ryle, 1949), confusing an approximate index (i.e. RSA) of a phenomenon (some general vagal process) with the phenomenon, itself.

Keywords

Respiratory sinus arrhythmia; Heart-rate variability; Polyvagal; Vagus; Parasympathetic; Cardiac vagal tone; Ventral vagal nucleus Ambiguus; Dorsal vagal motor nucleus; Neuroanatomy of the vagus; Autonomic; Vertebrate evolution; Sociality; Measurement of respiratory sinus arrhythmia

Introduction

The polyvagal hypotheses (e.g. Porges, 2011, Porges, 2021a) propose that the mammalian autonomic nervous system is comprised not only of two branches (sympathetic and parasympathetic): the parasympathetic branch can be further meaningfully separated into two additional systems, 1) a brainstem, dorsally situated vagal area and 2) a brainstem, ventrally located vagal area, in which each system exerts its own distinct influence upon vagally mediated heart rate control, and each is tied, respectively, either to defensive behaviors of immobilization or to prosocial responses.

According to the polyvagal hypotheses, the brainstem dorsal vagal motor nucleus (DVMN) putatively mediates massive slowing of heart rate (i.e. bradycardia) during phases of extreme fear- or threat-induced immobilization (emotional freezing or human psychological dissociation), for which sympathetic fight-or-flight reactions may not be adaptive. These supposedly dorsal vagal responses are characterized in the polyvagal literature as evolutionarily “primitive,” observed in “vertebrates that evolved long before mammals” (Porges, 2021a). The ventral vagal nucleus Ambiguus (nA), on the other hand, is seen as an advanced mammalian adaptation to promote modulation of heart rate and self-calming instrumental for affiliative social behavior. Activity of the ventral vagal nA is proposed to be enhanced during conditions of safety and positive social contact. Whereas the existence of the brainstem dorsal and ventral areas has long been known in vertebrate autonomic physiology, vagal neuroanatomy and evolutionary oriented comparative biology, the assumptions about the functions of each vagal area made in the polyvagal writings often appear to be at variance with past and current knowledge about the nA and the DVMN (e.g. Grossman, Taylor, 2007; Taylor et al., 2014; Duran et al., 2020; Sanches et al., 2019).

Additionally, a major limitation of the polyvagal conjectures, and in fact, all psychophysiological theorizing about the vagus and the psyche is the fact that there is, effectively, only one noninvasive and nonintrusive index of vagal activity, respiratory sinus arrhythmia (RSA),1 and that measure is only an imperfect and indirect marker of vagally mediated control of heart rate (Grossman & Taylor, 2007)— but of no other vagally mediated processes (see Jänig & Häbler, 2000), i.e. RSA provides no or very limited information about any other vagal processes beyond control of heart rate. Nevertheless, RSA is the linchpin for almost all psychophysiological speculations regarding the parasympathetic system, and this is very true for polyvagal hypotheses. Therefore, we will rely upon the existing physiological evidence regarding vagal influences on heart rate and dismiss conjectures about other systems that cannot yet be nonintrusively assessed.

The polyvagal hypotheses have become increasingly diverse over the years and often have borrowed substantially from prior existing psychological theories and evidence, e.g. attachment theory, social engagement literature and psychological trauma research (e.g. Bowlby, 1969; Campos et al., 1983; Izard, 1978; van der Hart et al., 1989). In such cases, these hypotheses consequently acquire their distinctiveness only in terms of their relationships to the underlying polyvagal premises.2 Therefore, we proceed, point-by-point, with a review of the existing evidence regarding each of the five basic premises of the polyvagal framework.

Conclusions

The polyvagal conjectures comprise a psychophysiological model based upon the foundational premises cited in this article. Therefore, the behavioral/psychological postulates must be evaluated in terms of the accuracy of underlying physiological assumptions. There is broad consensus among experts specialized in the vertebrate evolution of the autonomic nervous system, vertebrate evolution of sociality and neuroanatomy of the brainstem and the vagus nerve that each basic physiological assumption of the polyvagal theory is untenable. Much of the existing evidence, upon which these consensuses are grounded, strongly indicates that the underlying polyvagal hypotheses have been falsified. An earlier paper also provides several additional challenges to the polyvagal conjectures (Grossman & Taylor, 2007).

In a nutshell, specifically, there is no support for the continuing polyvagal assertion that the dorsal vagal motor nucleus mediates massive bradycardia in mammals and may be responsible for vasovagal syncope, or trauma-related dissociative or emotional freezing responses (e.g. Porges, 2021a). In fact, as reviewed above, there is a substantial body of evidence to the contrary. Nor is there evidence that the brainstem-vagal system in mammals “was repurposed in order to support and express sociality” (Porges et al., 2021). Because these notions remain such central assumptions of polyvagal thinking and the very source of the “poly” in “polyvagal”, psychological corollaries grounded upon the 5 basic premises must be called into question or provided with other explanations. There are alternative models which attempt to explore relations between the structure and function of vagal and psychological processes (Grossman and Taylor, 2007, Thayer and Lane, 2009). Although perhaps more plausible than the polyvagal conjectures, they also require further in-depth examination of their supporting physiological evidence.

Statement

The author did not use generative artificial intelligence (AI) technologies for preparation of this work.

Declaration of Competing Interest

The author reports no conflicts of interest.

Acknowledgements

I wish to express my sincere gratitude to Professors E.W. (Ted) Taylor, Tobias Wang (both comparative physiologists, and evolutionary biologists of the autonomic nervous system and respiratory-circulatory interactions), Alexander Gourine (cardiovascular autonomic physiologist), Winfried Neuhuber (vagal system neuroanatomist) and John Karemaker (cardiovascular autonomic physiologist) for commenting upon an earlier version of this article and/or for personal scientific exchanges, sometimes across several decades. My interactions with each demonstrate the value and the ease of truly interdisciplinary cooperation. I also thank each of the three anonymous reviewers for their comments.