Pressed for time? Jump to Summary and Conclusions.

If you’ve ever seen the terms “ventral vagal” or “dorsal vagal” outside of an advanced anatomy textbook, you’ve probably encountered polyvagal theory. This theory, introduced by psychologist Stephen Porges, makes specific claims about the evolution, anatomy, and physiology of the vagus nerve and autonomic regulation of the heart, and parlays those claims into hypotheses about the interplay between the autonomic nervous system and human psychology and sociality.

Polyvagal theory as an explanatory model, while receiving little to no acceptance in the fields of autonomic physiology or neurobiology, has become – dare I say – gospel in the communities of “trauma-informed” somatic and psychotherapy. (6, 7, 8)

Polyvagal theory also makes frequent appearances in communities that promote “rewiring” the autonomic nervous system as a way to treat illnesses such as chronic fatigue syndrome, POTS, and various autoimmune diseases.

I’ve even seen it in health and wellness spaces that aren’t focused on trauma or illness – for instance, on the Bulletproof YouTube channel, or in the Instagram posts of “pro-metabolic” nutrition influencers. It seems that polyvagal theory has become relevant for just about anyone interested in human health.

The comments below the Dave Asprey video give an idea of the enthusiasm and gratitude with which polyvagal theory is most often received. However, the theory has also been criticized by some scientists, most notably psychosomatic researcher Paul Grossman.

The exchanges between these two researchers have been largely unproductive, and I suspect this is in large part due to the fact that Grossman is critiquing polyvagal theory purely at the level of biology, while Porges conceptualizes the theory primarily within the contexts of experimental psychophysiology or broadly integrative “mind-body” research. Thus, I propose that polyvagal theory and its attendant controversy cannot be understood through analysis at the level of biology alone.

As such, in this article I’ll provide a critique of polyvagal theory as biology, as a model for psychophysiology, and as a biopsychosocial framework. I also include two additional levels of analysis that reflect the sociocultural roles that polyvagal theory has taken on: as direction and justification for clinical therapies, and as an “illness myth.”

*A note about references in the text: numbers in parentheses refer and link to footnotes providing additional context and info; citations are given by author last name and year.

What is Polyvagal Theory?

Because polyvagal theory has become somewhat of a sociocultural phenomenon among clinicians and patients, it’s likely that most of its proponents don’t actually understand it. Even the official website for the Safe and Sound protocol, a protocol that was developed by Porges himself, contains a description of the theory that is overtly unscientific and I know does not reflect Porges’ understanding of the autonomic nervous system. (1a)

Whether Porges should be held accountable for such statements made by his affiliates is another topic, but to avoid setting up a strawman for this critique, I’ve tried below to characterize the theory – as biology, as a model for psychophysiology, and as biopsychosocial framework – using text quoted directly from Porges himself.

As Biology: “The Vagal Paradox”

As biology, polyvagal theory makes specific claims about the anatomy and physiology of the autonomic nervous system, both in humans and in other vertebrates. The below is taken from the Polyvagal Institute website “Introduction to PVT” section, which should reflect Porges’ most up-to-date characterization of the theory. I’ve bolded some of the claims that will be addressed in the criticism sections below.

“Polyvagal Theory was introduced by behavioral neuroscientist, Stephen W. Porges, in his presidential address to the Society of Psychophysiological Research in Atlanta Georgia on October 8, 1994. The talk was later published in Psychophysiology 1995 with the title “Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A Polyvagal Theory.”  The title provides a succinct synopsis of the theory in which the phylogenetic transition from asocial reptiles to social mammals is discussed emphasizing the convergent shifts in the neural regulation of the autonomic nervous system and the adaptive biobehavioral consequences. Functionally, unlike their reptilian ancestors, mammals had a newer branch of the vagus providing cardioinhibitory influences on the heart that emerge from a ventral area of the brainstem (i.e., nucleus ambiguus).  In contrast, other classes of vertebrates (e.g., reptiles, amphibians, etc) had vagal cardioinhibitory pathways emerging only from a dorsal area of the brainstem (i.e., dorsal motor nucleus of the vagus). Thus, the theory explicitly brought attention to the adaptive function of the ventral vagal pathway in defining features of social mammals including the mutual downregulating of threat reactions, calming physiological state, and sociality.” (PVI, Oct 26 2022, emphasis mine) 

Originally, this polyvagal theory was an attempt to answer what Porges saw as a paradox in the parasympathetic (vagal) control of heart rate in neonates. From one of his review papers, published in 2021:

“Polyvagal Theory emerged from my research studying heart rate patterns in human fetuses and newborns. In obstetrics and neonatology, the massive slowing of heart rate known as bradycardia is a clinical index of risk and assumed to be mediated by the vagus. During bradycardia, heart rate is so slow that it no longer provides sufficient oxygenated blood to the brain. This type of vagal influence on the fetal and neonatal heart could potentially be lethal. However, with the same clinical populations, a different index of vagal function was assumed to be a measure of resilience. This measure was the respiratory oscillation in beat-to-beat heart rate variability (i.e., respiratory sinus arrhythmia), which was the focus of my research for several decades. Animal research demonstrated that both signals could be disrupted by severing the vagal pathways to the heart or via pharmacological blockade (i.e., atropine), interfering with the inhibitory action of the vagus on the sinoatrial node. These observations posed a paradox. How could cardiac vagal tone be both a positive indicator of health when monitored with heart rate variability and a negative indicator of health when it manifests as bradycardia?” (Porges 2021b; emphasis mine)

How indeed?

Porges’ solution was to propose that these disparate vagal effects on the heart are mediated by two anatomically and functionally distinct branches of the vagus nerve: the myelinated ventral branch that originates in the nucleus ambiguus (NA) and primarily serves the heart, lungs, and head; and the unmyelinated dorsal branch that originates in the dorsal motor nucleus of the vagus (DMNV) and primarily serves the subdiaphragmatic organs, but also has some efferent fibers to the heart.

This, he explains, solves the vagal paradox. The “ventral vagus” maintains parasympathetic tone to the heart in mammals and has a respiratory rhythm, generating respiratory sinus arrhythmia (RSA). Meanwhile, the “dorsal vagus” does not have a respiratory rhythm and is a vestige of reptilian autonomic wiring; it’s this branch of the vagus that mediates life-threatening bradycardia.

As Experimental Psychophysiology

These specific biological claims belie the fact that Porges himself is not a biologist. Instead, polyvagal theory made its debut in the field of psychophysiology – which, despite “physiology” in the name, is not a technical study of physiology but rather a subfield of psychology that introduced physiological metrics (such as heart rate and sweating) as variables in psychological research.

In this context, polyvagal theory serves to generate hypotheses that can be tested using these types of experiments.

“From the polyvagal perspective, RSA is a direct measure of the vagal efferent outflow originating in the nucleus ambiguus that influences the nicotinic preganglionic receptors on the sinoatrial node. Thus, the measurement of RSA provides a unique opportunity for psychophysiologists to monitor the central regulation via a peripheral measure of a neural circuit involved in the coordination of visceral state and the expression of emotion and social communication…Theoretically, RSA should closely parallel individual and intra-individual variations in emotion expression, social communication, and behavioral state.” (Porges 2006b, emphasis mine)

As Biopsychosocial Framework

Porges’ own preferred framing of polyvagal theory seems to be as a holistic and nonspecific biopsychosocial framework of sorts. From the PVI website:

“Functionally, Polyvagal Theory provides a foundation for an integrated and expansive brain-body science that emphasizes the bi-directional communication between visceral organs and brain structures through vagal pathways.  The theory is built upon the paradigm breaking research of several visionary scientists, who introduced concepts that have been reframed within the Polyvagal Theory including internal milieu (Claude Bernard), homeostasis (Walter Cannon), evolution (Charles Darwin), dissolution (John Hughlings Jackson), arousal (Robert Yerkes and John Dodson), fight/flight (Walter Cannon), and a unified nervous system integrating brain and body functions (Walter Hess). By extracting and combining accepted principles discovered by these foundational scientists, Polyvagal Theory provides a new understanding of the neural regulation of the autonomic nervous system that emphasizes the bi-directional communication between brain and visceral organs.” (PVI, Oct 26 2022, emphasis mine)

Porges’ most recent writings emphasize sociality and perceptions of safety in human health: the tagline on the PVI website is “the art and science of human connection,” and one of his most recent publications is titled Polyvagal Theory: A Science of Safety.

Having said all that, my best attempt to sum up polyvagal theory is: an explanatory model for the bidirectional integration of physical health with psychological and social health based on an evolutionary theory of the autonomic nervous system, with an emphasis on characterizing the different organismal states of receptivity or defense and exploring the relationships between these states and human health.

With that out of the way – on to the critical analysis! As a reminder, I’ll be tackling this at five different levels: biology, psychophysiology, biopsychosocial framework, therapy, and myth. First: biology!

Polyvagal Theory as Biology

Most of the criticisms leveled at polyvagal theory by Grossman and others relate to its specific physiological and evolutionary claims, and fall into three broad categories: 1) the comparative anatomy and physiology of mammals versus reptiles; 2) the role of vagal fibers from the DMNV in cardiac autonomic control; and 3) the nature of RSA. I cover each below, and then throw in my own two cents as a fourth criticism.

Reptiles vs. Mammals: Anatomy and Physiology of the Vagus Nerve

In Grossman P & Taylor EW 2007 and Taylor EW et al 2022, evolutionary biologist EW Taylor and collaborators critique Porges’ claims about the anatomy and physiology of the reptilian and mammalian autonomic nervous systems.

Throughout his writings, Porges either states directly or strongly (and repeatedly) implies that several features of the mammalian autonomic nervous system are unique to mammals: the existence of a second separate vagal nucleus; the myelination of vagal cardioinhibitory fibers; resting vagal tone to the heart; the cardio-respiratory syncing known as RSA.

On the level of anatomy, two of these claims are immediately shown to be erroneous: myelinated cardiac vagal fibers have been confirmed in sharks and fish (and suspected in all vertebrate groups), and dual vagal nuclei are seen in all vertebrate groups. Thus, Porges’ repeated naming of human myelinated cardiac vagal fibers as the “mammalian vagus” (for instance, in Porges 2011) cannot be understood as a scientific designation.

On the level of physiology, Taylor et al describe how most reptiles do, in fact, have resting cardiac vagal tone. In fact, all vertebrate groups show an inhibitory cardiac vagal tone, with changes in heart rate from the resting state most often mediated by vagal withdrawal.

Taylor et al also thoroughly cover cardiorespiratory interactions in 87 different species of vertebrate, from reptiles to amphibians to fish to birds, describing distinct vagally-mediated cardiorespiratory syncing almost across the board.

Based on this data, they suggest that cardiorespiratory interactions evolved early in phylogenetic history as a means of optimizing gas exchange and perfusion, which provides an evolutionary explanation for the phenomenon of RSA in mammals. Such cardiorespiratory syncing would have greatly improved the efficiency of gas exchange in animals with more primitive circulatory systems or episodic breathing.

The implication is that rather than being “uniquely mammalian modifications,” most of the ANS features Porges concerns himself with are in fact shared with other vertebrate groups and may be best explained by the evolutionary pressures of gas exchange, possibly making mammalian RSA a vestigial feature from the time before divided circulatory systems.

One additional point is relevant here. Despite the language Porges uses (2), mammals did not evolve from reptiles. Reptiles and mammals (if the terms are used to describe the classes Reptilia and Mammalia, respectively, as they usually are) are two separate phylogenetic groupings that each branched off from the amniotes clade.

While I have seen the common ancestor of mammals and reptiles described as “reptilian,” it’s clear that Porges uses the word “reptile” to refer to the reptiles we’re familiar with. We know little about the common ancestor of reptiles and mammals, and we certainly don’t have any data on their autonomic nervous systems.

The Role of the “Dorsal Vagus” in Cardiac Control

A central claim of polyvagal theory is that vagal fibers emerging from the DMNV can elicit “massive neurogenic bradycardia” as a vestigial defense mechanism in humans.

To my knowledge, there is currently no evidence to support this claim, while there’s a fair bit of evidence suggesting that the DMNV has limited to no ability to affect heart rate in mammals. Grossman and Taylor review some of this evidence in their 2007 paper, and Grossman has also collected quite a few references in this ResearchGate thread that appear inconsistent with Porges’ assertion that the DMNV can mediate massive bradycardia in mammals. Grossman has also pointed out that the two citations Porges provides in his book do not in fact support what he claims. (9)

Despite this, Porges continues to write as if this is proven. For instance, “without a functioning ventral vagus, the preterm neonate is predisposed to react with a ‘reptilian’ defensive response via the dorsal vagal pathway to stressors and challenges of birth. When recruited for defense, the dorsal vagal system may produce bradycardia and apnea.” (Porges 2021b)

It must be noted that the experimental techniques required to differentiate the effects of the two vagal nuclei are extremely invasive, and as such have only been conducted in animals. We are still far from having a perfectly clear and detailed understanding of cardiac vagal regulation in humans, but the broad consensus among experts in autonomic physiology is that the DMNV is not a significant contributor to heart rate control in mammals. There’s still room for future evidence to prompt a reevaluation of this consensus, but nothing currently supports the claim.

RSA and Cardiac Vagal Tone

Grossman and Taylor summarize this issue well:

“An additional and very essential implicit premise of the polyvagal theory is that RSA always reflects tonic vagal efferent discharge originating in the nA, and that dissociation between vagally mediated HR changes and RSA can be explained by divergent activities of the nA and the DMN. The theory assumes that nA activity is at all times associated with beat-to-beat changes in HR, i.e. RSA, whereas the DMN produces flat changes in HR that show no respiratory modulation or any other type of beat-to-beat variation. Therefore, according to this theory, vagally mediated HR reductions that are not accompanied by RSA increase are supposed to originate from the DMN; changes in RSA magnitude, on the other hand, from the nA. Hence the accuracy of RSA as a measure of mean levels of nA-generated vagal efferent discharge is critical to the theory, because RSA is the vagal measure used in studies to evaluate premises and postulates of the theory.” (Grossman & Taylor, 2007)

Perhaps the most extensive discussion of heart rate variability (and specifically RSA) as it relates to polyvagal theory is found in Porges’ 2006 paper The Polyvagal Perspective, and the relevant claim is stated within as “The functional output on the heart by the vagal efferent pathways originating in nucleus ambiguus may be monitored by RSA.” (Porges 2006b)

It is very well known and accepted within the field of autonomic physiology and heart rate variability (HRV) research that HRV metrics – including measurements of RSA – are not measurements of autonomic tone. I cover this issue (as it relates to HRV generally) in some detail in this section of my article about HRV, with a brief discussion of RSA specifically. In short, “tone” refers to the quantity of nerve traffic to the heart, while RSA is the pattern of nerve traffic. It is often highly correlated with the overall quantity of vagal traffic, certainly – but the two do dissociate, especially with changes in respiration rate and tidal volume.

Porges appears to use vague terms like “functional output” and “activity” interchangeably with the specific term “tone,” and perhaps this contributes to the confusion. Nevertheless, given that much of Porges’ career has revolved around HRV, this conflation seems inexcusable.

The following table on the Polyvagal Institute website presents an interesting summary of the arguments on both sides:

I’d like to give Porges the benefit of the doubt, but this table appears to be presenting polyvagal theory as unfalsifiable while neglecting to sincerely engage with any of the criticisms raised against it.

Much of Porges’ boldness in claiming that RSA is an accurate measure of vagal tone comes from his own proprietary method for measuring RSA, termed the “Porges-Bohrer” method. However, nobody else in the field seems to agree that Porges’ method has any notable advantages over other well-accepted methods, and may in fact have some minor disadvantages.

But more importantly, a thorough understanding of physiology makes it clear that the phenomenon of RSA itself, regardless of measurement, is a result of the patterning of vagal impulses, and that for physiological reasons – again, outside concerns of measurement – different impulse patterns can lead to varied RSA amplitude even while overall vagal tone remains stable. (10)

The Metaphorization of Autonomic Terminology

Based on my read of the arguments on both sides, it seems that a large part of the conflict may stem from Porges’ misuse of the terminology belonging to scientific fields that are not his own.

For instance, take the following description:

“The VVC [ventral vagal complex] represents the phylogenetically most recent stage and is unique to mammals. The VVC is characterized by a myelinated vagal system that can rapidly regulate cardiac output to foster engagement and disengagement with the environment. The VVC consists of the myelinated vagus and portions of other cranial nerves (i.e. V, VII, IX, XI) that regulate structures derived from the embryonic branchial arches (i.e. ancient gill arches). Collectively, these neural pathways regulate the branchiomeric muscles and have been categorized as special visceral efferent fibers. In mammals the branchiomeric muscles control facial expression, sucking, swallowing, breathing, listening and vocalization.” (Porges 1998)

In his various papers, Porges appears to use the above term “ventral vagal complex” somewhat interchangeably with the terms “social engagement system,” “ventral vagus,” and “smart vagus.”

In all of these cases, he’s referring to the neural “system” that supports social engagement and the suck-swallow-breathe-vocalize reflex characteristic of nursing mammals, which involves several cranial nerves in addition to the vagus (as well as higher brain structures where “social engagement” is concerned).

To an anatomist, the use of the term “vagus” or “vagal” to designate such a system would seem nonsensical at best; blatantly inaccurate at worst. To Porges, I imagine it’s an unimportant issue of semantics.

A similar semantic issue may contribute to the DMNV controversy. From Porges:

“Although recent research confirms that the unmyelinated vagal fibers originating in the DVC contribute to bradycardia in mammals, it is debated whether the unmyelinated vagal fibers, independent of the myelinated vagal fibers from the VVC, are capable of the massive bradycardia observed in mammals. Alternately, one might hypothesize that the massive bradycardia would require the recruitment of myelinated vagal pathways by the DVC following withdrawal of neural tone by the VVC. Thus, during periods when the VCC tone is depressed, the myelinaed vagal pathways originating in the nucleus ambiguus might come under control of the dorsal motor nucleus of the vagus.” (Porges 1998)

If an anatomist would find it nonsensical to refer to an entire system of cranial nerves as a “vagal” system, they’d find it absolutely preposterous to claim that an autonomic nucleus (ie, a bundle of nerve cell bodies) could “recruit” nerves that don’t originate from that nucleus. But to Porges, who is obviously using the DMNV as a metaphor for a physiological state of defense or shutdown, this apparently makes perfect sense.

This metaphorization of autonomic terminology is most obvious in all of the extra-academic manifestations of polyvagal theory: in pop psychology, among health influencers, even in clinical practice. The aforementioned characterization of polyvagal theory on the Safe and Sound website, which I will continue to consign to footnote status (1b) to avoid strawmanning polyvagal theory, is an excellent example of this. But you can even see it on the official Polyvagal Institute website:

The actual autonomic landscape of each of the listed emergent behaviors would be quite granular and nuanced depending on the specific internal and external threats to homeostasis at the time, so the autonomic descriptors given at the top have value as vague generalizations at best.

Revisiting the “Vagal Paradox”

These critiques leave the evolutionary and physiological foundations of polyvagal theory on shaky ground. But what of the “vagal paradox” that prompted Porges to formulate his theory to begin with? How can high “vagal tone” be both a sign of health and resilience when it manifests as high RSA, and a “negative indicator of health” when it manifests as bradycardia?

One answer is that, as explained above, RSA is not the same thing as “cardiac vagal tone.” It is a pattern of vagal modulation that reflects cardiorespiratory syncing.

But an answer that gets more at the heart (ha) of the issue is that the vagus is simply the messenger – not the message – and as Grossman expertly summarizes (11), there need not be a paradox in the fact that the same bundle of nerves can tell the heart to slow down in response to both ambient states of homeostasis and life-threatening situations.

Polyvagal Theory as Experimental Psychophysiology

The critiques of Grossman and others at the level of biology are most often met with – ironically – defensiveness from Porges, clinicians, and patients alike. This is probably because they perceive these critiques as attacks on the higher-level functions of polyvagal theory for which the importance is much greater. But these next three sections will show that such things are not, in fact, dependent on – nor do they validate – the questionable biological foundations of polyvagal theory.

Polyvagal Theory as the Successor to Arousal Theory

Porges entered the field of psychophysiology in the 1960s when it was still relatively new, and researchers were just beginning to use HRV metrics as variables when studying human behavior and cognitive processes.

As this new realm of inquiry brought psychologists into more intimate contact with physiology, the prevailing theoretical framework at the time for integrating autonomic physiology with behavior – arousal theory – started to lose some explanatory power.

As Porges puts it, arousal theory is implicitly a theory of “psychophysiological parallelism.”

“Psychophysiological parallelism is functionally a scientific strategy that assumes an isomorphic representation of a process with the gradations being mapped with equivalent precision on all levels. An alternate and more parsimonious strategy would be to organize the nervous system into a hierarchical format in which neurophysiological processes related to basic biologically determined survival needs are required to be managed successfully before higher brain structures are functionally given access to be activated for problem solving, creativity, and even sociality. Polyvagal Theory postulates that our biology is hierarchically organized with the basic survival needs, such as managing homeostatic functions, residing in foundational brainstem structures and optimal access and utilization of higher neural circuits being dependent on success at the foundational level.” (Porges 2022b)

(Anyone else get “Maslow’s hierarchy of needs” vibes here?)

And, again speaking to the field of psychology, Porges says “Frequently missed with our cortico-centric and cognitive-centric orientation is the importance of lower brain mechanisms in managing our basic survival-oriented reactions.” (Porges 2022b)

Viewed in this light, polyvagal theory represents a great leap forward in explanatory power over arousal theory. And because psychophysiological research operates at the bridge between behavior and observed physiological indicators like HRV, the anatomy and physiology behind those indicators generally remains in the realm of the abstract and theoretical, and a detailed understanding is not crucial to successfully carry out research.

Contributions of the Porges Research Group

Which brings me to the experimental contributions from Porges and collaborators. They’ve done quite a bit of fascinating work linking metrics of cardiac autonomic control – most recently a metric they’ve termed “vagal efficiency” – with various functional and psychological disorders. For instance, they’ve found that this measure of vagal efficiency is predictive of joint hypermobility in a group of adolescents with functional abdominal pain disorders, and is predictive of past childhood maltreatment in college students. And in a randomized controlled trial, baseline vagal efficiency predicted whether adolescents with functional abdominal pain disorders would experience improvements with auricular neurostimulation. (Kolacz et al 2021; Dale et al 2022; Kovacic et al 2020)

All of this is in addition to the work Porges has done with the Safe and Sound protocol, which I’ll describe later.

So despite its questionable biological foundations, it seems that polyvagal theory has served well in its role informing psychophysiological research. Not to say an updated and more accurate explanatory framework might not produce better hypotheses and sleeker experimental design; but the shortcomings of the current paradigm in no way invalidate any data that has been collected under its direction.

Polyvagal Theory as Biopsychosocial Framework

This article from traumageek.com highlights the fact that for most, polyvagal theory has almost entirely left behind its roots in autonomic evolution and lodged itself in the public sphere as a holistic framework integrating the mind-body-social aspects of human health and disease:

“In many cases, when a person says “polyvagal” they are not only referring to Porges theory as it was introduced in 1994, but also referencing a larger schematic which integrates PVT with attachment theory, research on emotional regulation, psychological stress models, and the other 4 models of the nervous system. (This is true for my blog The Polyvagal Neurodiversity Project.) The growing popularity of the polyvagal framework has been dismissed as “pop science,” but I believe it is popular with clinicians and survivors because of its implicit inclusion of other theories of neuroscience. In a polyvagal framework, PVT is an anchor concept that ties all these other theories together.” (Janae Elisabeth, Jan 2022)

Because the claims of physiology that are unique to polyvagal theory are inaccurate, the “anchor concept that ties all these other theories together” can be nothing more than the idea that threat detection and the state of the organism (receptive vs. defensive) are immensely helpful constructs through which to understand and approach human health, and that the autonomic nervous system is somehow involved in these states.

However, the concepts of threat detection and defensive states, knowledge that the vagus nerve is a crucial mediator of health and disease, and the other big concepts listed by Porges all predate polyvagal theory, and neither depend upon nor validate its biological claims.

The “reframing” provided by polyvagal theory has likely been helpful, simply because thinking about things differently is almost always beneficial for scientific inquiry and discovery, but the theory would need to be significantly overhauled (and likely renamed) to have validity as a biopsychosocial framework.

To illustrate the fact that polyvagal theory is distinct from and not required for this type of integrative science, below is an example first of a non-polyvagal biopsychosocial framework, and then a non-polyvagal model for the integration of the autonomic nervous system with sociality.

George Engel’s Biopsychosocial Model

The term “biopsychosocial,” which does a good job capturing the three levels of integration attempted by polyvagal theory, was coined in 1977 by psychiatrist George Engel in his paper The need for a new medical model: a challenge for biomedicine. An updated review of the model called The Biopsychosocial Model 25 Years Later: Principles, Practice, and Scientific Inquiry is available for free.

“In embracing Systems Theory, Engel recognized that mental and social phenomena depended upon but could not necessarily be reduced to (ie, explained in terms of) more basic physical phenomena given our current state of knowledge. He endorsed what would now be considered a complexity view, in which different levels of the biopsychosocial hierarchy could interact, but the rules of interaction might not be directly derived from the rules of the higher and lower rungs of the biopsychosocial ladder.” (Borrell-Carrio et al 2004)

As an overarching biopsychosocial framework, Engel’s model serves far better than polyvagal theory; rather than extrapolating a high-level framework from specific autonomic premises, it focuses on the high-level framework itself, leaving the model flexible to adapt to and embrace new and changing evidence at lower levels of inquiry.

Linking Autonomic Function and Sociality: An Alternative to Polyvagal Theory

As far as providing a specific physiological basis for biopsychosocial integration, a 2018 paper from Atzil et al entitled Growing a social brain provides an interesting counter to polyvagal theory. This paper can be compared and contrasted with Porges’ paper The Early Development of the Autonomic Nervous System Provides a Neural Platform for Social Behavior: A Polyvagal Perspective.

Both perspectives begin with the acknowledgement that the helplessness of newborns is a defining trait of mammals, and is most pronounced in humans. But while Porges argues that the “mammalian vagus” and its integration with other cranial nerves provides the neural platform for the development of sociality, Atzil et al argue that this integration of vagal pathways with neural pathways of sociality is not a cause of social behavior, but rather an effect of the early physiological allostatic regulation of the newborn.

They posit that the dependence of the infant on the caregiver for homeostatic maintenance (nourishment, warmth, autonomic regulation) is in fact the driving force behind the integration of these nerves and the development of sociality. Social interactions between infant and caregiver quickly become rewarding due to the repeated coupling of these interactions with the restoration of physiological allostasis (mostly through breastfeeding and skin-to-skin contact), and thus the still-developing newborn neural pathways involved in maintenance of the “internal milieu” become enmeshed with those involved in social engagement.

Thus, polyvagal theory’s emphasis on the specific brainstem anatomy of mammals vs. reptiles as being of the utmost significance for human sociality, with implied primacy of anatomy that then results in behaviors, is contrasted with a conception of the infant brain as adaptable and neuroplastic, allowing (nay, necessitating) early caregiving behavior to mold it into a social brain and thus intertwine the neural pathways involved in cardiorespiratory regulation with those mediating sociality.

These two views are not mutually exclusive, and I don’t see anything necessarily wrong with Porges’ argument that the anatomy of our autonomic nervous system provides the neural basis for sociality; certainly we have no reason to believe that the development and behavior of humans could remain the same if our anatomy and physiology were different.

But the difference in framing may have practical ramifications for both research and therapy, so it would likely behoove researchers, clinicians, and patients alike to remain open-minded to non-polyvagal models.

Polyvagal Theory as Therapy

I think a large part of the defensiveness with which criticisms of polyvagal theory are met is based on the notion that a “debunking” of the explanatory framework equates to a “debunking” of the practical therapeutic approach. And polyvagal theory has absolutely become entrenched in the minds of clinicians and patients as synonymous with the therapies it’s associated with.

It might seem self-evident that a therapy does not magically become ineffective if the proposed scientific basis for the therapy is revealed as bunk. If it works, it works – who cares why it works?

Well, everyone. Everyone cares, because it’s human nature to want to know why, especially in current Western culture. Acknowledging this fact, I’ll briefly review the therapeutic approaches most closely linked to polyvagal theory and their mechanisms of action (as best we understand them) such that the questionable claims of polyvagal theory can be safely abandoned without forgoing explanations altogether. (15)

The Safe and Sound Protocol

Fascinatingly, the Safe and Sound Protocol, which is the “only practical application of Polyvagal Theory” (as enumerated on the official website), has nothing at all to do with the vagus nerve. It instead uses computer-altered music to target and “exercise” the vestibulocochlear nerve, which provides neural regulation of the middle ear muscles to extract the sounds of human speech from background noise. (Porges et al 2014)

The idea of listening/sound therapy is not new (for instance, see the Tomatis method), although Porges et al 2014 (unsurprisingly) emphasizes the unique benefits of his method over others.

The protocol was designed to treat children with autisum spectrum disorder, who often present with auditory hypersensitivity and difficulty understanding speech. It has shown initial success in improving auditory hypersensitivity (Porges et al 2014; Porges et al 2013), and Rajabalee et al 2022 reports a case of remarkable improvement in a ten-year-old girl who had developed severe neurological symptoms following an infection.

“Vagus Nerve” Exercises

Another application of polyvagal theory is the class of techniques first laid out in Stanley Rosenberg’s book Accessing the Healing Power of the Vagus Nerve: Self-Help Exercises for Anxiety, Depression, Trauma, and Autism.

Although these are not “official” applications of polyvagal theory, Porges did write a forward to the book, the two have presented seminars together in both the US and Denmark, and the exercises laid out in the book are generally described as “polyvagal” by those who practice and share them.

Rosenberg had already been working with patients as a craniosacral therapist for decades and had founded a training school in Denmark before encountering polyvagal theory in 2001 and meeting Porges in 2002. As he describes it in his book:

“Porges’ Polyvagal Theory brought about a revolutionary advancement in my understanding of the autonomic nervous system. According to this theory, five cranial nerves (CNs) must function adequately in order to attain the desirable state of social engagement. These five nerves are CN V, VII, IX, X, and XI, and they all originate in the brainstem. Before I heard Porges speak, I had studied anatomy with Professor Patrick Coughlin, who taught us about each of the twelve cranial nerves, including the vagus nerve (CN X), and how to test their function. I had also learned specific biomechanical hands-on techniques from my craniosacral teacher Alain Gehin to improve the function of the twelve cranial nerves. So I was well prepared for an infusion of insight offered by the Polyvagal Theory. I adapted the techniques I had learned to successfully address a wide range of maladies with this new paradigm.” (Rosenberg 2017, p. xxx-xxxi)

In other words, Rosenberg was an extremely skilled and knowledgeable bodywork therapist with a decades-long track record of improving the health of his patients and training other therapists to do the same. What polyvagal theory offered him was a re-orienting nudge that lead to emphasizing treatment of the five cranial nerves (not just the vagus, mind you!) and a focus on social engagement as a desired patient-level outcome.

Although this new paradigm was obviously transformative in his practice, in no way are his techniques dependent on the flawed suppositions of the polyvagal theory described at the beginning of this article. All the exercises in his book address the function of all five cranial nerves related to social engagement, not just the ventral vagus, and they do so through non-vagus-mediated techniques.

For instance, according to his book, the “basic exercise” uses feedback to the occipital nerve and engagement of the oculomotor nerve to relax the suboccipital muscles and allow proper positioning of the C1 and C2 vertebrae, thereby increasing blood flow to the brainstem where the cranial nerves originate. The “salamander” exercises do something similar, while adding in thoracic mobility to improve breathing mechanics in addition to blood flow.

Somatic Experiencing

One final therapeutic approach that is intricately tied to polyvagal theory is “somatic experiencing,” developed by Peter Levine. This page on the official somatic experiencing website and Payne et al 2015 in Frontiers in Psychology give a pretty good idea of what it entails, but it’s essentially a body-focused (rather than mind-focused) therapy to release and heal past traumas through interoception, proprioception, and movement.

(Note that Pat Ogden’s sensorimotor psychotherapy is a similar body-focused approach, but while Levine’s model emphasizes the almost animalistic nature of defensive reactions and is primarily focused on treating trauma, Ogden’s model takes a decidedly human-centric view by incorporating bottom-up approaches with top-down approaches, providing flexibility to deal with more nuanced issues of the human psyche. The more animalistic emphasis of somatic experiencing is well reflected in its significantly stronger association with polyvagal theory.)

Like Rosenberg, Levine was treating patients long before encountering polyvagal theory. He had his transformative experience with the patient “Nancy,” which inspired his first book Waking the Tiger, almost a decade before meeting Stephen Porges in 1978.

Levine seems to have adopted the polyvagal framework as a physiological explanation for why somatic experiencing works; (15) he essentially states outright that he needed a firm scientific basis for the theory in order for it to be accepted in our secular Western society:

“People have sometimes described me as an almost mystical, shamanic healer. While I have been gratefully influenced by cross-cultural studies about shamanic healing and had opportunities to meet with various shamans and indigenous healers throughout the world, it still has been my lifetime task to prove this assumption wrong. Said in another way, for many years I desired to demonstrate that the methods I was developing were transferable in western secular society. Now that SE is widely accepted as a scientifically based approach, I feel freer to acknowledge its deep roots in shamanistic traditions.” (Peter Levine)

The neural intermediary proposed in Payne et al 2015 is not the “ventral vagus” and “dorsal vagus,” but rather the “Core Response Network,” which includes the autonomic nervous system as well as higher brain structures to “organize immediate, instinctive response to environmental challenges prior to extensive cortical processing.”

Hat tip for the reference goes to one of the scientists on ResearchGate, who made a point to say that the paper was not based on Porges’ thinking, and if it was, it would have been difficult to get published.

Polyvagal Theory as Myth

It’s all well and good to say that a therapy’s effectiveness doesn’t depend on the integrity of the explanatory framework, but that may miss the point. Below is a quote from a clinician on one of Grossman’s ResearchGate threads:

“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 dominated, (2) normal range, and (3) parasympathetically dominated – is the most useful part. I agree that it’s mythological, and that is a problem. 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.” (Andrew Cook, 20 Nov 2020, emphasis mine)

Why would someone abandon an approach they had experiential success with just because the explanatory framework was threatened?

This brings us to our final level of analysis: polyvagal theory as myth.

The paper Culturally adapted psychotherapy and the legitimacy of myth: a direct-comparison meta-analysis introduces the concept of “illness myth” as follows:

“That the explanation of illness is a central component in psychotherapy was seminally identified by Frank and Frank (1993), who viewed psychotherapy as a cultural healing practice with four essential components: (1) a confiding relationship with a culturally recognized and sanctioned healer, (2) a context and/or setting distinguished from the ordinary, (3) a rationale or myth providing a plausible explanation for the illness, and (4) a ritual or intervention believed by both to be effective means of restoring health. Frank termed the client explanatory model of illness the myth.” (Benish et al 2011, emphasis mine)

There are two key features of the illness myth that are relevant to polyvagal theory. The first is an ability to make sense of the patient’s subjective experience of suffering in light of their cultural beliefs and values.

Justifying Subjective Suffering in Western Culture

“A critical component of universal healing practices theory is the acceptability of the therapeutic explanation of illness provided to the client, which is embedded within a specific cultural context. That is, illness is a culturally shaped experience of distress manifesting diversely in its expression of bodily and mental symptoms, presumed etiology, expected course, social implications, and the relative importance of these expressions of suffering. Along this line of reasoning, effective psychotherapies offer adaptive explanations of the client’s suffering and provide therapeutic actions consistent with those explanations. What is important to the sufferer, then, according to the above theories, is not the scientific validity or falsifiability of the illness explanation but rather the congruence of the explanation with the client’s cultural beliefs about the illness.” (Benish et al 2011)

In Western medical and scientific culture, subjective experience is devalued in favor of reductive and mechanistic approaches. This fact has been elegantly demonstrated in some interesting experiments described in the papers The Seductive Allure of Neuroscience Explanations and The seductive allure is a reductive allure: People prefer scientific explanations that contain logically irrelevant reductive information. (4)

Polyvagal theory provides a model that reconciles patients’ subjective experiences of suffering with the reductive and mechanistic values of their culture. (12) It even bases the whole thing on the principles of evolution, which has become an immensely powerful cultural force.

(Is it a coincidence that two of the most wildly popular psychological frameworks in recent history, polyvagal theory and triune brain theory [3], have both been couched in evolutionary terms? I think not.)

For patients suffering from conditions that their culture doesn’t accept as “real” – whether it’s trauma, fibromyalgia, chronic fatigue syndrome, or any number of others – a model that not only acknowledges their suffering as real, but also points to the specific neurons causing it and how they evolved over the course of millennia…well, is it any wonder polyvagal theory has spread like wildfire among these communities?

The Unfalsifiability of Illness Myth

The second key feature of the illness myth that is relevant to polyvagal theory is unfalsifiability:

“Expressing explicit awareness of the provocative nature of the term myth, Frank noted that although Western psychotherapies do not invoke mystic powers to heal the afflicted, psychotherapy theories are analogues to ancient myths via a shared lack of scientific falsifiability.” (Benish et al 2011, emphasis mine)

Porges has characterized polyvagal theory as unfalsifiable in published articles, on his website, and on social media. For example: “The theory was not proposed to be either “proven” or “falsified,” but rather to be informed by research and modified.” (Porges 2021b)

He also provided the following response to Grossman’s criticisms:

There’s some debate in the realm of “philosophy of science” over whether a scientific theory can be “falsified.” Karl Popper, a renowned philosopher of science, maintained that falsifiability was necessary for a theory to be considered scientific at all. However, the point that the imperfect nature of research does not lend itself to such black and white claims of truth or falsity is a valid one.

It’s absolutely true that a theory is not “disproven” anytime data do not support it. The long and storied coexistence of Newton’s theory of gravity and Einstein’s theory of general relativity attests to the fact that a theory need not have perfect explanatory power to be valuable.

But we aren’t talking about the theory of gravity or the theory of relativity here. We’re talking about a theory for which the specific anatomical, physiological, and evolutionary claims upon which it is based have little to no supporting evidence and are summarily refuted by experts in each of those fields. Further, contrary to Porges’ assertions, Grossman and Taylor did indeed propose an alternative theory to explain the coordination of the heart and lungs known as RSA, one that is far more explanatory of existing data.

Ultimately, regardless of whether a scientific theory can technically be “falsified,” I’d argue that it is counter to the scientific spirit to continue to make specific assertions about anatomy and physiology that are unsupported, while declining to engage sincerely in discussions or collaborations with experts in those fields. It’s quite clear that Porges has not, in fact, allowed polyvagal theory to be “informed by research and modified.” (5)

It’s notable that across more than a dozen published review articles spanning from 1995 through 2022, although Porges’ focus has shifted noticeably away from specific autonomic physiology and toward the broader concepts of “safety” and “social engagement,” the original polyvagal myth and its attendant vocabulary has remained unchanged. I’d even suggest that the very language used – repetitive, narrative, and evoking quasi-moral imagery through persistent term pairings like “asocial reptiles” and “social mammals” – is more appropriate to storytelling and myth than to science.

The goal of the former is to remain unchanged and mold reality around it; the goal of the latter is to change and be molded by reality. It seems clear which one is more characteristic of polyvagal theory.

Concluding Thoughts

Summary

What is polyvagal theory? An explanatory model for the bidirectional integration of physical health with psychological and social health based on an evolutionary theory of the autonomic nervous system, with an emphasis on characterizing the different organismal states of receptivity or defense and exploring the relationships between these states and human health.

A critical analysis of polyvagal theory…

…as biology: At its inception, polyvagal theory was premised upon specific claims about evolutionary biology and the physiology of the autonomic nervous system, most of which are not supported by the current evidence. A large part of the problem appears to be Porges, coming from the field of psychophysiology, using the technical neuroanatomical terminology of the fields of physiology and evolutionary biology as metaphors for the higher-level phenomena he’s attempting to describe.

…as experimental psychophysiology: Polyvagal theory was proposed within the field of psychophysiology to replace arousal theory as an updated model of the autonomic nervous system, and has been used to inform and direct experiments that study the statistical correlation between measurements of RSA and various disorders, behaviors, or cognitive processes. While the underpinnings of polyvagal theory leave much to be desired from the standpoint of hard biology, it was undoubtedly a step in the right direction from the standpoint of the simplistic and outdated arousal theory, and the field of psychophysiology has likely benefited from this advancement.

…as biopsychosocial framework: Outside of academia, polyvagal theory has for many become synonymous with the idea that our biology, psychology, and sociality are intricately and bidirectionally interconnected, such that one might influence symptoms of psychological distress or asociality by influencing biology, and vice versa. While this type of thinking is both scientifically valid and sorely needed clinically, polyvagal theory was neither the first proposition of such an idea, nor are its questionable claims necessary for such an integration.

The vagus nerve can still play a vitally important mediating role between psychosocial and physiological health; the physiological regulation of the heart and lungs by the myelinated vagus can still be integrated and coordinated with the regulation of the structures of the face by other cranial nerves; emotional responses can still be mediated by lower physiological processes; and social interactions and perception of safety can still be of central importance to human health; all without RSA and myelinated vagal fibers being unique to mammals, the DMNV mediating neurogenic bradycardia, and measurements of RSA accurately depicting ventral vagal tone.  

…as therapy: Polyvagal theory has acted as both inspiration for the development or modification of practical therapies, and as post-hoc “scientific” justification for existing therapeutic approaches. As the former, it has undoubtedly benefitted clinicians and their patients by prompting the development and refinement of clinical techniques. As the latter, it is a symptom of the Western model of medicine in which a therapy is considered invalid in the absence of a reductive mechanism of action, regardless of its clinical effectiveness.

…as illness myth: In its written presentation, polyvagal theory exhibits several features that suggest a primary role as myth rather than science, including unfalsifiability, repetition of key imagery-invoking terms, and an unwavering consistency of message even in the face of sincere scientific critique. In clinical practice, polyvagal theory reconciles the suffering of patients with the values and narratives of their culture, thus fulfilling the all-important role of “illness myth” in their healing.

What We Have Gained From Polyvagal Theory

Based on this analysis, I think it’s clear that polyvagal theory is bad science. Or, to be more precise, it isn’t science at all – it’s myth. But to avoid throwing the baby out with the bathwater, I’d like to suggest several things we can take from polyvagal theory:

• Something for researchers and other curious minds to push against in the ceaseless pursuit of better explanations for human health and behavior
• An imperfect but important attempt to bring “hard” biology into the field of psychophysiology
• A reframing of the cranial nerves as highly integrated and relevant to psychosocial processes, which has already lead to new and improved therapies and may encourage new lines of scientific inquiry
• An illustration of the gulf between science and clinical practice (14)
• A resounding wake-up call to scientists and clinicians alike that there is an abject unmet need for mind and body to be reunited in the treatment of physical and mental illness, particularly in patients with maladies seen as “fake” in Western culture

Where to Go From Here

But alas, a myth has no place in scientific inquiry. And while polyvagal theory as myth has undoubtedly played a vital role in the healing journeys of many a patient, it has also undoubtedly done some harm. (13) It’s very easy to lose sight of what is eminently real, and to cling to treatment approaches that aren’t working, when one is in the grip of a powerful myth.

So where to go from here? In addition to the thoughts of Grossman and others (especially 15, 16, 17), I’ll add a few thoughts of my own:

For researchers: This may come as a surprise since I’ve just spent 13,000 words criticizing his brainchild and questioning his scientific integrity, but I think researchers ought to follow Porges’ lead – Grossman’s too, for that matter. If you have the chance to do something, anything, that builds a bridge between science and practice, or between one field of science and another – do it. Science needs more people who don’t merely “stay in their lane.” The one caveat, of course, is that standards of knowledge and scientific integrity must remain paramount.

For clinicians: Don’t be afraid to call BS on polyvagal theory. Metaphors are great, but should be understood and acknowledged as just that – metaphors. Not mechanisms. They should be held loosely and abandoned readily when they are shown not to reflect reality or serve the patient. There are more than enough incredible things about the human body and psyche that appear, to the best of our knowledge, to be true, that there is no need to cling to ones that aren’t. And where that fails, there’s no shame in saying “we don’t know yet exactly how this works, but damn if it doesn’t work.”

For all: Let’s divorce polyvagal theory and its unscientific assertions once and for all from both “mind-body” science and “mind-body” medicine. If both are to function optimally in the service of improving human health, both must interface as closely with reality as possible, and explanatory theories and frameworks must ever be abandoned and adopted anew to hew more and more closely to what is real.

Appendices

A note about references in the text: numbers in parentheses refer and link to footnotes or ResearchGate quotes (found below). Journal articles are linked and cited in the text by author and year, and all referenced papers, books, and articles are also listed below in the “References” section in order of appearance.

Footnotes

1a. The below is taken from the website for Porges’ Safe and Sound protocol:  

“The vagus nerve helps to regulate many critical aspects of human physiology, including the heart rate, blood pressure, sweating, digestion, and even speaking. As the body takes in information automatically through neuroception, the vagus nerve processes the signals and cues from the world around us and, in turn, determines how we react through three physiological states: 

• Parasympathetic / Ventral Vagal state — our centered “true self” state, where all social interaction, connection and cognition occurs 
• Sympathetic state — feeling of threat or danger, and feeling the need to either “fight” or “flee” from a situation to seek safety 
• Dorsal Vagal state — our “freeze” state, when we feel our lives are so immediately threatened that we become immobilized” 

1b. Aside from the clear “metaphorization” of the ventral vagal/sympathetic/dorsal vagal states above, it’s wildly inaccurate to claim that the vagus nerve processes external signals and determines how we react. The vagus nerve has no knowledge of any external data, nor does it have any way to directly communicate with the sympathetic nervous system. The vagus nerve merely carries information from the visceral organs to the brainstem (specifically the nucleus tractus solitarius), which can then be relayed to higher brain structures for integration with data from external perception, and then carries instructions back from the brainstem to the visceral organs.  

Porges clearly understands this, as evidenced by the following quote, but it’s unfortunate that he’s either unconcerned or fine with how polyvagal theory is portrayed on the official website of this company for which he is the Chief Scientific Advisor: “The Polyvagal Theory does not propose that the vagus is the ultimate cause of individual differences in social engagement behaviors or emotional regulation. The efferent vagal pathway originating in the nucleus ambiguus (i.e., manifested in RSA) is one of several output systems related to emotion and social engagement behaviors. In the Polyvagal Theory the source nuclei of the myelinated vagus are regulated by complex neural circuits involving both visceral afferents and higher brain structures that influence the brainstem source nuclei controlling both the myelinated vagus and the striated muscles of the face and head (i.e., the Social Engagement System).” (Porges 2006)

2. Two examples of Porges’ language that states or implies that mammals evolved from reptiles: “Although mammals and birds are phylogenetic descendants of reptiles, mammals are not ‘direct’ phylogenetic descendants of birds.” (Porges 2001) and “Polyvagal Theory focuses on differences, rather than similarities among vertebrate species and especially the neuroanatomical and functional changes observed during the transition from asocial reptiles to social mammals.” (Principle 5 of polyvagal theory, PVI website)

3. Polyvagal theory is astonishingly reminiscent of triune brain theory. This theory, proposed by Paul MacLean in the 1960s, has embedded itself in pop culture as the notion that we have a “lizard brain” underneath our “mammalian brain” (the limbic system) and our “primate/human” brain (the cortex). On the surface, polyvagal theory almost seems derivative, and in fact Porges mentions MacLean as a significant influence in several of his papers (for instance, Porges 2003a). Dr. Sarah McKay provides an interesting analysis of the triune brain theory in her article Rethinking the Reptilian Brain, and much is relevant to the sociocultural phenomenon that is polyvagal theory.

4. These experiments found that subjects preferred scientific explanations that included information from one level below the scientific field in question, even when that information didn’t actually improve the explanation (i.e. subjects preferred explanations for psychology that evoked neuroscience, biology that evoked chemistry, chemistry that evoked physics, etc). The effect was strongest for the psychology/neuroscience pairing, and was actually reversed for the the social science/psychology pairing (i.e. participants gave lower ratings to explanations for social phenomena that included reductive information about psychology). The authors speculate this may be due to a relatively positive view of neuroscience combined with a negative view of psychology in popular culture.

Hat tip for the references goes to Sarah McKay and her aforementioned critical article about the “triune brain theory.”

5. The following quote from Porges’ most recent publication (as of this writing) reveals unequivocally that he has not sincerely engaged with the criticisms of the theory, going so far as to present his conclusions as “uncontroversial” while entirely neglecting to mention the published controversy. The most he’s done over the span of his polyvagal publications is slightly modified some of his phrasing to be less resoundingly at odds with the available evidence, without any acknowledgement or frank discussion of the possible reasons for him doing so.

“Polyvagal Theory extracts from contemporary neuroanatomy, neurophysiology, evolutionary biology several basic uncontroversial conclusions that can be succinctly summarized: (1) mammals have two vagal pathways (i.e., supradiaphragmatic, subdiaphragmatic), (2) evolution and development provide insight into the changes in brainstem structures that enable mammals to be physiologically calm and socially interact. Functionally, mammals have neural attributes that efficiently, via rapidly responding cardioinhibitory fibers (e.g., myelinated ventral vagal pathways originating in nucleus ambiguus), calm autonomic state and promote social communication. The ventral vagal pathways also coordinate and repurpose circuits that evolved to support defense in socially relevant processes, such as play (i.e., ventral vagal influences constrain sympathetic reactivity), and intimacy (i.e., ventral vagal influences constrain dorsal vagal reactivity).” (Porges 2022b)

Selected Quotes from ResearchGate

I’ve included some key quotes from the various threads (linked below), but the threads themselves contain a great deal more evidence, anecdotes, exchanges between scientists and clinicians, shared personal correspondence between researchers, and even some behind-the-scenes drama that potentially sheds some light on the personalities involved, so definitely check out the original threads if you’re interested.

6. “As you know its practically impossible for somebody within the therapeutic community to talk about trauma without talking about Porges.” (Daniela Sieff, 4 Mar 2020)

7. “Many of my clinician friends talk about polyvagal theory like it was the law of gravity.” (Irwin Altrows, 31 Jan 2021)

8. “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.” (Leslie Ellis, 6 May 2020)

9. [the collected references mentioned in the text are listed and linked below; below is the Grossman quote:]

“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.”” (Grossman, 21 Oct 2017)

10. “Certainly the very first validation paper by Katona & Jih (1975, I believe; which, in fact, got this circus rolling) provides the basic rationale and method for applying respiratory sinus arrhythmia (RSA; i.e. high-frequency heart-rate variability) as an INDEX of cardiac vagal tone (essentially the extent to which heart rate, and no other physiological function is influenced by parasympathetic activation). Unfortunately, this paper has often gone unread and uncited in recent years and I will attach here a .pdf copy if I can find it easily. 

Two comments about this study: 1) it makes clear that cardiac vagal tone, as I just defined above, is not equivalent or synonymous with RSA, but that RSA may merely index vagal control of heart rate (and nothing else) under the specific conditions of the experimental procedure (perhaps not under all circumstances—as seems clear from subsequent research). 2) In the equation for predicting cardiac vagal tone by means of RSA, there is a variable that relates to respiratory parameters of breathing rate and breath volume. This variable must stay constant or be somehow experimentally or statistically controlled for the prediction of cardiac vagal tone to be accurate. In all honesty, back 40 years when I got started with this business, I, myself, overlooked this variable; only when I performed an experiment to examine the possibly confounding role of respiration (Grossman, Karemaker & Wieling, 1991) was it clear to me just how much breathing could muck up prediction of cardiac vagal tone when respiration changed within its usual range of natural variations. Despite the definitiveness of the two studies, this topic remains often ignored, debated or downright denied, despite a huge other bunch of supporting literature. I believe this occurs because many people are totally sold on the idea that RSA=cardiac vagal tone, [or] even worse RSA=vagal tone of all parasympathetic functions of the body, a kind of general vagal tone (Thomas Ritz gives clear evidence of that not being so, and there are many others too).

In the last few years, I have become increasingly aware of just how much the RSA literature assumes the latter, that RSA is literally vagal tone, and not just cardiac vagal tone. When researchers attempt to be a bit more careful, they call RSA a measure of parasympathetic control, almost always without considering the respiration in the very name of RSA. In fact, RSA is a phenomenon defined by, and operationalizing, the coordination of breathing cycle and heart rate. It is predominantly parasympathetically mediated, but may often say little to nothing, other than the vagus helps to coordinate breath and heart rate. This phenomenon seems very likely to have evolved as a help and perhaps safety valve for earlier vertebrates that didn’t have separation of circulation and ventilation (like we and other mammals do). It’s a specific phenomenon that under some conditions may reflect (pretty well) the degree of vagal influence upon heart rate at the moment. But RSA was certainly not devised by evolution for the latter purpose. So in my opinion, the whole literature should refer to RSA as a measure of vagal cardio-respiratory coupling, and no more, especially when other factors like respiratory rate and volume, concurrent cardiac sympathetic tone, physical activity etc. are not considered or controlled.” (Paul Grossman, 16 Dec 2021)

11. “Porges makes a similar serious category mistake when he assumes that either vagally mediated bradycardia or HRV (he actually means respiratory sinus arrhythmia [RSA]) is necessarily either a negative or positive indicator of health. He also clearly errs when he assumes that either phenomenon is equivalent to a general measure of cardiac vagal tone (i.e. the average extent of vagal control of heart rate during a specific condition or time period). Each of these two processes characterizes a distinct cardiac vagal phenomenon that need not at all be related to each other nor directly indicate either good or poor health:

Vagally mediated bradycardia is a phenomenon in which vagal traffic to the sinoatrial node of the heart profoundly and swiftly slows the heart rate. Such bradycardia often occurs under completely normal conditions like diving into cold water, bearing down during a bowel movement or just holding one’s breath for several seconds. Nevertheless, bradycardia can sometimes also spell risk, e.g. for a fetus in utero, during inflammatory disease or when there is specific chemical or metabolic dysfunction.

RSA, on the other hand, is the primarily vagus-mediated pattern of heart rate slowing during expiration and speeding during inspiration; it is a direct manifestation of the vagal contribution to coordinating heart rate and ventilation (breathing). Among healthy people, RSA is much diminished by movement and exercise, by rapid breathing, by normal ageing, and when cardiac vagal tone becomes extremely large or during sympathetic stimulation. RSA decrement, however, can also be a sign of dysfunction or disease, e.g. with fever, autonomic neuropathy, heart disease, obesity and poor physical fitness.

Contrary to Porges’ assumptions, each phenomenon emanates either exclusively or very primarily from the same ventrally located vagal nucleus Ambiguus in the brainstem, neither one to any significant extent from the dorsal motor nucleus. This evidence base seems very firm, and there is no evidence to the contrary that I know of or that Steve cites. Thus neither phenomenon is necessarily an index of health, RSA is not an index of cardiac vagal tone under all conditions, and consequently, there is no paradox when RSA and bradycardia do not necessarily correlate with each other.

The so-called paradox that Porges describes is artificial and derives from his erroneous assumption that RSA is equivalent to cardiac vagal tone, rather than just an approximate index of cardiac vagal tone, and then one with several caveats. Babies (and others) sometimes show bradycardia but not RSA, especially when cardiac vagal tone (i.e. the average vagal control of heart rate) is very large.” (Grossman, July 6 2022)

12. “I know a number of trauma survivors and clinicians who have taken the PV to heart. They know that it is disconfirmed, but they are still surrounded by it. I’ve posed a question to them today about how the PV theory helps them…They don’t actually understand it. Here are some of the answers:

• “I really loved it at first and know other practitioners who do as well because it helps having a model to explain how something not currently happening in the present moment is still continuously happening within the body. There is such a stigma against invisible illnesses that have huge impacts on a persons’ life and wellbeing, yet within the scientific evidence based model they have no explanation and the silent undertone is that people often conclude is that they are either making it up. I do also think it helps them connect with their trauma in a present moment way, because having something impact you from such a long time ago may not make sense to the brain/intellect, but the body is still living in that older pattern.” 
• “Hmmmm….I think people would say that when you tone up or tone down your vagal nerve (depending if you fight/flee or if you freeze/dissociate) then you will not react haphazardly. You will have more space to feel many different things and then you can respond logically to what is happening in your current environment.” 
• “My understanding was that vagal tone is more a way to explain how the nerve has been conditioned to respond and I really feel and think it just gives some validation to how someone may be feeling and that in and of itself can (and does) get people to start their road to recovery. In my experience with people who teach this I’m not seeing a big emphasis on ‘toning’ up or down…just the theory gives, again, some context and validating witnessing to the feelings.” 
• “The polyvagal theory gave me context and understanding of my freeze response and what I’ve been feeling all my life. Till then it made no sense, and I couldn’t wrap my mind around, or even understand, or consider there was an actual nervous system legit reason for this shut down that also held/holds so much charge to it. It seems in this day and age there is a need for some explanation to the seemingly unseen and unreasonable – so something that gives reasonable logic to how the body is responding makes sense that it could help people perhaps start the healing and relating to their body process for themselves. I am very logical, but my body doesn’t respond in kind- and it can take over my ‘logic’. So it seems that the polyvagal theory offers some sense making and gives some validation to these responses in the body – it did for me.”” (Karla McLaren, 20 & 24 Jul 2021)

13. “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.” (Karla McLaren, 6 May 2020)

14. “I believe that a gap between academic research settings and clinical settings (right down to our limited access to Pubmed full text/academic library privileges) sets the stage for this discussion thread. Paul, It is wonderful that you have made this effort to bridge the gap by reaching out through a community forum rather than strictly through scientific journals! We lay clinicians would rarely have access to this data….

…I am largely jumping into this conversation as a clinician (with my very nominal research background) because I’m afraid that this type of conflation by lay practitioners leads to another painful outcome that I am regularly wading through with the triune brain and “lizard brain” myth and its ongoing theoretical hegemony in my world as a trauma therapist. It’s disheartening for me to publicly admit that our applied field, with its larger disconnection from the scientific data, is slow to catch up. This problem leads to book, after book, building a narrative founded on theory that has long since been disavowed by updated science. I hope that I am not facing this with PVT in the future, but given what I am qualitatively observing in my community, I expect to see future books presenting PVT premises as foundational research in trauma and relationship treatment books.” (Julie Gustafson, 29 May 2021)

15. “The basic framework, that is, fight/flight/freeze/faint, etc., and the ways in which the perception of threat interrupts social engagement, are psychological and behavioral findings that came before PVT. The point of PVT was supposed to be a neuroanatomical/neurophysiological explanation for those findings. And although people are designing therapeutic and practice approaches that address that basic framework, they are using PVT as a catch-all for the explanations for those findings. And, as you say, which nerves are doing what aren’t all that important necessarily for the therapies to work properly, but PVT isn’t why those therapies are working. And if we focus on PVT as the explanation, we might miss other explanations which might open up other kinds of therapeutic approaches.” (Max Pearl, 24 Jul 2021)

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

So please believe your experience but, at the very least, leave room for some doubt about what caused your improvement. All the best.” (Paul Grossman, 1 Oct 2019)

17. “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-the–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).” (Paul Grossman, 7 Jul 2020)

References

Porges’ Review Articles

All of the single-author review articles Porges has written about polyvagal theory, in chronological order for easy reference. *I’ve also included three experiments/collaborative papers from his group that are directly related to polyvagal theory.

1. Orienting in a defensive world: mammalian modifications of our evolutionary heritage. A Polyvagal Theory. Psychophysiology, 1995.
2. Emotion: an evolutionary by-product of the neural regulation of the autonomic nervous system. Ann N Y Acad Sci, 1997.
3. Love: an emergent property of the mammalian autonomic nervous system. Psychoneuroendocrinology, 1998.
4. The polyvagal theory: phylogenetic substrates of a social nervous system. Int J Psychophysiol, 2001.
5. The Polyvagal Theory: phylogenetic contributions to social behavior. Physiol Behav, 2003a.
6. Social engagement and attachment: a phylogenetic perspective. Ann N Y Acad Sci, 2003b.
7. A phylogenetic journey through the vague and ambiguous Xth cranial nerve: a commentary on contemporary heart rate variability research. Biol Psychol, 2006a.
8. The Polyvagal Perspective. Biol Psychol, 2006b.
9. The polyvagal theory: new insights into adaptive reactions of the autonomic nervous system. Cleve Clin J Med, 2009.
10. The Early Development of the Autonomic Nervous System Provides a Neural Platform for Social Behavior: A Polyvagal Perspective. Infant Child Dev, 2011.
11. Cardiac vagal tone: a neurophysiological mechanism that evolved in mammals to dampen threat reactions and promote sociality. World Psychiatry, 2021a.
12. Polyvagal Theory: A biobehavioral journey to sociality. Compr Psychoneuroendocrinol 2021b.
13. Polyvagal Theory: A Science of Safety. Front Integr Neurosci, 2022a.
14. Heart Rate Variability: A Personal Journey. Appl Psychophysiol Biofeedback, 2022b.
15. *Sargunaraj et al. Cardiac rhythm effects of .125-Hz paced breathing through a resistive load: implications for paced breathing therapy and the polyvagal theory. Biofeedback Self Regul, 1996.
16. *Reed et al. A neural explanation of fetal heart rate patterns: A test of the polyvagal theory. Dev Psychobiol, 1999.
17. *Porges et al. Heart rate and respiration in reptiles: contrasts between a sit-and-wait predator and an intensive forager. Brain Cogn, 2003.

Critical Papers and ResearchGate Threads

1. Grossman P & Taylor EW. Toward understanding respiratory sinus arrhythmia: relations to cardiac vagal tone, evolution and biobehavioral functions. Biol Psychol, 2007.
2. Taylor et al. An overview of the phylogeny of cardiorespiratory control in vertebrates with some reflections on the ‘Polyvagal Theory’. Biol Psychol, 2022.
3. Grossman. ResearchGate (main project): Examining Porges’ “Polyvagal” suppositions (2016, ongoing)
4. Grossman. ResearchGate (question): After 20 years of “polyvagal” hypotheses, is there any direct evidence for the first 3 premises that form the foundation of the polyvagal conjectures? (2016, ongoing)
5. Grossman. ResearchGate (question): Does anyone know of research documenting large heart-rate decrease during episodes of psychological dissociation? (2016, ongoing)

References re: Role of DMNV in Bradycardia

1. Cheng et al. Projections of the dorsal motor nucleus of the vagus to cardiac ganglia of rat atria: an anterograde tracing study. J Comp Neurol, 1999.
2. Cheng Z & Powley TL. Nucleus ambiguus projections to cardiac ganglia of rat atria: an anterograde tracing study. J Comp Neurol, 2000.
3. Cheng et al. Domoic acid lesions in nucleus of the solitary tract: time-dependent recovery of hypoxic ventilatory response and peripheral afferent axonal plasticity. J Neurosci, 2002.
4. Cheng et al. Attenuation of baroreflex sensitivity after domoic acid lesion of the nucleus ambiguus of rats. J Appl Physiol, 2004.
5. Cheng et al. Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence. Am J Physiol Regul Integr Comp Physiol, 2004.
6. Farmer et al. Brainstem sources of cardiac vagal tone and respiratory sinus arrhythmia. J Physiol, 2016.
7. Geis GS & Wurster RD. Cardiac responses during stimulation of the dorsal motor nucleus and nucleus ambiguus in the cat. Circ Res, 1980.
8. Gourine et al. Cardiac vagal preganglionic neurones: An update. Auton Neurosci, 2016.
9. Gray et al. Parasympathetic control of the heart. III. Neuropeptide Y-immunoreactive nerve terminals synapse on three populations of negative chronotropic vagal preganglionic neurons. J Appl Physiol, 2004.
10. Verberne, Anthony JM. Differential cardiac parasympathetic innervation–what is the functional significance? Am J Physiol Regul Integr Comp Physiol, 2004.

Additional Papers and Books Mentioned

• Atzil et al. Growing a social brain. Nat Hum Behav, 2018.
• Benish et al. Culturally adapted psychotherapy and the legitimacy of myth: a direct-comparison meta-analysis. J Couns Psychol, 2011.
• Borrell-Carrio et al. The Biopsychosocial Model 25 Years Later: Principles, Practice, and Scientific Inquiry. Ann Fam Med, 2004.
• Dale et al. Childhood Maltreatment Influences Autonomic Regulation and Mental Health in College Students. Front Psychiatry, 2022.
• Engel GL. The need for a new medical model: a challenge for biomedicine. Science, 1977.
• Hopkins et al. The seductive allure is a reductive allure: People prefer scientific explanations that contain logically irrelevant reductive information Cognition, 2016.
• Kolacz et al. Cardiac autonomic regulation and joint hypermobility in adolescents with functional abdominal pain disorders. Neurogastroenterol Motil, 2021.
• Kovacic et al. Impaired Vagal Efficiency Predicts Auricular Neurostimulation Response in Adolescent Functional Abdominal Pain Disorders. Am J Gastroenterol, 2020.
• Payne et al. Somatic experiencing: using interoception and proprioception as core elements of trauma therapy. Front Psychol, 2015.
• Porges et al. Respiratory sinus arrhythmia and auditory processing in autism: modifiable deficits of an integrated social engagement system? Int J Psychophysiol, 2013.
• Porges et al. Reducing Auditory Hypersensitivities in Autistic Spectrum Disorder: Preliminary Findings Evaluating the Listening Project Protocol. Front Pediatr, 2014.
• Rajabalee et al. Neuromodulation Using Computer-Altered Music to Treat a Ten-Year-Old Child Unresponsive to Standard Interventions for Functional Neurological Disorder. Harv Rev Psychiatry, 2022.
• Rosenberg, Stanley. Accessing the Healing Power of the Vagus Nerve: Self-Help Exercises for Anxiety, Depression, Trauma, and Autism. 2017.
• Weisberg et al. The Seductive Allure of Neuroscience Explanations J Cogn Neurosci, 2008.

Other Critiques of Polyvagal Theory

James C Coyne on medium.com – various critical articles regarding PVT
RIP Polyvagal Theory by Shin Shin Tang (medium.com)
The Problem with the Polyvagal Theory by Max Pearl
Evolution of a Theory: Polyvagal is Not Dead by Janae Elisabeth
The Dark Side of Polyvagal Theory by Brian Dunning