Polyvagal Theory: Summary, Premises & Current Status
Abridged by Polyvagal Institute with Permission, February 2023
Below is an abridged version of the most recent commentary from Dr. Stephen Porges. For the complete paper, please refer to the unabridged PDF version.
Autonomic state as a neural platform. Polyvagal Theory (PVT) conceptualizes autonomic state as a neural platform influencing behavioral, physiological, and psychological responses. Rather than assuming a cause-and-effect or stimulus-response model that assumes a psychophysiological parallelism (see Porges, 2022), the theory proposes that autonomic state functions as an intervening variable mediating the response.
Hierarchy of autonomic states: An emphasis on two vagal pathways. The model can be conceptualized as a stimulus-organism-response (S-O-R) model in which autonomic state is expressed and experienced along a continuum from fear-related immobilization involving dorsal vagal mechanisms, to fight-flight mobilization involving sympathetic mechanisms, and finally to a calm socially accessible state involving ventral vagal mechanisms. This sequence is hierarchical, with the latter state functionally having the capacity to co-opt the other states to enable hybrid states of mobilization without fear (play, dance) and immobilization without fear (shared moments of intimacy). From an evolutionary perspective, the sequence is a hierarchical representation of the evolutionary history of the vertebrate ANS (Autonomic Nervous System) as it became encoded in the ANS of humans and other social mammals.
The newest circuit, dependent on the ventral vagal complex, is the product of a ventral migration of cardioinhibitory neurons in the brainstem to the ventral nucleus of the vagus from the dorsal nucleus of the vagus. This ventral migration appears to have been completed in the earliest mammals as a defining characteristic of their transition from ancient extinct reptiles about 220 million years ago. The integration of cardioinhibitory neurons into the ventral vagal complex provided a circuit that integrated suck-swallow-vocalize-breathe processes with a newer mammalian, myelinated cardioinhibitory ventral vagal pathway that is expressed as RSA (Respiratory Sinus Arrhythmia) in the heart rate pattern. This circuit, which initially links ingestion through nursing with behavioral calming, provides the basic structures that enable co-regulation and connectedness through the lifespan.
According to the theory, survival challenges trigger a process of dissolution (or evolution in reverse) that disinhibits the phylogenetically older defense circuits of fight/flight or freeze/collapse. Dissolution disrupts homeostatic functions and predisposes visceral organs to disease. Within the PVT model, disruption of homeostatic functions operationally defines a physiological state of stress and psychological states of anxiety and threat. In contrast, when the ANS successfully supports homeostatic function, feelings of safety and opportunities to co-regulate and connect are spontaneously emergent. PVT is an integrative model emphasizing brainstem regulation of the ANS. PVT does not preclude the important influences of both bottom-up signals, through interoception, or top-down influences, via memories, visualizations, or associations, on these regulatory circuits.
Retrospective context. When initially formulated (Porges, 1995), PVT was conservatively organized upon several premises or inferences extracted from the literature. These premises were plausible explanations of important phenomena observed in psychophysiology and in perinatology for which the neurophysiological mechanisms had not been identified. By proposing these premises, the scientific community could confirm or refine these inferences through more in-depth exploration of the published literature and empirical research. The premises of PVT provided a new framing of questions that tied the neuroanatomy and neurophysiology of the ANS to clinical conditions and psychophysiological processes.
PVT focused on a plausible explanation of the ‘vagal paradox’ in two disparate disciplines, perinatology and psychophysiology. Functionally how could the vagus be the pathway for both RSA and bradycardia? The publication of the premises functionally framed the scientific questions for subsequent empirical research to evaluate specific clinical conditions and psychophysiological processes in which this paradox was observable. By proposing plausible relationships and identifying the specific metrics to map ventral vagal (i.e., RSA) and dorsal vagal (i.e., bradycardia) function, the research in these disciplines could incorporate a deeper neurophysiological understanding of the mechanisms underlying these observations. With this new perspective, it was optimistically hoped that vulnerabilities could be monitored to improve clinical outcomes and predict behavior.
PREMISES OF PVT, DERIVED FROM THE SCIENTIFIC LITERATURE
As I developed the theory, I extracted principles from the literature that I summarized as premises (see below) upon which a theory could be established to generate testable hypotheses. From my perspective the premises were not controversial, but logically derived from the literature. The conceptualization of PVT required a ‘transdisciplinary’ approach, because the assumed foundational disciplines of clinical medicine and psychophysiology did not have the tools to conceptualize the questions generated by PVT. Since the premises were dependent on my interpretations of the literature, I welcomed alternative interpretations. Below are the five premises as presented in the first publication of the theory (Porges, 1995).
Premise 1: Neurogenic bradycardia and RSA are mediated by different branches of the vagus and need not respond in concert.
Premise 2: Neurogenic bradycardia associated with orienting is a phylogenetic vestigial relic of the reptilian brain and is mediated by DMNX [dorsal vagal nucleus].
Premise 3: Withdrawal of cardiac vagal tone through NA [nucleus of the ventral vagus, nucleus ambiguus] mechanisms is a mammalian adaptation to select novelty in the environment while coping with the need to maintain metabolic output and continuous social communication.
Premise 4: The ability of NA to regulate special and general visceral efferents may be monitored by the amplitude of RSA.
Premise 5: Emotion, defined by shifts in the regulation of facial expressions and vocalizations, will produce changes in RSA and branchiomotor tone mediated by NA.
CURRENT STATUS OF PREMISES
Premise 1 and Premise 2 relate to the proposed mediation of neurogenic bradycardia and RSA being dependent on different vagal circuits with the ventral vagal nucleus regulating RSA and the dorsal vagal nucleus regulating neurogenic transitory bradycardia. The literature reviewed in previous papers outline the theory (e.g., Porges, 1995, 2007) provided conclusive evidence that in mammals, the two branches of the vagus are profound regulators of autonomic function relevant to adaptive biobehavioral reactions. A more recent review confirms these conclusions (see attached, Porges under review). Moreover, empirically the two indices are identifiable in the beat-to-beat heart rate pattern.
Premise 3 is supported by hundreds of publications across several laboratories documenting the reduction of cardiac vagal tone via a depression of RSA during metabolic demands and attentive challenges.
Premise 4 proposes that the role of the nucleus ambiguus in the ventral vagal complex enables RSA to index the status of the system, which was later labeled as the “social engagement system” (Porges, 1998).
Premise 5 further proposes that the ventral vagal complex is a nexus for the expression of features of emotion (e.g., vocal intonation, facial expressions), which in turn are also mirrored in RSA (see Porges, 1998; Porges et al., 1994).
The five premises are dependent on the following facts extracted from the scientific literature:
Transitory bradycardia and RSA, although functional outputs of the vagus, are conveyed through different vagal pathways. In general, transitory bradycardia is a survival reaction in response to threat cues. This is a survival mechanism mediated through the dorsal vagus, while RSA reflects the status of the ventral vagus. RSA reflects the functional support of homeostatic functions through ventral vagal pathways. During challenges and threats the two pathways may work synergistically, resulting in depressed RSA during episodes of bradycardia. This does not preclude the potential influence of both vagal pathways on tonic heart rate levels or transitory heart rate responses in safe contexts during states of optimal ventral vagal tone.
The three primary neural systems involved in autonomic regulation form a phylogenetically ordered response hierarchy, which is mirrored in development and responds in a predictable order when under survival challenge.
The ventral vagal nucleus, nucleus ambiguus, is part of an integrated ventral vagal complex controlling the striated muscles of the face and head via special visceral efferent pathways that are involved in sucking, swallowing, breathing, vocalizing, and listening. These structures are involved in nursing and develop into a social engagement system to detect and signal safety and threat to conspecifics. This system is involved in the adaptive expression of emotion.
The current widespread interest in noninvasive vagal nerve stimulation is revealing that stimulating the afferents of vagus, as well as afferent pathways of the facial and trigeminal nerves, will stimulate ventral vagal tone.
CURRENT STATUS OF PVT
The foundation of Polyvagal Theory (PVT) is based on the extraction of well accepted principles from the scientific literature. These included the well documented phylogenetic and ontogenetic sequence of brainstem structures regulating cardioinhibitory processes that form the basis of a response hierarchy consistent with the Jacksonian principle of dissolution. Given its strong scientific foundation, there has been little criticism of the theory in the scientific literature. There have, however, been misrepresentations of the theory that have been used to argue that the theory is not scientifically supported. In general, the misrepresentations can be traced to two sources: publications by Edwin W. Taylor and colleagues, and social media posts by Taylor’s colleague, Paul Grossman.
Grossman and Taylor have systematically structured a straw man argument based on misrepresentations of PVT to create the appearance of scientifically valid arguments. In Taylor’s case he has used false attributions of PVT to highlight the importance of his findings. In contrast to Taylor, Grossman has not conducted research to generate data to falsify PVT. Instead, Grossman has elaborated on Taylor’s misrepresentation to position himself in social media as the ‘debunker’ of PVT. Since the points of contention are not supported by facts, the work by Grossman and Taylor fails to challenge any of the tenets embedded in PVT. Rather than identifying points of disagreement, their straw man argument is dependent on faulty attributions of the theory and NOT on PVT. The net result of their efforts has been to sow confusion around the theory, especially among those not familiar with the foundational papers.
The above explanation of the theory and its supporting literature document the features of PVT that have been obfuscated by Grossman and Taylor. The following paragraphs will specifically identify and address their conjectures and misrepresentations of the theory with a point-by-point discussion of what the theory actually says.
Misrepresentation of the scientific bases of PVT. Grossman has used social media to promote his claim that there is no scientific evidence for Premises 1 and 2. Although Taylor’s research is not relevant to PVT, Grossman frequently cites Taylor’s publications to support his claims (Campbell et al., 2005, 2006; Monteiro et al., 2018; Sanches et al., 2019; Taylor et al., 2006, 2022). Interestingly, other than stating that the Premises are false, Grossman has provided no alternative interpretation of the literature. In addition, other than depending on Taylor’s misrepresentations, he has not reported any documented contradictions between the literature and PVT. Unfortunately, others, who have assumed that his statements were scientifically sound, have quoted him and set off a cascade of misinformation in social media.
Misrepresentation of the uniqueness of mammalian RSA in PVT. Taylor and his group blur the well-documented distinctions between mammalian RSA and heart rate-respiratory interactions in other vertebrates. As emphasized in the theory and throughout this paper, mammalian RSA is dependent on the ventral vagus and the functional output of ‘myelinated’ cardioinhibitory vagal fibers originating in the ventral vagus. In contrast, in other vertebrate species heart rate-respiratory interactions involve the dorsal vagal nucleus and communicate to the heart, in general, via unmyelinated fibers. As described in the sections above, there is scientific consensus that neuroanatomical structures and neurophysiological pathways involved in producing mammalian RSA are distinguishable from respiratory-heart rate interactions in other vertebrates. However, in building his argument, Taylor obfuscates this distinction and redefines RSA as being inclusive of all manifestations of respiratory-heart rate interactions observed in all vertebrates. With his definition of RSA, he argues that if species other than mammals express RSA (i.e., his definition of RSA as any form of heart rate-respiratory interaction) then PVT is false.
Taylor and his colleagues repeatedly press their inaccurate argument, since they have incorrectly assumed that heart rate-respiratory coupling being solely mammalian is a foundational principle of PVT. Following their logic, observations of heart rate-respiratory coupling in other vertebrate species would be inconsistent with the theory. Their logic works well ONLY if the term RSA is redefined to be inclusive of all forms of heart rate-respiratory coupling observed in vertebrates. Then, since PVT uses the construct of RSA, they could assume that any statement regarding the uniqueness of RSA as being mammalian would be false. However, their strategy misses two important points about RSA that relate to PVT: 1) the specific vagal pathways mediating RSA in mammals, unlike their ancestral vertebrates, originate in the ventral vagus, and 2) RSA is a portal to the function of the ventral vagus enabling the testing of polyvagal-informed hypotheses and is NOT a foundational construct of the theory.
Misrepresentation of the role of myelinated vagal fibers in PVT. Consistent with the scientific literature, PVT proposes that only mammals have a myelinated cardioinhibitory vagal pathway originating from the ventral vagus. The foundational PVT papers have consistently stated that these two features, in combination and not independently, reliably distinguish mammalian RSA from respiratory interactions observed in other vertebrate species. Even with these strong statements qualifying the neuroanatomical structures involved in mammalian RSA, Taylor and his colleagues have misrepresented PVT by stating incorrectly that PVT assumes that only mammals have a myelinated vagal pathway (Monteiro et al., 2018). Consistent with their ’straw man’ argument, with this ‘new’ PVT attribution, Taylor and his group highlight their finding of a myelinated cardioinhibitory pathway originating in the dorsal vagal nucleus in the lungfish as falsifying PVT. They make their argument despite the fact that the cardioinhibitory vagal pathway in lungfish originates in the dorsal vagal nucleus. Taylor’s statements misrepresent the theory’s foundational papers that limit the neurophysiological origin of mammalian RSA to myelinated cardioinhibitory vagal pathways originating ONLY in the ventral vagus. He and his colleagues have repeatedly misrepresented the theory as stating that only mammals have myelinated cardioinhibitory pathways without qualifying their anatomical origin in the ventral vagus. In this manifestation of misrepresenting the theory, they have repurposed the word myelinated from being associated ONLY in mammals with cardioinhibitory pathways originating in the ventral vagal nucleus to a general feature of cardiorespiratory interaction independent of nucleus of origin (i.e., either ventral or dorsal vagal nucleus).
Taylor and colleagues have questioned the assumption that the dorsal vagal nucleus is an evolutionarily older structure than the ventral vagus. The literature including Taylor’s work (Taylor, 1999) has reliably documented in modern vertebrates representing groups of vertebrates, which evolved prior to mammals, that the prominent cardioinhibitory vagal neurons originated in the dorsal nucleus of the vagus. Thus, it is indisputable that estimating an evolutionary timeline through phylogeny, cardioinhibitory neurons originated first in the dorsal nucleus of the vagus and then consistent with Taylor’s own work (2022) migrated ventrally. In the earliest (now extinct) mammals this ventral migration was sufficiently complete to embed cardioinhibitory functions with activities of branchiomotor neurons (i.e., special visceral efferent pathways) that regulate the striated muscles of the face and head promoting ingestion (e.g., nursing) and social communication via facial expression and vocalizations.
RSA has historically been used to describe a mammalian heart rate rhythm. It has a history of use that has been agnostic of the heart rate-respiratory interactions of other vertebrates. In fact, Taylor in his earlier papers (i.e., prior to 2000) uses the term RSA only when discussing mammals. Perhaps, Taylor’s atheoretical agenda, to document that respiratory-heart rate interactions are a highly conserved phenomena across several vertebrate species, has contributed to his repeated, inaccurate statements regarding their underlying neural mechanisms. Although the phenomenon is highly conserved during evolution and even evidenced in mammals, the underlying mechanisms have been modified through evolution (e.g., Richter & Spyer, 1990). These points are emphasized in PVT. The foundation of PVT focuses on the structural and functional consequences of mammalian modifications of this highly conserved system. This point was unambiguously stated in the title of the paper introducing PVT (Porges, 1995) - Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A polyvagal theory.
Taylor’s generalization of common mechanisms underlying heart rate-respiration interactions across vertebrate species has its limitations. Evolution continues to repurpose and modify how the mammalian autonomic nervous system is both structured and functions. If we do not acknowledge the evolutionary repurposing of structures, we would be vulnerable to being criticized as accepting ‘recapitulation’ theory, i.e, a disproven theory that assumes evolution not only preserves structure, but also function.
The scientific method seeks to distinguish valid points from conjectures. Theories flourish only if they are useful in describing phenomena that can inform future investigations. Of course, theories must be modified and informed by empirical research and, when necessary, replaced by alternative theories that are more effective in explaining naturally occurring phenomena. If we use this as an acceptable standard, then PVT provides a testable model describing how the autonomic nervous system reacts to threat and safety. The theory specifically provides an understanding of the core features of the mammalian nervous system needed to co-regulate and trust others. It also provides insights into the consequences of autonomic state for mental and physical health. Perhaps, most importantly, the theory gives voice to the personal experiences of individuals who have experienced chronic threat (i.e., trauma and abuse) and structures an optimistic journey towards more optimal mental and physical health. It is this core, described by PVT, that links our biological imperative to connect with others to neural pathways that calm our autonomic nervous system. These systems, in the context of mammalian physiology, are foundational processes through which behavioral experiences can lead to sociality and optimal health, growth, and restoration.
Copyright 2023, Stephen W. Porges | References