Polyvagal Theory: Summary, Premises & Current Status 

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.     

1. 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. 
    

2. 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.
    

3. 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). 
    

4. 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.
    

5. 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.