2.14
Polyvagal Perspectives: a Book Review
In August 2024, Porges published a new book. Initially, we considered integrating it into our already-written chapters and updating them accordingly. However, this soon seemed overwhelming, so we wrote a dedicated review instead. The book’s primary interest lies in examining what Porges has retained from the original theory 30 years later, and how much he may have altered under the pressure of modern research.
In the first chapter, THE VAGAL PARADOX: A POLYVAGAL SOLUTION, we encounter the same tentative language (“if we are right,” “it is possible,” “we might,” “hypothetically”) that we found in earlier articles (e.g., Porges, 1995). This non-committal style creates an illusion of reasoning without solid evidence or a clear stance, making the arguments harder to refute directly. Over time, this repetitive reliance on speculative claims borders on the ad nauseam fallacy—repeating weak assertions until they appear credible through sheer repetition.
On page 6, Porges discusses the dorsal vagal (DVMN) effect on left ventricular contractility (inotropic). As noted in the Dorsal chapter, Porges fails to mention how new optogenetic technology supports a positive inotropic effect of the DVMN (Machhada, 2020). Improved contractility contradicts his concept of dorsally induced death. He then pivots to the vagal paradox: the same vagus is positive and negative. Quoting Richter (1957)—a dated source who never used the term “dorsal” and instead suggested a psychological cause, “hopelessness,” during rat drowning experiments—Porges makes the parasympathetic tone the cause of death.
In distinguishing mammals from reptiles, Porges notes that “at birth, mammalian offspring can functionally suckle” (p. 9) and “lactation depends on a functional ventral vagal complex.” However, he neglects that swallowing is regulated by the NTS (nucleus tractus solitarius), a crucial part of the dorsal vagal complex. Bieger and Neuhuber describe this in detail in Neural Circuits and Mediators Regulating Swallowing in the Brainstem (2006). Sucking requires coordination between breathing and swallowing, which the VVC alone cannot facilitate. Additionally, the NTS integrates gustatory afferent signals (taste).
Porges reiterates the tenuous hypothesis that the VVC extracts the voice from airborne acoustic signals, contrasting it with reptilian bone conduction—a theory supported by the singular work of Borg and Counter (1989). However, low-frequency sounds, like a cat's 20-30 Hz purr (Herbst, 2023) or Tibetan monks’ chanting, are not inherently threatening.
Again, Porges emphasizes a distinction between RSA (respiratory sinus arrhythmia) and heart-breath interactions, stating the former occurs only in mammals, while the latter applies to all vertebrates.
In EVOLUTION: PARALLELS BETWEEN ONTOGENY AND PHYLOGENY, Porges claims that evolution repurposes neural regulation of the ANS to support social behavior. However, evolution’s only 'purpose' is species survival, making Porges’ interpretation teleological—biologists do not view evolution as having a specific purpose.
Later (p. 12), Porges concedes that “new molecular techniques, which were not available when the theory was proposed, often do not agree with the fossil record.” He then dismisses this contradiction as irrelevant to PVT, stating that “the phylogenetic sequence relevant to PVT is reflected in the embryology of modern mammals, including humans.” This is a classic example of circular reasoning. Porges assumes phylogeny mirrors ontogeny, and when new evidence challenges phylogeny, he dismisses it by reinforcing the link to ontogeny, closing the argument to critique.
In EVOLUTIONARY TRANSITION FROM REPTILES TO MAMMALS, Porges references a “common ancestor,” citing Meet the Ancient Reptile That Gave Rise to Mammals (Geggel, 2016), which describes a cynodont as the ancestor of mammals. However, the split between synapsids (leading to mammals) and sauropsids (leading to reptiles) occurred 326 million years ago (mya), not 220 mya as stated—making the cynodont a mammaliamorph synapsid, not a reptile.
Porges states that “since there is evidence that the earliest mammals could lactate” (Vogel, 2018), they likely had a functional ventral vagus coordinating with ingestive structures, similar to modern mammals. Yet, all jawed vertebrates possess branchiomotor neurons controlling prey capture, biting, and swallowing. The development of lactation significantly predates nursing, as detailed in The Evolution of Milk Secretion and Its Ancient Origins (Oftedal, 2012).
The section on VENTRAL MIGRATION OF CARDIOINHIBITORY NEURONS repeats the error of an “ancient reptilian ancestor” and the “repurposing” of cardioinhibitory wiring. Nosaka’s (1979) hypothesis about ventral migration and defensive behavior (more migration = more aggression) is presented as a speculative explanation for bradycardia in mammalian prey species. Once again, Porges quotes Richter (1957), who supposedly describes “spontaneous bradycardia” in drowning rats. But upon reading Richter's work, it's clear that the rats were manipulated into “hopelessness” and forced to swim until they drowned. Hardly spontaneous.
Porges also asserts, without evidence, that branchiomotor nuclei (ancient gill arches) developed interneuronal connections with ventral cardioinhibitory neurons. A circular argument follows: the social engagement circuit, as an anatomical structure, communicates autonomic state to conspecifics (e.g., mother-infant). However, this “system of interneuronal communication” between brainstem nuclei remains unproven. Porges' argument mirrors the “limbic system” theory, wherein social behavior is attributed to an anatomical structure (the VVC), which, in turn, justifies the existence of said structure—a circular fallacy.
Finally, Porges excludes the XII cranial nerve from the ventral vagal complex, ambiguously noting no evidence of interneuronal communication “between the nerve and the vagus. “However, what exactly does “the vagus” refer to here?
MONITORING DEVELOPMENT OF THE VENTRAL VAGUS VIA RSA describes the embryo's development. Porges repeats the error of conflating the maturation of ventral vagal cardiac neurons with the process of myelination, which continues even after birth. Brainstem nuclei, such as VII (facial) and X (vagal), are active before complete migration and myelination. Fetal HRV is observed well before complete myelination, which increases the transmission speed.
Porges reiterates that RSA is a unique mammalian feature tied to the nucleus ambiguus. However, the definition of RSA is functional rather than strictly anatomical. Taylor (2014), Grossman, and Monteiro (among others) describe cardio-respiratory interactions beyond Porges' narrow, polyvagal framework. The PVT is essentially a “locationist” theory that is fixated on the anatomical concept of ventral vagal complex (VVC). We do not see lungfish (Monteiro, 2018), with their myelinated fibers, as outliers (as Porges does). Instead, they are “living cousins” that shed light on the evolutionary processes leading to tetrapods, including humans. Porges adheres to a monophyletic ladder model, necessitating the dismissal of any exceptions. From a cladistic perspective, evolution is more of a labyrinth with many “ladders.” Some evolutionary processes are repeated (e.g., endothermy, transition to land, middle ear bones), often occurring in parallel or even reverting to earlier stages (e.g., mammals returning to water, snakes losing their legs). The cited authors bring much-needed flexibility to the rigid polyvagal construct.
Regarding premature infants, there is no need for the social engagement hypothesis. Early skin-to-skin contact (SSC) (Bedetti, 2023), one of the four components of kangaroo care (KC), serves as an effective alternative to incubators in low-income countries. This intervention relies on tactile, olfactory (mother's scent), and auditory (mother's heartbeat) stimuli — none of which are part of the “smart vagal” system.
In DISSOLUTION, Porges co-opts the hierarchical Jacksonian dissolution process (which refers to functional regression from cortical to subcortical activity) to describe the autonomic nervous system (ANS). This is an attribution fallacy or false comparison (see Polyvagal Fallacy). Porges claims, “Under challenge, there is a progression that could be characterized as either evolution or development in reverse.” However, he also acknowledges that phylogeny alone does not provide sufficient evidence for dissolution. Does this imply we can abandon the polyvagal phylogenetic yo-yo (where, under threat, we regress to reptiles, sharks, or hagfish)? This remains unclear.
A TEST OF PVT: DISSOLUTION IN THE NEONATAL INTENSIVE CARE UNIT is quite argumentative. Porges quotes an article he co-authored (Reed, 1999): “Functionally, withdrawal of vagal tone originating in the nucleus ambiguus renders the pacemaker susceptible to sympathetic influences and to the more primitive unmyelinated vagal pathways originating in the dorsal motor nucleus of the vagus, which may contribute to clinically relevant bradycardia.” Again, we see the same suggestive, tentative language (“it may”). In this case, whether the sympathetic system is genuinely responsible for bradycardia is also unclear. The subsequent paragraph repeats this notion. Respiratory function, linked to HRV, is again absent from the discussion. If respiratory movements are impaired (as in the fetus or newborn), HRV should also be affected.
In the newborn, respiratory arrest poses a greater risk than cardiac arrest, as most neonatal cardiac arrests are secondary to respiratory issues like hypoxia. When a newborn experiences respiratory failure, the heart may eventually stop due to oxygen deprivation, leading to cardiac arrest.
DORSAL VAGUS THROUGH THE LENS OF PVT: AN UPDATE uses the same hedging language: “It is possible, ... they may be, ... under certain cases might be.” Later, Porges writes, “The possibility of ... has been suggested as being consistent with the PVT (Porges, 2001).” Referring to himself in the third person is strange. He later adds, “It is important to note that the dorsal vagus has a beneficial function in humans.” Porges cites gastric ulcers and colitis as examples of “dorsal” pathology, ignoring (cherry-picking) conditions like bronchial asthma, which is a “ventral” manifestation.
Furthermore, colitis is an autoimmune disorder. The “dorsal” and sympathetic systems maintain the anti-inflammatory reflex, while specific adrenergic centers in the medulla are responsible for blood pressure—not the DVC. Porges confuses two dimensions: blood pressure and bradycardia. They are not equivalent.
REPURPOSING THE DORSAL VAGUS: SPECIES SPECIFICITY makes the “dorsal” responsible for irritable bowel syndrome in trauma survivors. Current research reveals a much more complex picture, including a dysregulated brain-gut axis, microbiome imbalances, and inflammatory mechanisms similar to post-concussion dysregulation caused by head injury (Blanke, 2021; El Baassiri, 2024). Porges then attempts to link the “dorsal” to perinatal mortality, misquoting Machhada. The “dorsal” protective role is not limited to normal conditions; on the contrary, the DVMN is active during myocardial infarction and supports the sympathetic system (positive contractility) both during and after the event (see Gourine, 2019). The DVMN is not responsible for hypotension (depressor center) or vasovagal syncope (Alboni, 2015).
In THE VAGAL BRAKE: A MEASURE OF VENTRAL VAGAL EFFICIENCY, Porges reminds us that, according to “a large body” of literature, HRV is related to mental health outcomes. While this is generally the case, some studies (e.g., Beauchaine, 2019) provide more cautious conclusions. Moreover, as Porges himself notes, HRV is related to mental health, not causally linked (a cum hoc, propter hoc fallacy).
In NEUROCEPTION, Porges tries to justify the term “neuroception” as distinct from perception. However, perception can also be both conscious and unconscious, positive or negative. Declaring that neuroception is related to “cortical areas located in or near the temporal cortex” without evidence is highly speculative and “locationist.” Porges describes a bottom-up information pathway similar to interoception. Yet, he omits that this route is mediated by the NTS (part of the dorsal vagal system) and neglects the role of proprioception (from striated muscles).
In POLYVAGAL THEORY: PRINCIPLES, Porges again presents the five main principles of the PVT. His misunderstanding of “tonic immobility” (e.g., Why didn’t they run or fight?) as a cause of post-traumatic shame is apparent. This immobility is muscular, not autonomic. The amygdala and PAG orchestrate the paralysis, not the autonomic nervous system. Porges proposes an algorithm summarizing the switch from “dorsal” and sympathetic defensive strategies to social activities like play (sympathetic) and intimacy (dorsal). He insists on placing the ANS as “a part of an integrated response, not just a covariate.” So, is the ANS a cause or a part, as he seems to suggest elsewhere?
Later, Porges uses the expression “spinal sympathetic” for the first time, which is odd. This reminds us that anatomically speaking, the sympathetic nervous system is primarily related to the spinal cord. What about the classic “fight-or-flight” response? This sympathetic response to threat extends beyond the classical “spinal sympathetic.”
In his discussion of immobilization, Porges equates it with death-feigning, which is incorrect. “Tonic immobility” is an involuntary response, while death-feigning is a strategic behavior with purpose. Later, Porges quotes Richter (1957) about death-feigning responses, but Richter doesn’t use this term. The rats in his study gave up, hopeless. Death-feigning is a tactic; hopelessness is not.
Porges continues to hypothesize: “Potentially, gut symptoms may result from a dampened ventral vagal circuit that creates vulnerability to dorsal vagal recruitment in defense.” This is intriguing but speculative and based on co-authored articles (with Porges as the last author).
Porges also describes the “ventral migration of cardioinhibitory neurons integrating with the regulation of the striated muscles of the face and head.” This is fictional. The NAext does not control the striated muscles of the face and head.
Finally, Porges asserts: “Since neuroception does not involve perception or appraisal of causality, it is difficult to modify through cognitive channels.” This supports the view that PVT is fundamentally a bottom-up theory of emotions that downplays the role of cognitive processes in emotional construction.
The final section, CURRENT STATUS OF PVT, focuses on the ongoing debate between Porges and Grossman (and indirectly Edwin Taylor and his group). We addressed part of this in Polyvagal Fallacies (Strawman fallacy), and Grossman has already responded (2023). A critical review of PVT extends far beyond the RSA controversy.
Summary: In reviewing the first chapter of Polyvagal Perspectives, we observe Porges reiterating the core claims of the PVT. The following chapters present many of the same arguments. Since further commentary would risk repetition, we have stopped there.
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