A new wave of messages has recently surfaced, claiming that polyvagal theory (PVT) has been scientifically debunked. The trigger is an article by Paul Grossman titled Why the Polyvagal Theory Is Untenable. Despite an adequate response from Stephen Porges, the piece has left a number of therapists and psychologists in doubt. But when you place the criticism alongside the theory itself, a striking pattern emerges: Grossman is once again—and still—largely arguing against a version of PVT that its founder, Stephen Porges, never actually described.
Alongside the work I am doing on several in-depth articles on the subject, I came across a video by Justin Sunseri this week in which he clearly explains several key points. I decided to write a summary about it.
The Vagal Paradox: Two Different Questions
Polyvagal theory begins with a neurological puzzle that Stephen Porges called the vagal paradox. His question was concrete: how can one and the same nerve—the vagus nerve—be both life-protecting and life-threatening? If RSA (respiratory sinus arrhythmia) is understood as a marker of healthy vagal regulation, how do we explain that other vagal responses—such as bradycardia (a slow heart rate) and apnea (cessation of breathing) in premature infants—are associated with life-threatening dysregulation? This paradox formed the basis for Porges’ hypothesis that the vagal system is divided into distinct functional units.
Grossman reformulates this question and turns it into a measurement problem: RSA is simply an imprecise measure of vagal cardiac tone, and that explains the apparent contradiction. But in doing so, he answers a different question than the one Porges was asking. Porges was not asking whether RSA is a reliable measurement instrument. He was asking why the same nerve produces opposing survival outcomes. That is a neurobiological question, not a methodological one.
This distinction matters. The vagal paradox was the driving force behind Porges’ research into the brainstem, which ultimately led to the identification of two anatomically distinct vagal pathways arising from different brainstem nuclei and serving fundamentally different functions. Grossman does not address the vagal paradox in the form Porges posed it, nor does he engage with the anatomical distinction between different vagal circuits that Porges proposed as its explanation.
RSA as a Measurement Tool, Not a Foundation
A large part of Grossman’s article is devoted to the shortcomings of RSA as an index of vagal cardiac tone. If RSA is unreliable, the reasoning seems to go, then the entire theoretical edifice of PVT collapses. But this misrepresents what Porges himself has written about RSA.
In a 2023 publication, Porges explicitly states that RSA is a window onto the function of the ventral vagus—a measurement tool for testing polyvagal-informed hypotheses—but not a foundation of the theory itself. The comparison to a thermometer is illuminating here: if a fever thermometer measures inaccurately under certain conditions, it does not follow that fever as a criterion for infection is untenable. Criticism of the instrument does not touch the underlying reality it is trying to measure.
Grossman cites the relevant 2023 article by Porges. He is therefore aware of it. Why he nonetheless treats RSA as the pivot around which the entire theory turns remains unclear.
Freeze and Shutdown: Two Different States
Another point of criticism concerns the relationship between bradycardia and the freeze response. Grossman argues that bradycardia does not occur during freeze and uses this as an argument against the theory. But in polyvagal theory, freeze and shutdown are described as two distinct states.
Shutdown is a dorsal vagal response: a limp, passive collapse—think of a mouse going limp in a cat’s mouth. Bradycardia fits within this as a physiological response. Freeze, by contrast, is a combined state: immobility resulting from the simultaneous activation of the dorsal vagal system and the sympathetic nervous system. The body is still, but internally under high tension—comparable to a panic attack in which someone freezes. In that combined state of activation, bradycardia is precisely what one would not expect.
So bradycardia does indeed not occur during freeze—exactly as both Grossman and PVT assert.
Admittedly, the terminology around freeze, shutdown, and collapse is not always consistent in the literature; this is an area where confusion regularly arises. Grossman does not make this distinction either, which considerably weakens his argument on this point.
Myelinated Nerves in Non-Mammals
Grossman points to research showing that non-mammals—sharks, fish, and reptiles—also possess fast-acting myelinated nerves capable of directly influencing heart rate. His conclusion: if this anatomy is not exclusive to mammals, it cannot represent a special mammalian innovation for social engagement.
But polyvagal theory never claimed otherwise. Porges has clarified this point repeatedly: the theory is not about whether fast-acting vagal nerves are exclusive to mammals. It is about the evolutionary relocation of the brainstem nucleus from which those nerves originate. In mammals, a so-called ventral shift is described: an evolutionary reorganization of vagal control, in which—alongside the older projections from the nucleus dorsalis motorius (hence the dorsal vagus)—a prominent role emerges for vagal pathways originating in the nucleus ambiguus, located more ventrally in the brainstem (hence the ventral vagus).
This organization is functionally crucial, because the nucleus ambiguus is closely connected to nuclei involved in facial expression, vocalization, and auditory processing. This gives rise to an integrated system in which cardiac regulation and social communication are intertwined. That is the evolutionary claim of PVT—not that fast vagal nerves are uniquely mammalian.
Social Behavior in Reptiles
Grossman notes that modern reptiles display far more complex social behavior than was long assumed: long-term pair bonding, shared parental care, and social learning. As an argument against polyvagal theory, this misses the mark—and Porges has responded accordingly.
PVT is not concerned with the social behavior of modern reptiles as such, but with the specific evolutionary transition from a common extinct ancestor to mammals. Whatever modern reptiles have developed since then follows a separate evolutionary trajectory. To the extent that similarities in social behavior exist, these can be understood as examples of convergent evolution, in which comparable behaviors arise via different underlying biological systems.
Moreover, the theory describes a very specific integration: the coupling of cardiac regulation to facial expression, voice, and hearing, such that social signals—a warm tone of voice, eye contact, a smile—can bring about physiological calming in others (co-regulation). That is something quite different from the social behavior Grossman describes in reptiles.
For Whom Did Grossman Write His Article?
Beyond the substantive objections, something about the article’s design stands out. The abstract and introduction are explicitly directed at therapists and other practitioners who use PVT in their work. The final three of the twelve conclusions address psychology and treatment and encourage care professionals to abandon the theory.
That is remarkable, because the article contains no new arguments against PVT. Grossman is repeating positions he has been publishing for years, to which Porges has responded on multiple occasions. The article presents itself in scientific terms while simultaneously targeting readers who do not systematically follow the primary literature.
That makes it harmful to a fair assessment of PVT: those unfamiliar with the theory’s original formulations have little basis for evaluating the criticism on its merits. The gap between what Grossman argues against and what Porges actually claims only becomes visible when you place theory and critique side by side. The effect is already apparent: therapists and various popular psychology channels have adopted the conclusions without checking whether the criticism described actually corresponds to the theory.
Since this is not the first time Grossman has applied this strategy, it is difficult to characterize it as an innocent mistake.
Work to Be Done
That does not mean Grossman has no valid points. The question of how ventral vagal activity can be measured reliably remains open, even setting aside RSA as a foundation of the theory. The phylogenetic claims—concerning the evolutionary reorganization of vagal circuits in the transition to mammals—are plausible but less robustly supported than the anatomical part of the theory. And the terminology around freeze, shutdown and collapse is not always consistent within the PVT community itself, which complicates comparative research. These are real issues, and they deserve more serious attention than they have so far received.
Conclusion
Scientific criticism is valuable, and polyvagal theory is not immune to questions or refinement. There are legitimate debates about the degree to which RSA is useful as a proxy for ventral vagal activity, about how robust the evolutionary claims are, and about the precise anatomical boundaries of the social engagement system.
But Grossman’s article is largely not about any of that. It argues against a vagal paradox that Porges never formulated, treats RSA as a foundation that Porges himself has explicitly relativized, conflates freeze with shutdown, and misses the evolutionary core of the theory concerning the nucleus ambiguus. When you place the sources side by side, it becomes clear that the heart of the criticism does not connect with the heart of the theory.
Polyvagal theory is not dead. It is the subject of an ongoing scientific debate, and that is precisely where it belongs—only, that debate ought to concern different questions than the ones Grossman is asking.
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