Wednesday, March 18, 2026

The polyvagal theory is dead - and HRV isn't a simple indicator of arousal

I was recently struck by Baxter's Substack post (its title copied to be the title of this MindBlog post), which noted work critical of Porges' Polyvagal  theory (or PVT) published iin the journal Clinical Neuropsychiatry, because it calls into question one idea commonly derived from this theory that I have accepted (and repeated in several MindBlog posts): that heart rate variability can be taken as a simple indicator of calm (higher HRV and parasympathetic nervous activity) versus arousal (lower HRV and sympathetic nervous system activity).  A number of bio-monitors such as the Apple Watch and the Oura Ring report ongoing HRV measurements.  Here is a clip from her article, and then the abstract of the multi-author paper she references.

Psychological safety, social engagement, co-regulation, emotional freezing, dissociation — these are real phenomena, supported by decades of research that predate PVT. They come from attachment theory, trauma research, and somatic practices. The (critical paper’s authors explicitly state that body-mind therapeutic methods “may confer benefits on their own.”

So the work stands.

What doesn’t is the specific neuroanatomical story Porges constructed to explain these states, i.e. what drives them. This is the now-familiar three-tier hierarchy: dorsal vagal shutdown, ventral vagal social engagement, sympathetic activation.

Porges got the clinical observations right—or rather, he built upon clinical observations that were already well-established. But the mechanism is wrong.

Concerningly, Porges continued to assert that mechanism for thirty years, even as the evidence mounted against it, and apparently misrepresenting and distorting the work of other scientists to support his claims. Rather than engage with criticism of his theory, Porges ignored the overwhelming scientific consensus and instead promoted this inaccurate framework as sound, misleading practitioners and clients alike.

There is good news in all this mess—for clinicians at least. What you observe in your clients is real. Hyper-arousal is real. The need for safety and co-regulation is real. People really do dissociate, numb, and freeze when overwhelmed. Your interventions still work. They just don’t work for the reasons PVT said they did.

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Here is the Grossman (+38 co-authors) summary:

This article specifically appraises--based upon the current state of knowledge of autonomic function and vertebrate evolution--several major elements of the PVT, as described in Porges (2025a) and elsewhere. These include: 1) the validity of PVT assumptions that respiratory sinus arrhythmia is a direct measure of the extent of central vagal drive to the heart; 2) PVT characterizations regarding the neuroanatomy and functions of two major brainstem vagal nuclei, the ventrally situated Nucleus Ambiguus and the Dorsal Motor Nucleus of the vagus nerve; 3) PVT assertions regarding the evolution of the vagus nerve; 4) PVT claims about the specificity of mammalian social behavior in relation to nonmammalian vertebrates, and 5) PVT interpretations of earlier seminal physiological literature. All co-authors agree that major tenets of the PVT are not supported by past or current knowledge and, in several instances, are inconsistent with the broader evidence base. Since the topics addressed constitute fundamental premises of the PVT, we conclude that the PVT is untenable, because it is not defensible based on existing neurophysiological and evolutionary evidence. The psychological elements composing the superstructure of the PVT are primarily derived from earlier psychological literature and are neither clarified nor strengthened by PVT constructs that lack evidence. This article does not intend to address alternative explanations about relations between vagal function and psychological processes, although such explanations do exist. 

The text of this article is mind-numbingly detailed and complex, as is a rebuttal of the critique by Porges in the same issue of Clinical Neuropsychiatry.   

 

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