Critiques of
Polyvagal Theory:
A Comprehensive Analysis

Stephen W. Porges, PhD

Distinguished University Scientist,
Kinsey Institute, Indiana University

Overview

Polyvagal Theory has contributed a biologically grounded framework for understanding autonomic regulation, safety, and social engagement, informing research and clinical practice across neuroscience, psychology, medicine, and education. As the theory has gained wider visibility, it has also become the subject of critique across academic and public forums. This page provides a concise, evidence-based clarification of Polyvagal Theory’s core claims, scope, and scientific grounding, with the goal of supporting accurate evaluation through reference to primary sources and contemporary neurophysiology.

The published criticisms of Polyvagal Theory, particularly those by Paul Grossman and E. W. Taylor, exhibit a recurring pattern of misinterpretation and factual inaccuracy. Despite multiple clarifications in the peer-reviewed literature (Porges, 2007b, 2022, 2023, 2025a, 2025b), these critiques continue to introduce conceptual errors into both academic discourse and clinical application. Grossman’s 2023 critique reiterates themes first advanced by Taylor, drawing heavily on his anatomical and evolutionary misreadings, framed in a rhetorically authoritative style that may mislead readers unfamiliar with the theory’s foundational literature.

In addition to peer-reviewed publications, public-facing sources—particularly the Wikipedia entry on Polyvagal Theory—have played a role in disseminating inaccuracies. That entry prominently cites two critiques: Neuhuber and Berthoud (2022) and Doody, Burghardt, and Dinets (2023). While both articles were peer-reviewed, their appearance in a special issue of Biological Psychology edited by Grossman suggests an editorial alignment that likely shaped both their thematic and conceptual framing.

The critique by Neuhuber and Berthoud exemplifies an anatomical-functional misinterpretation. While questioning the functional interpretation of vagal pathways proposed by Polyvagal Theory, they do not dispute the core neuroanatomical distinctions—specifically, the separation between the dorsal motor nucleus of the vagus (DMNX) and the nucleus ambiguus (NAmb), nor the contrasting myelination of their efferents. However, they omit a critical tenet of the theory: that the Social Engagement System (SES) derives from structures of the embryological pharyngeal arches and that communication between the cardioinhibitory vagus and the SES is largely indirect, with the exception of direct pathways involving the trigeminal nerve. Wikipedia, in summarizing this critique, distorts it further—presenting it as a categorical refutation of the anatomical foundation of Polyvagal Theory, which the original article does not claim.

Similarly, the critique by Doody, Burghardt, and Dinets misrepresents the theory’s phylogenetic framing. They challenge what they interpret as a rigid binary between "asocial reptiles" and "social mammals." However, Polyvagal Theory is explicitly mammalian-centric and defines social behavior through a mammalian lens. It emphasizes that sociality, in the context of Polyvagal Theory, is rooted in a mammalian-specific autonomic innovation—the ventral vagal complex—responsible for regulating the Social Engagement System. While reptiles may exhibit adaptive social behaviors, these behaviors are mediated through different signaling systems and neural architectures and serve different evolutionary functions. Thus, social behavior in reptiles, although evolutionarily adaptive, is not equivalent to mammalian sociality as defined by Polyvagal Theory. By conflating behavioral analogy with neurophysiological homology, the critique overlooks the theory’s domain-specific scope. Public summaries, including Wikipedia, further amplify this misrepresentation, overstating the critique and ignoring Polyvagal Theory’s focus on hierarchical autonomic evolution.

Crucially, the problem is not merely that these articles exist, but that they have been filtered through a public platform in a way that both exaggerates and misrepresents their content. This layered mischaracterization—shaped by personal bias and not by accurate scholarship—contributes to the dissemination of misleading information. It underscores the need for scholarly evaluation grounded in direct engagement with primary sources, rather than interpretations shaped by editorial alignment, selective emphasis, or secondary dissemination.

To clarify the nature of these misinterpretations, Table 1 identifies the recurrent domains of error present in critiques of Polyvagal Theory, outlining how they manifest and the consequences they carry for accurate theoretical interpretation.

Table 1 Porges Core Domains of Misrepresentation.png

As shown in Table 1, these domains span anatomical, physiological, evolutionary, conceptual, and methodological dimensions. While the specific content of critiques varies, they consistently fall within this typology of error— undermining the coherence and scientific validity of Polyvagal Theory by misrepresenting core constructs or applying flawed evaluative criteria. This structured framework provides a diagnostic lens through which to assess the epistemic integrity of both academic and public-facing criticisms.

While Table 1 identifies recurrent error domains across critiques, Table 2 maps these distortions more
specifically to key publications—highlighting how Taylor’s foundational misrepresentations established
patterns that were subsequently reproduced and extended in later critiques, particularly those by
Grossman. Citations of Taylor and his colleagues (e.g., Campbell et al., 2006; Monteiro et al., 2018;
Sanches et al., 2019; Taylor et al., 2022) indicate recurrent patterns across publications; specific
dominant error types for individual articles are detailed in a later typological summary (see Table 4) and
the annotated bibliography.

As shown in Table 2, Taylor’s publications repeatedly collapse anatomical distinctions and confuse phylogenetic constructs central to Polyvagal Theory. Grossman’s later writings amplify these misrepresentations, embedding them in critiques that are rhetorically authoritative but empirically misaligned. This inheritance of error contributes to a layered mischaracterization of Polyvagal Theory across both academic and public domains.

While Tables 1 and 2 categorize general and foundational misrepresentations, Table 3 engages directly with major criticisms advanced by Grossman—evaluating them against established empirical and neurophysiological evidence.

Table 3 consolidates the principal claims advanced by Grossman (2007, 2023) and evaluates them against contemporary empirical and neurophysiological findings. Across anatomical, physiological, evolutionary, and interpretive domains, these critiques consistently reflect misunderstanding rather than empirically grounded disagreement—reinforcing the need for evaluation rooted in primary literature.

Table 3 functions not merely as a summary of neuroscientific evidence that refutes Grossman’s criticisms, but also as a demonstration of the internal coherence of Polyvagal Theory. By aligning with contemporary findings across neuroanatomy, physiology, developmental psychobiology, and evolutionary biology, the theory maintains conceptual integrity and cross-disciplinary consistency—highlighting its explanatory robustness rather than vulnerability to reductionist critique.

Taken together, the critiques addressed here—whether anatomical, physiological, evolutionary, or conceptual—reveal more about the interpretive lens of their authors than about the validity of Polyvagal Theory itself. The persistence of mischaracterization, particularly in public-facing summaries, underscores the necessity of returning to primary sources when evaluating the theory’s claims. As this analysis demonstrates, Polyvagal Theory remains a coherent and empirically anchored framework, whose interdisciplinary reach continues to inform both basic neuroscience and translational applications.

Methodological Misrepresentation and the RSA Artifact Claim

Grossman’s repeated assertion that RSA is merely a respiratory artifact stems from his reliance on the peak-to-trough method of RSA quantification—a technique long recognized as methodologically flawed. First critiqued by Byrne & Porges (1993) and later confirmed by Lewis et al. (2012), this method violates key statistical assumptions, is overly sensitive to respiration and signal trend, and fails tests of normality and stationarity. In contrast, the Porges–Bohrer method is more responsive to vagal blockade, less influenced by respiratory variables, and more suitable for valid parametric analysis.

Despite longstanding critiques, Grossman has continued to apply the peak-to-trough approach, producing systematic bias and a misleading interpretation of RSA’s relationship to ventral vagal tone. His refusal to adjust analytic methods or acknowledge empirical refutations has allowed this error to persist across more than two decades of publications.

As a result, many of the published criticisms of Polyvagal Theory are not grounded in competing evidence, but in a singular,
uncorrected methodological flaw. Addressing such errors is critical to restoring scientific accuracy and analytic accountability in
discourse surrounding Polyvagal Theory.

Is Grossman Critiquing Polyvagal Theory or a Misrepresentation of It?

Close analysis of Grossman’s critiques (2007, 2023) indicates that his arguments frequently engage a version of Polyvagal Theory that diverges from its formulation in the primary literature. This divergence arises through selective quotation, reliance on outdated models of vagal physiology, and misinterpretation of comparative neuroanatomical evidence. As a result, premises are attributed to Polyvagal Theory that it does not advance (e.g., that RSA is unrelated to respiration or that NAmb exists only in mammals), and these attributed positions are subsequently challenged.

This pattern reflects a categorical misunderstanding rather than a disagreement grounded in competing empirical data. In particular, Grossman repeatedly conflates functional analogy with neuroanatomical homology, overlooking the phylogenetic rationale articulated within Polyvagal Theory. Similarly, the failure to distinguish between DMNX and NAmb obscures the anatomical basis of the theory’s hierarchical model of autonomic regulation.

Although the foundational papers of Polyvagal Theory are frequently cited in these critiques, the points under criticism are not linked to an accurate representation of the theory’s original neurophysiological claims. Instead, Grossman’s commentaries rely on a highly siloed treatment of specific neuroscience subdisciplines—such as comparative anatomy or neurophysiology—without engaging integrative theoretical models that relate structure, function, development, and behavior. Consequently, the critiques focus disproportionately on secondary interpretations and downstream clinical applications rather than on the core constructs articulated in the foundational literature. Framed as methodological critique, this body of work perpetuates misrepresentations first introduced by Taylor and colleagues, substituting metaphor for mechanism and evaluating a version of Polyvagal Theory that was never advanced in its primary sources.

Ethical Implications

Misrepresentations of Polyvagal Theory have generated epistemic harm—confusing clinicians, misguiding educators, and undermining translational clarity. These consequences are not merely academic; they obstruct the accurate application of a theory grounded in validated neuroanatomy, robust physiological metrics, and a coherent neuroethological model of autonomic regulation.

Recent findings strengthen the empirical foundation of Polyvagal Theory. For example, Strain et al. (2024) demonstrated via optogenetic activation that neurons in the DMNX—a key component of the dorsal vagal complex—produce bradycardia and modulate anxiety-like behavior without triggering locomotor suppression. This distinction aligns with Polyvagal Theory’s differentiation between dorsal-mediated threat responses and immobilization without fear, addressing longstanding misconceptions, including those perpetuated in the Biological Psychology special issue edited by Grossman.

This context raises further ethical concerns. The guest-edited issue featured multiple critiques of Polyvagal Theory—such as Neuhuber and Berthoud (2022) and Doody et al. (2023)—without offering rebuttals or scholarly responses. Given Grossman’s established opposition to Polyvagal Theory, the absence of countervailing views introduces potential editorial bias. Such asymmetry risks misrepresenting scholarly consensus and propagating error in both academic and public domains.

As Porges (2025b) notes, scientific critique should engage with theories as they are written—not as caricatures. Ethical scientific discourse demands fidelity to evidence, currency in interpretation, and transparency in method. These standards are essential not only for accurate evaluation of Polyvagal Theory, but for preserving the integrity of scientific exchange more broadly.

Misrepresentation in Public Discourse

Several criticisms frequently attributed to Polyvagal Theory—such as oversimplification or over-commercialization—are, in fact, critiques of how the theory has been represented or applied by third parties, not flaws inherent to the theory itself.

Oversimplification: Claims that Polyvagal Theory oversimplifies autonomic-emotional relationships often stem from secondary interpretations that disregard its neurophysiological depth. Constructs such as the “vagal brake” and “neuroception,” while empirically supported, are frequently reduced to metaphor in popular discourse. These simplifications reflect a lack of engagement with the primary literature, not intrinsic features of Polyvagal Theory.
Over-commercialization: Polyvagal Theory has been adapted in coaching, wellness, and branding contexts that may lack
scientific rigor. While this trend raises valid concerns about translational ethics, the theory itself embeds ethical considerations and should not be held accountable for distortions introduced by external actors.
Critique of the anatomical distinction between NAmb and DMNX: Neuhuber and Berthoud (2022) argue that the
anatomical separation proposed by Polyvagal Theory lacks empirical support. However, their critique overlooks well-established evidence differentiating NAmb and DMNX—including their embryological origins, efferent myelination, and functional specificity. Transcriptomic data (Coverdell et al., 2019; Jalil et al., 2023) reveal molecular markers unique to NAmb neurons related to autonomic function and myelination. Strain et al. (2024) further demonstrated that selective optogenetic activation of DMNX neurons induces bradycardia and modulates anxiety-like behavior, confirming the functional and behavioral relevance of the dorsal vagal complex as described in Polyvagal Theory.
Phylogenetic critiques based on non-mammalian vagal structures: Some critiques cite vagal features in lungfish or reptiles
to challenge Polyvagal Theory’s evolutionary claims. These arguments conflate functional analogy with phylogenetic homology. Polyvagal Theory does not suggest that vagal regulation is exclusive to mammals; rather, it identifies the NAmb-mediated, myelinated vagus integrated with cranial social engagement as a mammalian adaptation. Equating general vagal function across species with this specialized system reflects a misunderstanding of Polyvagal Theory’s evolutionary specificity.

It is essential to differentiate between a theory’s empirical foundation and its public portrayal. The Wikipedia entry on Polyvagal Theory exemplifies this conflation, often treating misuse or misrepresentation by third parties as if they reveal flaws in the theory itself. This constitutes a category error in scholarly evaluation.

These criticisms, when examined closely, reveal not theoretical vulnerabilities but challenges in accurate dissemination. Upholding the scientific integrity of Polyvagal Theory requires precise communication and ethical stewardship by those who apply it in clinical, educational, and public domains.

Typology of Errors in Critiques of Polyvagal Theory

To synthesize the recurring issues identified across critiques of Polyvagal Theory, Table 4 presents a typology of common error categories. These range from rhetorical misrepresentations to empirical and methodological missteps. Each error type is defined, exemplified by its appearance in published critiques, and paired with its resulting scientific distortion.

This diagnostic classification underscores a central concern of the current document: that the most persistent and visible criticisms of Polyvagal Theory often fail to engage with the theory on its empirical and conceptual terms. Rather than offering grounded scientific challenges, these critiques frequently reflect misunderstandings of evolutionary biology, neuroanatomy, and methodological validity—or arise from editorial and translational dynamics external to the theory itself.

Table 4 Porges Typology of Recurrent Errors.png

Conclusion

A comprehensive evaluation of the published criticisms of Polyvagal Theory reveals a recurring structure of error: the most influential objections—across anatomical, physiological, evolutionary, and conceptual domains—are repeatedly traceable to the scholarly contributions and editorial influence of Paul Grossman. Whether via direct authorship, collaboration with E. W. Taylor, or editorial curation of the 2023 Biological Psychology special issue, Grossman has played a central role in shaping the public and academic discourse around Polyvagal Theory.

This concentration of dissent, particularly when amplified through publication venues that exclude rebuttal, raises legitimate concerns about scholarly objectivity and the simulation of consensus. Scientific critique must rest on accurate representation of a theory’s foundational claims, not caricature or rhetorical deflection. As this manuscript has shown, many critiques of Polyvagal Theory misrepresent its core constructs, often via a small number of categorical errors that recur across publications and platforms.

Such repetition should not be mistaken for convergence or consensus. Rather, it underscores the need for greater epistemic accountability in both scholarly and public domains. Readers and evaluators are urged to consult the primary literature directly, where the empirical foundations and conceptual architecture of Polyvagal Theory are most clearly articulated.

References

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Campbell, H. A., Taylor, E. W., & Egginton, S. (2005). Does respiratory sinus arrhythmia occur in fishes? Biology Letters, 1(4), 484–487. https://doi.org/10.1098/rsbl.2005.0365

Note: Conflation of Analogy and Homology — Treats fish cardiorespiratory coupling as homologous to mammalian RSA, mistaking functional similarity for phylogenetic continuity and overlooking the NAmb-based, myelinated mammalian specialization central to Polyvagal Theory.

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Note: Conflation of Analogy and Homology — Uses reptilian RSA-like coupling to imply evolutionary equivalence with mammalian RSA, bypassing Polyvagal Theory’s emphasis on mammalian NAmb innovations and SES integration.

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Note: Mischaracterization of Theoretical Claims (incl. Strawman Arguments) — Recasts Polyvagal Theory as claiming reptiles are “asocial” and treats the theory’s mammalian-specific autonomic innovation argument as a denial of reptilian sociality, conflating behavioral analogy with Polyvagal Theory’s neuroanatomical scope.

Grossman, P. (2023). Fundamental challenges and likely refutations of the five basic premises of the polyvagal theory. Biological Psychology, 180, 108589. https://doi.org/10.1016/j.biopsycho.2023.108589

Note: Mischaracterization of Theoretical Claims (Strawman Argument) — Attributes claims to Polyvagal Theory that it does not make (e.g., mammalian exclusivity of RSA). Misrepresents the theory's anatomical specificity and physiological nuance. Fails to acknowledge the distinct cardioinhibitory myelinated pathways of the nucleus ambiguus (NAmb) and their integration with cranial motor systems that constitute the Social Engagement System, as well as the coordinating role of the common cardiopulmonary oscillator in mammalian autonomic regulation.

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Note: Mischaracterization of Theoretical Claims (incl. Strawman Arguments) — Sets up a strawman of Polyvagal Theory’s evolutionary and vagal claims, borrows Polyvagal Theory constructs without proper attribution, and collapses NAmb/DMNX distinctions while relying on invalid RSA framing.

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Note: Conflation of Analogy and Homology —Infers evolutionary homology from functional similarity in lungfish cardiorespiratory interactions, overlooking Polyvagal Theory’s emphasis on mammalian-specific neuroanatomical reorganization, particularly NAmb-linked myelination and integration with the Social Engagement System as evolutionary innovations.

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Note: Anatomical Oversight — Reduces Polyvagal Theory to a simplistic “dual vagus” narrative while bypassing developmental, myelination, and hierarchical distinctions between NAmb and DMNX. Ignores afferent pathways and omits the Social Engagement System framework, thereby overlooking Polyvagal Theory's emphasis on integrated functional circuits and evolutionary organization.

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Note: Conflation of Analogy and Homology — Relabels reptilian coupling as RSA homologous to mammalian NAmbmediated RSA, disregarding PVT’s mammalianspecific neuroanatomical and behavioral integration.

Strain, M. M., Conley, N. J., Kauffman, L. S., Espinoza, L., Fedorchak, S., Castro Martinez, P., … Boychuk, C. R. (2024). Dorsal motor vagal neurons can elicit bradycardia and reduce anxiety-like behavior. iScience, 27(3), 109137. https://doi.org/10.1016/j.isci.2024.109137

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Note: Conflation of Analogy and Homology — Interprets respiratory–cardiac coupling in fish as evidence of evolutionary continuity with mammalian respiratory sinus arrhythmia, without addressing the mammalian-specific NAmb-linked, myelinated vagal pathways and their integration with the Social Engagement System emphasized in Polyvagal Theory.

Taylor, E. W., Wang, T., & Leite, C. A. C. (2022). An overview of the phylogeny of cardiorespiratory control in vertebrates with some reflections on the “polyvagal theory.” Biological Psychology, 172, 108382. https://doi.org/10.1016/j.biopsycho.2022.108382

Note: Mischaracterization of Theoretical Claims (incl. Strawman Arguments) — Reframes Polyvagal Theory as asserting mammalian exclusivity of cardiorespiratory coupling, and critiques this reformulated claim rather than engaging the theory’s stated emphasis on mammalian neuroanatomical specialization, particularly ventral vagal complex integration supporting social engagement.