R.I.P. Polyvagal Theory
By: Shin Shin Tang
Tags: Trauma, Therapy, Mental Health, Polyvagal Theory, PTSD

Photo: Shin Shin Tang. Image description: A black ink drawing of a tombstone that says “R.I.P. Polyvagal Theory (1994–2021) with a heart at the top and a few flowers at its base.

What therapist doesn’t love Polyvagal Theory? Since 2009, when Dr. Stephen Porges first publicly shared his theory of how trauma affects the nervous system, it has been widely embraced by not only mental health therapists but yoga instructors, meditation teachers, and just about anyone interested in treating trauma. Polyvagal Theory has also been lauded by giants in the field of traumatic stress such as Bessel Van Der Kolk, Pat Ogden, and Peter Levine. As a clinical psychologist myself, I, too, believed Polyvagal Theory offered exciting implications for healing through the nervous system.

What is Polyvagal Theory?

Polyvagal Theory centers upon the vagus nerve, which extends from the brain stem to all the internal organs including the heart, lungs, and stomach. The vagus nerve has many functions, one of which is to be the conduit of the parasympathetic nervous system, which is responsible for stimulating “rest and digest” activities such as decreasing respiration and heart rate, and increasing digestion. The vagus is essential in calming the nervous system, especially after experiencing a stressor.

According to Porges (1995), the three premises of Polyvagal Theory are (as paraphrased by me for my fellow non-neuroscientists):

Respiratory sinus arrhythmia (RSA), or changes in heart rate that typically synchronize with breathing, and neurogenic bradycardia, a sudden and extreme drop in heart rate, are mediated by different branches of the vagus nerve. RSA is regulated by the ventral branch and neurogenic bradycardia by the dorsal branch. These branches can operate independently of each other. There is a phylogenetic hierarchy of the two main branches of the vagus, dorsal and ventral. The dorsal vagus is a vestigial relic of the reptilian brain and is responsible for neurogenic bradycardia. The ventral vagal branch is a uniquely mammalian adaptation that allows mammals to detect novelty, actively engage with the environment, and socially communicate. It does this by withdrawing vagal tone, which has the effect of increasing heart rate. Dubbed by Porges the “smart vagus,” the ventral vagus is absent in other vertebrates such as fish, snakes, and birds.

In other words, if the vagus nerve were like a brake system of a car, the ventral vagus would be the brake pedal, slowing down heart rate gradually. When a person encounters a stressor, releasing the ventral vagus brake allows for increased heart rate and potentially activiation of the “fight or flight” response if needed.

On the other hand, the dorsal vagus would be the emergency brake and is responsible for the “freeze response” that appears as a sudden and extreme drop in heart rate, reduced respiration, and muscle immobility.

Debunking Polyvagal Theory

While the overall function of the vagus nerve is not in dispute, a growing number of scientists are pointing to evidence that refutes Polyvagal Theory (For an extensive discussion, see Paul Grossman’s (2016) question on ResearchGate). According to neuroscientific research, it’s unlikely that any of the three premises is true.

Regarding premise number 1, neuroscience research has repeatedly found that the dorsal branch of the vagus has little effect on heart rate (Cheng et al., 2002; Cheng et al., 2004; Farmer et al., 2016; Geis & Wurster, 1980; Verberne, 2004). Grossman (2016) has also argued that the evidence the Porges has presented in support of the effects of the dorsal vagus on neurogenic bradycardia is scant and flawed.

Regarding premises number 2 and 3, many studies have found evidence that the ventral vagal exists among lizards and fish. Therefore, it is not a uniquely mammalian adaptation as Porges asserts (e.g., Barbas-Henry, 1984; Campbell et al., 2006; Grossman & Taylor, 2007; Monteiro et al., 2018; Taylor et al., 2010; Taylor et al., 2014).

I feel a bit like the Grinch who stole Christmas for saying this, but we need to stop teaching Polyvagal Theory to our clients and students. Sometimes a theory doesn’t pan out even though it sounds great — that’s science for you.

Can anything be salvaged from Polyvagal Theory?

In light of the evidence, I do not think so. However, there are many aspects of the trauma response that are still real phenomena such as neurogenic bradycardia and the traumatic freeze response. They just cannot be explained by Polyvagal Theory. That we are wired for connection is also likely to be true, though again not in the way that Polyvagal Theory describes.

Finally, the vagus nerve is amazing in its own right — for example, 80–90% of its nerve fibers are afferent, meaning they carry information from the body to the brain rather than the other way around (Berthaud & Neuhuber, 2000). In this manner, the vagus plays a central role in transmitting information along the gut-brain axis (Breit et al., 2018; Enders, 2018).

I understand if the debunking of Polyvagal Theory is difficult to accept for the nerdy neuroscience-loving therapists among us. I personally found it so disappointing I had to process my emotions by drawing a tombstone. I encourage you to delve into the primary sources yourself with an open mind starting with the references below.

References

Berthoud, HR & Neuhuber, WL (December 2000). “Functional and chemical anatomy of the afferent vagal system”. Autonomic Neuroscience. 85 (1–3): 1–17. doi:10.1016/S1566–0702(00)00215–0. PMID 11189015. S2CID 30221339

Breit, S., Kupferberg, A., Rogler, G., & Hasler, G. (2018). Vagus nerve as modulator of the brain–gut axis in psychiatric and inflammatory disorders. Frontiers in psychiatry, 9, 44.

Cheng ZX, Guo SZ, Lipton AJ, and Gozal D. (2002). Domoic acid lesions in nucleus of the solitary tract: time-dependent recovery of hypoxic ventilatory response and peripheral afferent axonal plasticity. Journal of Neuroscience, 22: 3215–3226.

Cheng Z, Zhang H, Guo SZ, Wurster R, Gozal D. (2004). Differential control over postganglionic neurons in rat cardiac ganglia by NA and DmnX neurons: anatomical evidence. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 286:R625–33

Enders, G. (2018). Gut: The Inside Story of Our Body’s Most Underrated Organ (Revised Edition). Greystone Books Ltd.

Farmer DG, Dutschmann M, Paton JF, Pickering AE, McAllen RM. (2016). Brainstem sources of cardiac vagal tone and respiratory sinus arrhythmia. J Physiology, 594(24):7249–7265. doi: 10.1113/JP273164.

Geis, G. S., & Wurster, R. D. (1980). Cardiac responses during stimulation of the dorsal motor nucleus and nucleus ambiguus in the cat. Circulation research, 46(5), 606–611.

Grossman, P., & Taylor, E. W. (2007). Toward understanding respiratory sinus arrhythmia: Relations to cardiac vagal tone, evolution and biobehavioral functions. Biological psychology, 74(2), 263–285.

Grossman, Paul. (2016). Re: After 20 years of “polyvagal” hypotheses, is there any direct evidence for the first 3 premises that form the foundation of the polyvagal conjectures?. Retrieved from: https://www.researchgate.net/post/After-20-years-of-polyvagal-hypotheses-is-there-any-direct-evidence-for-the-first-3-premises-that-form-the-foundation-of-the-polyvagal-conjectures

Monteiro, D. A., Taylor, E. W., Sartori, M. R., Cruz, A. L., Rantin, F. T., & Leite, C. (2018). Cardiorespiratory interactions previously identified as mammalian are present in the primitive lungfish. Science advances, 4(2), eaaq0800. https://doi.org/10.1126/sciadv.aaq0800

Porges, S. W. (1995). Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A polyvagal theory. Psychophysiology, 32(4), 301–318.

Verberne, A. J. (2004). Differential cardiac parasympathetic innervation — what is the functional significance?. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287(2), R485-R486.