Both more broadly and specifically: Why does the polyvagal group of hypotheses still enjoy such broad popularity and acceptance when its most basic biological premises regarding vagal control have been largely—perhaps completely—refuted, and the one measurable linchpin to the polyvagal (respiratory sinus arrhythmia, or a proxy thereof) has long been shown not even to be a consistently reliable index of vagal activity of any kind, influenced as it is by mutiple other factors?
The five most basic premises of the polyvagal collection of hypotheses have by now been soundly refuted (see https://www.sciencedirect.com/journal/biological-psychology/special-issue/105P98LLB4B). Additionally, the sole noninvasive, nonintrusive index of vagal control (respiratory sinus arrhythmia, or its empirical surrogates, e.g. high-frequency heart-rate variability or root mean squared successive differences of heart rate—upon which polyvagal speculations almost exclusively rest—has long and repeatedly been demonstrated to be, at best, seriously affected by nonvagal influences (e.g. sympathetic effects upon the heart, arterial carbon dioxide level, changes in respiratory pattern and brainstem respiratory pacemakers) rendering this measure as not a specific index of vagal activity of any kind (e.g. Article Sympathetic restraint of respiratory sinus arrhythmia: Impli...
).Additionally numerous meta-analyses of these measures‘ relations with psychological regulatory processes and trauma yield small or extremely small degrees of association, often yielding correlations