Learning Somatics without learning Autonomic Physiology
Learning somatics without learning autonomic physiology is literally building a house in quicksand. Autonomics are the primary governor of the body’s physical and energetic structure. This includes bones, joints, connective tissue, fascia, muscles. Starting with anything other than the autonomic physiology will lead to situation where you have over-indexed on some element of structure that is not at the root of what is organizing how the body structures, moves, and relates. Learning autonomics changes the WHY of everything.
-Natureza Gabriel
ANNOUNCING THREE ADVANCED OPEN SHORT-FORM COURSES ON ZOOM
You may take these as a three-part series, or as stand-alone classes, but they will build upon one another. Individually classess are $200. Classes meet from 8 to 11 am Pacific on Saturdays with two weeks between them.
SATURDAY JULY 25 - AUTONOMICS OF BREATH
For three decades, heart rate variability has served as the field's preferred noninvasive window into autonomic function — a choice driven largely by the computational affordances of the 1970s rather than by the richness of the signal itself. Heart rate is a discontinuous output that captures only a fraction of what the autonomic nervous system is doing at any given moment. Respiration, by contrast, is continuously updated by the brainstem's central pattern generators and encodes the full dynamic negotiation between the Connection System, the Movement System, and the Grounding System in real time. Breath is not merely a correlate of autonomic state — it is one of its primary expressive and regulatory channels.
In this three-hour class, we will examine the neurological architecture of respiratory control, the specific ways in which breathing both reflects and actively reshapes present-moment autonomic state, and what becomes clinically visible when breath is read with the precision the signal actually affords.
LEARNING OBJECTIVES
1. Articulate why respiratory sinus arrhythmia and HRV, while valuable, capture only a subset of the autonomic information encoded in the breathing signal, and describe the neurological basis for breath's superior fidelity as an autonomic index.
2. Identify the brainstem central pattern generators governing respiration and explain how breathing rhythm reflects the cooperative coordination — or hierarchical decoupling — of the three autonomic systems under different neurochemical conditions.
3. Apply a breath-based observational framework in clinical settings to distinguish present-moment autonomic state more precisely, and recognize how conscious and assisted respiratory interventions work through autonomic channels rather than psychological ones.
AUGUST 8 - THE PERINATAL AUTONOMIC CASCADE
At the most fundamental level, birth is a transition from marine to terrestrial existence. The fetus lives in a neutrally buoyant, pressure-equalized environment, without gravitational gradients to manage cardiovascularly, without pulmonary gas exchange, without the requirement to source nutrition from outside the body. In the first moments and hours after birth, a precisely ordered series of neurological and neurochemical transformations must occur to prepare the physical body for this entirely novel reality. We call this the Perinatal Autonomic Cascade: a sequential initialization of autonomic systems — cardiovascular, respiratory, gravitational, visceral — each stage dependent on the successful completion of the one before it. The cascade is exquisitely sensitive to neurochemical context, particularly the presence of oxytocin. Disruption at any stage — through difficult delivery, separation, pharmacological interference, or insufficient oxytocin — results in incomplete initialization that may* be retained in the autonomic architecture throughout the lifespan, with measurable consequences for physiological regulation, somatic organization, and clinical presentation. This class presents the theoretical model, the clinical evidence for retained incomplete initialization, and the conditions under which completion may be possible.
LEARNING OBJECTIVES
1. Describe the major stages of the Perinatal Autonomic Cascade — including lung inflation, suck-swallow-breathe coordination, genital/pelvic neural ignition, cardiovascular pressurization through inspiratory hemodynamics, respiratory-gravitational adaptation, and the sequential integration of anterior vagal and posterior spinal architectures — and explain why each stage is prerequisite to the next.
2. Explain the role of oxytocin as the neurochemical substrate enabling cooperative coordination among autonomic systems during the cascade, and identify the categories of perinatal disruption most likely to produce incomplete initialization with lasting clinical consequences.
3. Recognize clinical presentations that may reflect retained incomplete perinatal initialization — including patterns of autonomic dysregulation, somatic organization, and sensory calibration anomalies (generally ascribed generically to a ‘difficult birth’ if noted at all) — and describe the neurochemical and neuroceptive conditions required for evocation and completion of retained cascade stages.
*this is some of our newest, and possibly most profound research, and the data set upon which it is built is both very convincing, and statistically small. While applying some of the general principles of autonomic physiology regarding retained allostatic loads seems defensible, we are still deeply involved with exploring this and are hesitant to make categorical assertions about what happens when elements of the cascade are incomplete. Our certainty about this is likely to have increased somewhat by the time the class occurs.
AUGUST 22: THE TLR (TONIC LABRYNTHINE REFLEX) AS GENERAL PURPOSE VESTIBULAR-PROPRIOCEPTIVE RECALIBRATION MECHANISM
The tonic labyrinthine reflex is conventionally understood as a primitive developmental reflex that integrates and is superseded in the first months of postnatal life. Our clinical research suggests this framing is incomplete. The TLR — a full arc from extension through flexion driven by vestibular input — appears to function as a general-purpose recalibration mechanism available throughout the lifespan, deployable whenever the relationship between vestibular input and somatic mass requires fundamental reorganization from a new baseline. We have documented spontaneous TLR arcs in numerous clinically distinct contexts including during completion of the Perinatal Autonomic Cascade in an adult patient, and following restoration of proprioception after eight years of complete loss in a case of complex regional pain syndrome (both adult cases). In all cases the reflex appeared endogenously, without instruction, at precisely the moment of vestibular-somatic recalibration. In this class, we will review the neurological architecture of the reflex, examine these two clinical cases in detail, and explore what spontaneous TLR expression means for the treatment of impact injuries, vestibular compromise, and conditions involving disrupted proprioceptive mapping.
LEARNING OBJECTIVES
1. Describe the neurological substrate of the tonic labyrinthine reflex — including its vestibular, brainstem, and proprioceptive components — and articulate the evidence from clinical cases that the reflex serves as a general-purpose recalibration mechanism beyond its conventional developmental role.
2. Analyze the two presented clinical cases to identify the specific conditions under which spontaneous TLR arcs emerged, the mechanistic rationale for their appearance in each context, and what the reflex accomplished neurologically in each instance.
3. Identify clinical presentations — including sequelae of impact collisions, vestibular injury, and conditions involving proprioceptive loss — in which the conditions for TLR-mediated recalibration may be present, and describe the facilitation principles that support rather than interrupt spontaneous reflex expression.