Peter’s Doctoral Thesis is online

Dr. Peter Levine’s 1976 Doctoral dissertation, Accumulated Stress, Reserve Capacity, and Disease, is now available online as a PDF. For those of you interested in reading one of Peter’s earliest documents regarding the connection between ANS discharge and the releasing of system stress, please enjoy. I have attached the abstract as well. We are looking to convert it to word and .html as well.

 

Abstract

The underlying theme of this paper is that the accumulation of stress affects the reserve capacity of an organism, both in the maintenance of its functional integrity and inthe resolution of subsequent exposures to stress. Stress isdefined in terms of a reaction resulting from stimuli whichsufficiently activate the autonomic nervous system (ANS) andis either resolved or accumulated depending on whether the pre-stimulus baseline is re-established or not.

Accumulated stress profoundly influences the totality of organismic functioning, and is expressed essentially through three bi-polar effector systems: In the realm of the autonomic, the effector system is the sympathetic and parasympathetic visceral outflow. For the somatic, it is paired movers, like extensor/flexors; and metabolically stress is expressed (though less distinctly) by, for example, catabolic/anabolic and inflammatory/anti-inflammatory endocrine reactions.

Model of Shutdown - after prolonged exposure to fight-or-flight-stress (sympathetic), the parasympathetic (relaxation system) overtakes it, causing a drop in heart rate and blood pressure.

Model of Shutdown – after prolonged exposure to fight-or-flight-stress (sympathetic), the parasympathetic (relaxation system) overtakes it, causing a drop in heart rate and blood pressure.

The response to stress is defined as occurring sequentiallyin two phases, charge and discharge: When the charging(sympathetic) phase is followed by a parasympathetic discharge of equal magnitude, then pre-activation homeostasis is reestablished and the stress is said to be resolved. On the other hand, it is shown that under certain physiologic conditions (and behaviorally where mobilization–i,e.,somatic response to stress–is blocked), the charge phase is no longer balanced by rebound. In these cases activation is not resolved and the stress becomes incorporated within the organism, as a diminished adaptational capacity.

The basic physiologic relations of the autonomic, sympatheticand parasympathetic, can be represented by a simple mechanical analogy (the “Zeeman Machine”) which exhibits properties described by a relatively new branch of mathematical topology, Catastrophe theory. The visualization gained by this re-presentation offers new insights into the nature and mechanisms by which stress accumulates. It also suggests paradigms by which stress, once it has already become internalized, may be successively resolved towards re-establishinga fuller adaptational range/reserve capacity.

In this regard, various holistic systems of healing areseen to focus their efforts towards detecting and treatingthese accumulation imbalances and reduced capacities evenbefore they become symptomatic and pathologic. It is the view of this work that a wide range of “stress diseases” with varied symptoms and obscure aetiologies are the final– pathologic — expression of this loss in resiliency. That the accumulation of stress is the underlying stratum in certain disease syndromes is tested by measuring autonomic levels underlying certain blood pressure responses of a hospitalized population. It is not possible, however,to measure the sympathetic and parasympathetic components directly (since they are expressed as a single output vector, blood pressure). For this reason a systems analysis of the cardio-vascular system, based on well known experimental parameters, but with variable set point and gain levels, is constructed. A set of blood pressure response curves is generated and compared with the hospitalized population. The fit of these with the experimental data is surprisingly good. In addition, the prognosis for five groups in the hospitalized population is predicted accurately by the model, where as no such predictions could be made on the basis of the raw data.The accumulation of stress, defined in terms of the autonomic nervous system, influences many, if not all, other systems. The concept of an autonomic hypothalamic “hub”around which behavior is organized and executed is illustrated to clarify some of these extended relationships. Specifically,the hypothalamic links between autonomic-endocrine, as well as somatic mobilizing systems, are examined in this context. In addition, examples illustrating the potential for the wide and varied symptomatologies of their “mis-integration” (autonomic-endocrine-somatic) in the stress diseases are presented. Some possibilities for pre-symptomatic diagnosis, whereby stress accumulation is detected before the development of debilitating symptoms and tissue pathologies, are investigated as well. These stress diseases are shown, in a selected set of examples, to have underlying patterns of unresolved stress that can be understood in terms of their topologic configurations in catastrophe space.

Dr. Levine’s Thesis.

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