This chapter reviews three major models in psychology relevant to the present work—the biopsychosocial model, complexity/NLDST, and embodiment. In Young (Development and causality: Neo-Piagetian perspectives. New York: Springer Science + Business Media, 2011), I reviewed in depth the first two of these models. All three models are considered wide-ranging, integrative ones.
However, each of the models includes limitations—for example, each possesses properties that make it difficult to apply clearly to the domains that have been considered under its scope.
In this regard, the biopsychosocial model suffers from a lack of precise mechanisms in how its major components might interact to produce a behavior at issue (e.g., illness, psychopathology) or how the treatments under its guise might work. Also, the NLDST approach provides a generic approach to describing system states and their change, as well as the processes that might bring about the change, but it has not made the widespread inroads in psychology predicted for it. Part of the reason might lie in the different approaches that are espoused under its umbrella (as well as its complex mathematics and its different approach to variability in behavior, which is considered “noise” in many of the standard approaches in psychology but the primary subject matter in this approach to psychology).
Finally, the embodied approach is only beginning to prosper as a potentially unifying one in psychology, and it too needs to work on specific mechanisms than entrain development and change, or else it will be considered simply as a redescription of behavioral phenomena rather than a model with sufficient explanatory transformative acumen. Certainly, this present work is dedicated to integrating these various integrative models in psychology and providing them with a reliable and valid suite of change mechanisms that can help explain stability/instability and gradual/abrupt changes in behavior.
As for key terms in this chapter, there are a few for the biopsychosocial approach, given its prevalence throughout the present book. I refer to the psychological component of this model as the “personal” one because all three components are involved in the psychology or behavior and it makes no sense to consider one of the components of the term as especially psychological when, in essence, all three are psychological in nature. It is important to note that the three components involved in the model are not as distinct as their separate presentation might indicate.
Some examples of the biological, psychological (personal), and social components of the model included in the present book follow. These examples are taken from throughout the book and not uniquely from this chapter that is being summarized here.
For the biological component of the biopsychosocial model, among others, the present work examines the influence on behavior of genes/epigenetics; Gene × Environment (G × E) interactions and correlated G × E (rGE); the brain and brain networks (the Connectome, structural, and functional); lateralization and hemispheric specialization; evolution, life history theory, and differential susceptibility; as well as the stress response and its major physiological systems (hypothalamic pituitary adrenal (HPA) axis; sympathetic adrenal medullary (SAM) system), and critical molecular biochemicals and neurotransmitter components (cortisol, norepinephrine, glucocorticoid receptors) and their action on neurons and the brain.
For the psychological (personal) component of the biopsychosocial model, among others, the book examines aspects of the self; self-control/regulation (cognitive, emotional); executive function; relevant cognitive acquisitions, including belief; resilience and coping; personality and temperament; motivation and attention; and free will and resource (ego) depletion.
For the social component of the biopsychosocial model, among others, the book explores cultural and societal influences; socioeconomic status (SES), minority status, and other demographics; prenatal influences, early adversity, early life experiences; parenting, parenting style, and schooling; maltreatment, abuse; buffering the environment, etc.
Clearly, free will is a major anchor of the present book. Another component to the personal agency in behavioral causation that I introduce in this chapter concerns passion. I review the definition of passion and also the questionnaire currently in use in evaluating it and, in both regards, develop better ones.
As for the complexity and NLDST, they especially refer, in particular, respectively, (a) to complex adaptive systems, networks, and agents and (b) to attractors, self-organization, emergence, fractals, and circular causality. They also refer to collective autocatalytic sets and to complexity pyramids, as well as to control and order parameters, respectively.
The key terms and concepts in the embodiment model of behavior are proliferating. The embodiment model has been differentiated into strong, secondary, hybrid, and radical versions. A similar model is that of radical enactivism. It has been applied to cognition, affect, the brain (e.g., the mirror system), and even the extended mind, inter-brain, embodied attunement, and conjoined people (through joint attractors). It incorporates extended concepts of behavior, such as body-becoming-mind and the brain–body–environment landscape, yet also quite basic ones, such as chemosignals in intersubjectivity and force dynamics in language and sociality. Some of its concepts are rarified, such as having a hypergrip on affordances and also hermeneutic realism. As for my contributions to the area of embodiment, I develop the concepts of embodied causation or etiology and of causal or etiological embodiment. Also, I refer to the human species as Homo Causa in this chapter and to the causalization process as inimical to who we are and how we become.