Allostasis and the human brain: Integrating models of stress from the social and life sciences

Abstract

We draw on the theory of allostasis to develop an integrative model of the current stress process that highlights the brain as a dynamically adapting interface between the changing environment and the biological self. We review evidence that the core emotional regions of the brain constitute the primary mediator of the well-established association between stress and health, as well as the neural focus of wear and tear due to ongoing adaptation. This mediation, in turn, allows us to model the interplay over time between context, current stressor exposure, internal regulation of bodily processes, and health outcomes. We illustrate how this approach facilitates the integration of current findings in human neuroscience and genetics with key constructs from stress models from the social and life sciences, with implications for future research and the design of interventions targeting individuals at risk.

Figure 1

The role of central and peripheral allostatic accommodation in predicting reported health outcomes from stressor exposure. Dotted lines indicate active feedback.

Figure 2

The relative roles of stressor, cognition, and context in the allostatic model of stress. Dotted lines indicate active feedback. Dashed arrow between perception and central allostatic accommodation to a current stressor (bypassing complex representation of sensory stimuli and possibly awareness) indicates that this pathway is currently under debate in the literature (see text).

Figure 3

The allostatic model, including the role of central and peripheral allostatic load in the response a current stressor. Interaction would be expected between allostatic load and major pathways in central allostatic accommodation (not shown).

Figure 4

Allostatic model across development (simplified).

Figure 5

Linking health outcomes across generations: the role of genetics in a simplified allostatic model of stress includes the main effects of genetic inheritance on the stress physiology and choice of environment, gene × environment (G × E) interactions that affect the stress response, and epigenesis as a potential means to inherit parental allostatic load.

Figure 6

a. Schematic illustration of the midline frontal-brainstem axis involved in brain-body information transfer regulating peripheral autonomic, endocrine, and immune function. We argue that this axis is a key component of central allostatic accommodation, as discussed here (reprinted from Neuroimage, 47, R.D. Lane, & T.D. Wager, The new field of brain-body medicine: What have we learned and where are we headed? p. 1136 (2009), with permission from Elsevier). b. Figure showing areas of significantly lower gray matter volume (in yellow) in healthy adults who were within a mile and a half of the World Trade Center on 9/11/01 more than three years prior to imaging, relative to comparison group (reprinted from Neuroimage, 40, B. Ganzel, P. Kim, G. Glover, & E. Temple Resilience after 9/11: Multimodal neuroimaging evidence for stress-related change in the healthy adult brain. 791, (2008), with permission from Elsevier).