If social touch influences how the body reacts to challenges, how might this be mediated? In a very general sense, the physiological relationship between bodily challenges and bodily reactions can be viewed in terms of “stressors” and “stress responses.” Social touch may tap into the complex dance between the bodily systems that defend the organism against external challenges or stressors—stress responses—and those that calibrate the stress responses to avoid spending too much or too little energy. Such calibration mechanisms are referred to here as “stress buffers.” This section sketches a conceptual overview of stress responses and stress buffering in order to further explore the possibility that affective, social touch plays a stress buffering role.

The term “stress responses” usually refers to activation of specific systems in the body that allow prompt, sometimes life-preserving, reactions to events. These systems invigorate responses to short-term challenges by making energy quickly available to the body’s cells, as well as facilitating behavioral and bodily adjustments to such challenges. For example, neurochemical cascades in the hypothalamic-pituitary-adrenal (HPA) axis help to mobilize glucose in muscle and organ cells to produce energy (McEwen 1998). The sympathetic-adrenal-medullary (SAM) axis can similarly jump-start cardiac and respiratory responses in order to facilitate fast oxygen delivery to muscles and other cells (McEwen 1998; Gunnar and Hostinar 2015). In these stress-response systems, the body’s efficient use of its energy economy and the effective, adaptive modulation of behavior are key.

Under typical circumstances, such stress responses are adaptive. But they can also have a dangerous flip side (Valentino and Van Bockstaele 2015). For example, some HPA and SAM stress responses occur at the expense of important immune and inflammatory processes. In the longer term, chronic activation can impair growth and healing, flatten stress responses, and even shrink hippocampal neurons involved in learning (Miller et al. 1994, Sapolsky 1994; Herman and Cullinan 1997; Sapolsky 2005). Further, because the body is a complex mesh of dynamically interacting systems, blunted or dysfunctional responses can also create asymmetric pressures on other systems, which often heighten their own activity in response to decreased or badly-coordinated stress reactions elsewhere in the body (McEwen 2004). Stress responses are best suited to meet acute, one-off challenges, for example when one is facing aggression, braking to avoid a car accident, or running from a bear. In such emergencies stress responses are cost-effective, even considering the short-term negative impact on the body. Stress responses are therefore not a bad thing in themselves, but under some circumstances, the efficiency of these systems—in terms of energy expenditure, efficacy, and flexibility of response—can be compromised (eg, Schulkin 2011).

The timing of stress responses is also vital. The brain’s networks integrate information from multiple sources, domains, and levels, and exert descending control over peripheral regulatory systems. The scope for the body’s peripheral systems to anticipate and predict challenges before they occur is limited, compared to that of the brain. Through a wider range of learning and predictive abilities, the brain can engage stress responses in anticipation of a stressor. That is, they can be proactive as well as reactive (Herman et al. 2003; IJzerman et al. 2015). It may indeed be the case that the anticipatory or proactive category of stress responses carries especial risk of maladaptation under conditions of chronic stress (Herman et al. 2003). Proactive stress responses can also involve anxiety, in which activation of stress responses extend beyond the immediate context. Anxiety-related HPA and SAM activation is associated with an increased risk of cardiac disease (Ouakinin 2016).

Systems such as the HPA and SAM axes operate most efficiently within a certain “zone”, and less efficiently outside this zone. (This general idea has been discussed elsewhere, eg McEwen 1998). This is likely to be true of most systems which keep the body functioning under changing circumstances. For example, thermoregulatory systems (discussed in the next section) protect the body’s tissues from straying outside a specific temperature range and getting too hot or too cold. The general energy-efficiency-centered range in allostatic regulatory systems will be referred here to as an “Efficiency Zone” (EZ; see Fig. 1). The term “Efficiency Zone” is coined here as a general label for processes and effects that have been noted and discussed in the literature, for example in Sterling (1988).

Fig. 1 Schematic illustration of physiological stress responses along an axis of efficiency. Different forms of response on the left extreme are in the efficiency zone (EZ; green), providing flexible, adaptive, and energy-efficient responses to stress challenges. The right extreme represents dysfunctional responses, which carry the danger of maladaptivity and the potential of deleterious consequences. Stress buffering mechanisms are likely to have most relevance at the right edge of the EZ (yellow). A stress buffering mechanism mitigates or prevents energy efficiency losses among regulatory systems, while also allowing adequate responses to external challenges Full size image

Physiological responses to stress and challenge are expected to be within an EZ under these conditions:

1) responses are easily modulated and adaptive, for example cortisol release showing a sharp, well-timed response.

2) responses return to baseline after the stressful event, without becoming blunted or attenuated.

3) responses are acute and infrequent.

4) responses are well-tuned during a developmental sensitive period (eg, in infancy or early childhood, see Hostinar et al. 2014).

So when stress responses fall outside the extremes of an EZ, the costs of activation (or lack thereof) can begin to outweigh the benefits. For example, frequent dilation of blood vessels in a SAM-mediated response to stress, or their frequent constriction in chronic cold exposure (Castellani and Young 2016), can result in reduction in vessel elasticity and thus reactivity. Outside the EZ, then, risks from within can begin to overshadow risks from without.

However, in maintaining allostatic balance, the body may enlist “buffers” that anticipate and attenuate responses that fall outside the EZ. Overall, the stress buffer idea can be operationalized as responses that offset or mitigate the negative effects of responses outside the EZ, or those that provide some check against the loss of efficiency. Some of these buffering mechanisms may have a genetic basis, as suggested by evidence that certain gene variants can confer a degree of protection, or “resilience,” to stress (eg, Osorio et al. 2016). Some may have developed via natural selection in evolutionary history, such as the comparatively phylogenetically recent ability of the parasympathetic vagal nerves to mitigate sympathetic arousal (Porges 2007). Finally, some buffers may arise from more plastic mechanisms based on learning, experience, and early development. This can involve, for example, developmental time windows (Hostinar et al. 2014), changes in gene transcription and expression (Champagne et al. 2008, Burbridge et al. 2016), and even some forms of gene competition within an individual genome (Champagne et al. 2009). This broad scope for buffering mechanisms gives rise to a tentative generalized definition: a stress buffer is any mechanism or process that mitigates, attenuates, offsets, or prevents energy efficiency losses among regulatory systems, while remaining adequately responsive to external challenges.

If social touch indeed plays such a stress-buffering role, this may involve an interplay between conserved mechanisms of physiological regulation, and those more plastic pathways that change during the course of an individual life, providing flexibility of response and sensitivity to relevant short-term events. It is therefore reasonable to predict that social touch could modulate neural systems which protect bodily safety via regulation of physiological responses, such as the comparatively well-studied systems of cortisol release and regulation. Any such buffering role for affective, social touch might apply to anything between acute, reactive responses within the EZ (eg, a bad day at the office), or straying outside the EZ (eg, chronic anxiety). In a sense, then, our stress-regulatory systems could even extend outside the body envelope to include other people. But what is the current evidence that it does so?