Evidence for individual differences in stress response

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James Wallace

Stress can be defined as the physiological and behavioural reactions in organisms when environmental demands exceed adaptive capacity in response to actual or perceived threats (Sparrenberger et al., 2009; Pinel and Barnes, 2018). Stress is an adaptive brain-body response, designed to maintain homeostasis (i.e. stability) through hormone secretion, or ‘stress mediators’, controlled by the hypothalamic-pituitary-adrenal (HPA) axis (McEwen and Seeman, 1999). This manifests as the evolutionary ‘fight-or-flight’ response and is essential for survival. 

HPA activation causes the hypothalamus in the brain to produce small protein molecules called a neuropeptide (i.e. which neurons use to communicate) which stimulates the adrenal cortex to release cortisol in humans (Kortea et al., 2005). Differences in the secretion levels of these hormones, in part, correlates with individual stress response variability, or ‘response stereotypy’. This mechanism is well-recognised (Sparrenberger et al., 2009, cited in Kasprowicz et al., 1990, Root et al., 2009). Indeed, while many individuals show potent biological responses to mild stressors, others seem behaviourally unaffected even by life-altering events (Ellis et al., 2006). The long-term consequences for the stress-susceptible comprise maladaptive neuronal, behavioural and immune function changes which cause health risks, such as depression, post-traumatic stress disorder (PTSD), anxiety disorders, tissue damage and disease, enlarged adrenal glands, as well as metabolic and cardiovascular dysfunctions (Kinlein et al., 2015; Schneiderman et al., 2005). By contrast, stress-resilient individuals can remain largely impervious to similar adversity (Ellis et al., 2006). This spectrum of stress-related impacts is known as allostasis, the process that maintains homeostasis through change (McEwen and Seeman, 1999). This essay will now consider selected associated theories and evidence.   

Evolutionary

Evidence which supports Darwinian evolutionary theories is considerable, much of which is drawn from animal studies. Kortea et al (2005) described the ‘Hawk–Dove’ metaphor, which claims stress reactivity is a function of evolution-directed behavioural responses. According to the theory, Hawks adopt aggressive behaviour while Doves are cooperative and passive. These differences are due to genetic-environmental driven biases in how nervous and endocrine systems interact which, in turn, influences behaviour, coping and emotional styles and, consequently, stress response (Kortea et al., 2005). The theory of adaptive phenotypic plasticity further supports this evolutionary account. The theory purports that a genotype (i.e. an individual’s assortment of genes) can be biased towards the development of certain phenotypes (i.e. a distinct set of characteristics), in response to environmental conditions. Phenotypic plasticity in response to different environments is regarded as a primary genetic-environmental driver of adaptive individual differences, including in respect of stress response (Ellis et al., 2006). Kortea et al (2005) wrote that Hawks are characterised by low HPA axis reactivity (i.e. stress-resilient), while Doves are characterised by high HPA axis reactivity (i.e. stress-vulnerable). These gene-environmental interaction variations, in part, result from structural neurobiological differences in the hippocampus, the brain region which regulates responses during and after stressful situations (Kortea et al., 2005). However, the generalisability of evolutionary trends in animal research to humans varies. Elsewhere, studies suggest genetic factors partially determine individual differences in diurnal HPA axis rhythms, controlled by light-dark and awake-sleep patterns, which influence responsiveness to stressors (Ebner and Singewald, 2016). 

Environmental 

Studies show the quality of one’s early environment, exposure to adversity, parental style and socioeconomic (SES) status all influence neural and endocrine system development. In turn, this influences stress-resilience or susceptibility development in adulthood (Cameron et al., 2005). Traumatic events, such as physical or sexual abuse in early life, increase endocrine and autonomic responses to stress in adulthood, while early parental loss can increase HPA responses to stress (Cameron et al., 2005). In addition, studies have shown that low socioeconomic status (SES) is associated with increased exposure to chronic stressors (Cameron et al., 2005). Elsewhere, emerging evidence suggests personality traits may be predictors of response stereotypy. However, evidence to date is equivocal. Xin et al (2017) wrote that neuroticism is associated with greater negative psychological responses, including higher perceived stress (cited in Bibbey et al., 2012), while other studies reveal no relationship (Garcia-Banda et al., 2011). Personality and environmental adversity can impose a bidirectional influence on stress reactivity. For example, levels of neuroticism and emotionality correlate with response stereotypy, as well as with proneness to stressful events (Sparrenberger et al., 2009), while intensity, severity and controllability of the stressor are also factors (McEwen and Seeman, 1999; Ebner and Singewald, 2016). Furthermore, individual protective factors, such as one’s resources, self-esteem and optimism can also be material influences.

Physiological

Evidence for physiological variability in response stereotypy is considerable. Variations can be identified in cardiovascular metrics (i.e. blood pressure, heart rate, immune system, etc) through increased levels of secreted stress hormones by HPA axis activation (Pinel and Barnes, 2018, Hirotsun et al, 2015). Clinical studies have also demonstrated the connection between sleep and stress response. Hirotsun et al (2015) wrote that sleep deprivation can lead to maladaptive changes in the HPA axis, which triggers neuroendocrine dysregulation and, in turn, changes in metabolism, energy utilisation and blood pressure. Cardiovascular activity is another cited variable which can illuminate stress reactivity differences. Bibbey et al (2012) wrote that cardiovascular activity is correlated with differences in secreted cortisol levels in the HPA axis, as well as in the sympathetic–adrenal–medullary (SAM) system (cited in Lovallo, 1997). However, García-Prieto et al (2006) pointed out that cortisol is a circadian hormone which fluctuates in levels throughout the day, which renders mean values redundant in stress measurement.

More broadly, studying the physiological consequences of stress is problematic due to variability in the classification methods of stressed and non-stressed individuals (García-Prieto et al., 2006). Further, psychological tests show weak associations with the physiological responses to stress (García-Prieto et al., 2006, cited in McEwen, 1998). Finally, a study by Llabre et al (1998) provided empirical support for stress reactivity differences by gender and ethnicity.

Conclusion

Individual stress reactivity is complex and not easily disentangled. However, a review of this subject’s extensive literature suggests individual differences in stress responses emerge within and across the interplay of physiological, environmental and genetic factors. Moreover, the nature of stressor itself, its intensity, duration and repetition also influence response stereotypy.

This essay was submitted as part of my MSc in Psychology at Leeds Beckett University in January 2020. Students are reminded copying this essay is plagiarism. 

Suggested citation:

Wallace, J. (2020). Evidence for individual differences in stress response. Retrieved from: www.james-wallace.uk

Reference List 

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