A&O – DEEP – STRESS defined





First we must be clear about the difference between stressors (stimuli) and the stress response (process)

In casual conversation these are often used interchangeably, but that is a convenience we cannot allow the researcher, requiring much more precise definitions.  (Looked at in depth, the stress response can be a stimulus that feeds back to modulate specific components.  For example, chronic stress can facilitate the expression of acute stress episodes by changing catalysts that act in the adrenal gland to affect the proportion of specific stress hormones synthesized and released.) 


Stress, to Sibly & Calow (1989)[i] is “an environmental condition that reduces Darwinian fitness when first applied” and is developed in terms of optimal life-cycle strategies.   To Koehn and Bayne (1989)[ii], stress is “any environmental change that acts to reduce the fitness of an organism” (p.158). and is developed in terms of physiological energetics.  A version, they admit, of “Brett (1958): “any environmental factor which extends the normal adaptive response of an animal, or which or which extends the normal functioning to such an extent that the chances of survival are significantly reduced.”   Bradshaw  and Hardwick (1989)[iii] emphasize evolutionary mechanisms emphasizing genotypic and phenotypic plasticity.  

In modelling stress, Sterling and Eyer (1988) used the term allostasis, to refer to a predictive regulatory aspect of homeostasis that emphasized “stability through change.” (cited by McEwen 1998)[iv] and the cost of allostasis maintained over time was termed allostatic load” by McEwen and Stellar (1993; cited by McEwen 1998) and can be regarded as a significant issue for understanding biological fitness and disease.   Sapolsky (2003) considers stress anything that upsets homeostasis (look at his readable review in Scientific American (excerpts))


Greenberg (2002) defined stress in terms of biological needs, adapting Maslow’s motivational scheme and considering the cost of needs not met.  The powerful anticipatory aspect implicit in allostasis as developed by McEwen was accommodated in Greenberg’s definition of stressors as “real or perceived challenges to an organism’s ability to meet its real or perceived needs.” (p526) The evolutionary dimension is built in by regarding stressors as representations of selection pressures, ultimately acting on natural selection (Greenberg et al. 2002).  Adaptive scope, in this scheme represents the tolerance at any level of organization for stress before additional processes are activated.  Thus, stress at the cellular level can ramify though successive levels of organization, but only as needed and eventually, if necessary, recruiting cognitive mechanisms to identify and cope with the stressor.   


An example from a real classroom experience: It was freezing outside but the classroom was cozy.  Coats were hung up on the side of the room, the 80 students were getting comfortable, and I began class.      The room however was cooling off rapidly and after a while I saw people adjusting their postures and eventually someone got up and retrieved their coat and then another asked timidly if I could adjust the thermostat.   It took some time. The first adjustments are wholly non-conscious:  as temperature fell, muscle tone would increase to generate some metabolic heat–but when not enough to compensate, peripheral vasoconstricting reflexes would act to prevent bloodflow to the surface of the body from radiating out needed warmth.  The core of the body would be protected.  Then postures would change to minimize exposed surface area… and finally conscious awareness was roused and cognitive processes kicked in to try to solve the problem.


STRESS is CONSTANTLY in play but only concerns us when it challenges our ability to meet NEEDS (and that also makes it more likely to reach conscious awareness). Of course, each individual’s thresholds for awareness are different, depending of congenital dispositions interacting with experiences  We can speak of most stress as SUBCLINICAL or PRECLINICAL–of insufficient magnitude to represent a challenge.  The possibility of conscious awareness (as in the example above) reflects thresholds for different levels of response at different levels of organization.  Amongst the routine stressors are mismatches between some physiological (or cognitive) intention and outcomes, the vast numbers of which are detected (and errors corrected) non-consciously.  SO: we need to accommodate the fact that at some level, adjustments are always being made and the fact that stress as it is commonly identified as an autonomic nervous system and/or endocrine response


STRESS and ART.  The constellation of cognitive functions that characterize the creation of art and its appreciation (projective and receptive functions) are deeply involved in the machinery of coping with STRESS:   

A line by Percy Bysshe Shelley that I found last week recalls my observation and belief that diarizing often begins in times of personal stress:

“Most wretched men

Are cradled into poetry by wrong:

They learn in suffering what they teach in song”


(from “Julian and Maddalo” (1818) l. 544) (recalls a Wounded Healer)







[i]SIBLY, R. M. and CALOW, P. (1989), A lifecycle theory of responses to stress. Biological Journal of the Linnean Society, 37: 101-116. doi:10.1111/j.1095-8312.1989.tb02007.x

Abstract. Stress is here defined as an environmental condition that reduces Darwinian fitness when first applied. Optimal stress responses (i.e. those that maximize Darwinian fitness) are calculated for different levels of growth and mortality stress, and are found to depend critically on the shape of the trade-off curve relating mortality to growth rate. If the trade-off does not change shape when stress is applied, then the optimal strategy is to spend less on personal defence for both mortality and growth stresses. However, if stress does change the shape of the trade-off the predictions may be modified, or reversed. This optimality analysis is rigorous and easy to apply. What is more difficult, is to establish the shapes and positions of trade-off curves in particular cases. This problem is discussed and some suggestions are made. The theory’s predictions are applied speculatively to biogeographical data on marine animals and are found to be qualitatively successful, although some of the needed data are lacking. The applications and testability of the theory in the study of ageing and a variety of other processes are considered.

[ii] RICHARD K. KOEHN & BRIAN L. BAYNE (2009) Towards a physiological and genetical understanding of the energetics of the stress response. Biological Journal of the Linnean Society 37(12):157 – 171.  DOI:10.1111/j.1095-8312.1989.tb02100.x   https://www.researchgate.net/publication/230085233_Towards_a_physiological_and_genetical_understanding_of_the_energetics_of_the_stress_response

Abstract. We consider stress as an environmental change that results in reduction of net energy balance (i.e. growth and reproduction). Reduced energy balance restricts the environmental range of an organism and may change the environmental optima at which maximum production can be achieved. We emphasize individual differences in net energy balance and the interrelationships among genetic heterozygosity, rate of protein synthesis, efficiency of protein synthesis and whole organism measures of both routine and maintenance metabolic rate. Lastly, we consider the consequences of genetically determined individual differences in metabolic maintenance costs within the context of variable environments and how genetic/environmental interactions can define individual responses to environmental extremes.

[iii] A. D. BRADSHAW K. HARDWICK (1989) Evolution and stress—genotypic and phenotypic components  Biological Journal of the Linnean Society, Volume 37, Issue 1-2, 1 May 1989, Pages 137–155, https://doi.org/10.1111/j.1095-8312.1989.tb02099.x

Abstract.  Since stress can be defined as anything which reduces growth or performance, it follows that, if appropriate genetic variability is present, classical evolutionary changes in populations are to be expected in any situation where a consistent stress is occurring. There is now considerable evidence for such evolution, producing constitutive adaptations in plants in response to stress, which are specific to the stress concerned. Stress may however operate in a temporary or fluctuating manner. In these situations, facultative adaptations, able to be produced within a single genotype through phenotypic plasticity, will be more appropriate. Very different specific phenotypic response systems, both morphological or physiological, can be found in plants in relation to different fluctuating stresses, operating over a wide range of time scales. These response systems are under normal genetic control and appear to be products of normal evolutionary processes. They can however have quite complex features, analogous to the behavioural response systems in animals.

[iv]McEwen BS (1998) Stress, adaptation, and disease. Allostasis and allostatic load. Ann N Y Acad Sci. 1998 May 1;840:33-44.

Abstract.  Adaptation in the face of potentially stressful challenges involves activation of neural, neuroendocrine and neuroendocrine-immune mechanisms. This has been called “allostasis” or “stability through change” by Sterling and Eyer (Fisher S., Reason J. (eds): Handbook of Life Stress, Cognition and Health. J. Wiley Ltd. 1988, p. 631), and allostasis is an essential component of maintaining homeostasis. When these adaptive systems are turned on and turned off again efficiently and not too frequently, the body is able to cope effectively with challenges that it might not otherwise survive. However, there are a number of circumstances in which allostatic systems may either be overstimulated or not perform normally, and this condition has been termed “allostatic load” or the price of adaptation (McEwen and Stellar, Arch. Int. Med. 1993; 153: 2093.). Allostatic load can lead to disease over long periods. Types of allostatic load include (1) frequent activation of allostatic systems; (2) failure to shut off allostatic activity after stress; (3) inadequate response of allostatic systems leading to elevated activity of other, normally counter-regulated allostatic systems after stress. Examples will be given for each type of allostatic load from research pertaining to autonomic, CNS, neuroendocrine, and immune system activity. The relationship of allostatic load to genetic and developmental predispositions to disease is also considered.  PMID: 9629234  https://www.ncbi.nlm.nih.gov/pubmed/9629234