In the field of health psychology, there is still much debate as to what constitutes an acute stressor versus a chronic stressor. The importance of this clarification is crucial for researchers in this field, because stress is a key factor in many areas of research including coping processes, health behavior, disease progression, and psychoneuroimmunology among others. Many researchers have defined acute vs. chronic stress in the context of their own work, but these definitions varied from one another and illustrate the existing uncertainty as to what precisely differentiates an acute stressor from a chronic stressor. Watch this TED Talk by Dr. Firdaus Dhabar, Associate Professor at Stanford School of Medicine, on the positive effects of the stress response. Pay close attention to how he defines “acute” versus “chronic” stress:
In his TED talk on the positive effects of stress, Dhabar defines acute stressors as “short duration stressors…when you need the response, you mount it but then you shut it down.” This characterization of an acute stressor can be parsed into two main features: (1) short duration and (2) the activation and deactivation of the stress response. This definition bears a similarity to the definition offered by Joshua Smyth and colleagues in a recent paper on an analysis of the pathway between stress and disease. Smyth and his colleagues mention both a short duration and the return to homeostasis as two important features of what they term “pure” acute stressors. However, note that an interesting distinction is made in the Smyth et al. article, delineating “pure” acute stress from a more nuanced perspective of acute stress. We’ll get back to this nuanced perspective of acute stress a little bit later in the post. First, I want to examine the different conceptualizations of chronic stress defined by Dhabar as well as by Smyth.
As heard in his TED talk, Dhabar defined chronic stressors as “lasting for months to years”. However, Smyth and colleagues offer a different approach, conceptualizing a chronic stressor as any stressor that deviates from being a “pure” acute stressor. They go on to specify three main conduits through which pure acute stressors become chronic: (1) repeated activations, (2) low or slow adaptation, and (3) delayed or failure to return to homeostasis. These pathways bear a similarity to those suggested by McEwen (1998) through which stress leads to allostatic load (a great read if you have the time!). The focus of Smyth’s paper, however, was not to identify the effect of stress on biological systems, but to identify what delineates an acute stressor from a chronic one.
Arguably, the most important contribution from the Smyth article was the conceptualization of acute and chronic stress as overlapping concepts. Many researchers in health psychology are concerned with what separates the experience of acute stress from chronic stress, but perhaps these two hypothetical constructs are not as mutually exclusive as we once thought. By placing acute and chronic stress on a continuum of physiological response, researchers are able to take a more nuanced perspective as to how stressors affect a variety of variables (e.g. disease progression, inflammatory response, psychological well-being, etc.)
Using this definition, we can explore stress from amore complex outlook. Let’s take a classic example of an acute stressor—one that is commonly referred to as a “daily hassle”—sitting in traffic. According to the Smyth definition, being stuck in traffic would be characterized as a “pure” acute stressor if the traffic was only present for a brief amount of time and if the driver’s stress response returned to homeostasis shortly after the traffic subsided. However, what if this particular driver encounters a similar traffic scenario every day on her commute to work (not an outlandish notion, especially if she lives in LA)? Would sitting in traffic for this driver still be considered an acute stressor or would it be a chronic stressor because it repeatedly activates her physiological stress response? The continuum approach to chronic vs. acute stress allows us to claim that it is, indeed, both. The isolated event of sitting in traffic fits the definition of acute stress, but if the repeated activations are appraised as stressful or threatening for the driver, her commute (conceptualized as combination of daily stressors from traveling to and from work) may be characterized as a chronic stressor.
This example makes a lot of intuitive sense, because we know that many professionals consider commute time as an important factor when deciding upon a particular job offer or an apartment location. Sitting in traffic during a commute to work is not solely an “acute” or a “chronic” stressor in and of itself. Although the isolated event may be acute, the daily build up (or repeated activations) of those events may lead to a chronic stressor (largely dependent on whether or not the driver appraises traffic as stressful). This example is only the tip of the iceberg when it comes to delineating acute from chronic stressors. More complex stressors may be harder to parse, and you may imagine the many questions that arise when exploring the role of multifaceted stressors such as grief, divorce, or financial strain.
It may be compelling to place acute and chronic stress onto a continuum as suggested by Smyth and colleagues rather than to separate them into two distinct categories. Although my traffic example only explored one of the suggested pathways through which acute stress becomes chronic, similar cases can be explored through the other contributing factors. Research in health psychology may progress further into examining stress from a variety of perspectives, identifying which (if any) contributing factors predict certain diseases more than others. The clinical implications would be to develop interventions geared at specific physiological signatures associated with such pathways that lead to chronic stress, illuminating several new avenues of research in this area.
1. Firdaus Dhabar: The Positive Effects of Stress http://www.youtube.com/watch?v=nsc83N-Q1q4
2. Smyth, J., Zawadzki, M., & Gerin, W. (2013). Stress and Disease: A Structural and Functional Analysis. Social and Personality Psychology Compass, 7(4), 217-227.
3. McEwen, B. S. (1998). Stress, adaptation, and disease: Allostasis and allostatic load. Annals of the New York Academy of Sciences, 840(1), 33-44.
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