Science and the Socio-Cultural History of Stress
Welcome to Part II in my three-part series on Stress and the Medicalization of Life. Stress as a cultural model has its own socio-cultural history. This means that it has a social life and a past, like any other cultural concept. It is not simply a facet of human physiological reality – an objective fact discovered and elaborated by scientists. It is a creation specific to a culture, a place, and a time. The way we use the word stress today is of relatively recent origin; stress as a cultural model has a shallow socio-cultural history. Although the word stress was loosely associated with ill health by ordinary people during the 19th and early 20th centuries, it rarely appeared in the psychiatric and psychological literature until after W.W.II (Pollock 1988: 381). Medical historian Anne Harrington (2008) credits two men with the term stress as we use it today. The first is Walter B. Cannon (1871-1945), the Harvard physiologist best known for inventing the concepts of “homeostasis” and the “fight or flight response.” The second is Czech-born endocrinologist Hans Seyle (1907-1982), whose research and subsequent media campaign made stress the household word it is today.
Linking Emotions, Physiology, and Illness
W.B. Cannon was interested in the physiological responses produced by our emotional reactions to experiences (Pollock 1988). This interest developed out of his research into peristalsis (how food moves through the digestive tract). Cannon discovered that peristalsis was inhibited in his subjects (mainly domestic cats) whenever they became enraged or distressed (Harrington 2008). Because of this discovery he began to question why and how emotions and digestion might be related. To find out, he developed a new experiment that involved placing cats in ‘safe cages’ and then bringing in dogs to sniff and bark at them. He found that cats threatened in this way generally had higher levels of the hormone adrenaline in their blood samples. It was already known at the time that animals injected with adrenaline showed a particular physiological response that included increases in blood pressure and blood sugar, pupil dilation, inhibited digestion, and piloerection (hair standing on end). No one understood, however, why these particular physiological changes appeared to be associated with emotional arousal (Harrington 2008: 146). To explain the connection Cannon drew on a Darwinian perspective and adaptation to develop a model he called the ‘fight or flight response’ (Pollock 1988, Harrington 2008).
Cannon theorized that all of the physiological responses induced when a cat feels threatened help it to either fight or flee its adversary. The fight or flight response involved mobilizing physiological resources to a heightened state that improved the animal’s chances of fighting or fleeing its enemy. Assuming the animal overcame the threat (and escaped being another critter’s breakfast), its physiology would return to a normative state natural to the species. Cannon termed this physiological regulatory process ‘homeostasis’.
Cannon’s next move was key to the subsequent development of the modern concept of stress: he extended his model to human beings (Harrington 2008: 146-47). Where he made his real leap was in suggesting that the daily experiences of modern life chronically stimulated the fight or flight physiological response in people, preventing the homeostatic systems from returning physiology to a resting state. Cannon speculated that chronic emotional arousal following crises, or just the everyday pressures of modern life, could be a direct cause of illness in people (Pollock 1988: 384). Yet, Cannon generally didn’t use the word stress in the way we use it today to describe the uniquely pathogenic (disease-causing) nature of modern life (Harrington 2008: 148).
Inventing the Mechanical Model of Stress
Common use of the word stress originated in laboratory research conducted in 1935 by Hans Seyle (Harrington 2008, Viner 1999, Pollock 1988). In his experiments, Seyle exposed rats to adverse environmental conditions, like temperature extremes over long periods, and then measured their physiological responses. Seyle found that if the rats survived long enough a typical combination of physiological changes would result: adrenal hyperactivity (over-production of cortisol; what today we know as the primary ‘stress hormone’), atrophy of the lymph nodes, and peptic ulcers (Seyle 1936, 1976). He believed that a common factor or force existed across the environmental conditions to which he exposed his rats and that this force accounted for the combination of physiological changes he had measured. In the model Seyle developed based on his early research, stress referred to the generalized response of the organism to environmental demands. This response is an innate physiological mechanism that prepares the organism for action in the face of threats to survival (Helman 2014).
Seyle’s model, which he termed the General Adaptation Syndrome (GAS), clearly built upon the fight or flight response and homeostasis concepts developed earlier by Cannon (Harrington 2008). In the GAS model, Seyle used the term “stressors” to refer to any environmental influence that produces a combination of physiological changes in the rat body, which he called “the stress response.” In his experiments, stressors included things like exposing rats to temperature extremes, forced exercise in mechanical wheels over long periods, and sewing their eyelids open and then subjecting them to continuous bright light (Harrington 2008). The GAS model laid out the stages in an organism’s physiological response to stressors. The first stage of the response (the alarm reaction) included the initial physiological response to the stressor or force applied to the organism. In the second stage (the resistance or adaptation stage), the organism adjusted to the physiological condition and used this response to cope with the stressor (to fight or flee in the wild). Also, in this stage, the physiological reaction reversed and the body returned to normal (homeostasis), assuming the stressor was removed. The organism also recovered with increased resistance to the original stressor. The third stage (the exhaustion stage) occurred only if the stressor was continuous. If the stressor persisted, the organism’s physiological reaction to the stressor would also persist. If homeostasis was not restored the organism would develop pathologies (disease) and ultimately suffer a premature death (Harrington 2008, Helman 2014, Pollock 1988).
Although they may seem quite similar, there are some important differences between the models developed by Cannon and Seyle. Cannon’s model was about the way emotion mediates between an organism’s physiological response to threats in the environment and illness. Seyle’s model was about a mechanical, non-specific physiological response to an external common factor (any kind of physical damage). Seyle’s stress response did involve emotion, but it wasn’t defined by it (Harrington 2008: 148). His model was much more mechanistic than Cannon’s. Seyle intentionally borrowed the mechanistic approach to stress common in physics and engineering at the time and translated it into the world of biology (Pollock 1988).
Like Cannon before him, Seyle could not resist the urge to apply the GAS model to the experiences of modern humanity. He believed that his experiments explained the prevalence of many illnesses broadly considered the ‘plagues’ of modern life in Western societies. They included heart disease, arthritis, various mental illnesses, and high blood pressure (Harrington 2008). These modern ills had become so frequent, yet were so different, Seyle reasoned that they must be explainable by a non-specific common factor. By 1950, Seyle had coined the term stress to designate this factor and speculated that it was the cause of a whole host of physical and mental illnesses associated with modern life (Harrington 2008: 150).
When Seyle published his model, it was not well received by other endocrinologists, including Cannon. Seyle’s detractors noted that stress was unobservable, immeasurable, too flexible as a concept, and thus not amenable to scientific hypothesis testing (Viner 1999: 396). His leap from the environmental stressors (physical damage) he applied to rats to the human organism’s response to the pressures and complexities of modern life (economic and social) entailed yet another problematic conceptual leap. This leap involved speculation that the ‘stressors of modern life’ were analogous to the mechanical physical forces he applied to rats. He assumed that stressors in the human social world would cause the same nonspecific physiological response (the stress response), which would in turn result in pathogenesis in humans. Presumably, emotion and cognition would both mediate between stressors and the stress response and between the stress response and pathogenesis in humans. But how and to what extent was not elaborated in Seyle’s model. His rat-human analogy included a kind of sleight of hand wherein physical stressors were replaced by the social, emotional, and psychological stressors experienced by humans.
Stress as a Household Word
Seyle quickly decided not to bother with trying to convince other scientists of the validity of his theory through further experimentation. Instead, he launched his own media campaign to get his ideas out to the public and professionals working in other fields. He wrote magazine articles for publications like The Reader’s Digest and gave public lectures. He reached out to special interest groups, to medical clinicians dealing with psychosomatic illnesses, and particularly to military psychiatrists dealing with shell-shocked WW II veterans (Harrington 2008). Seyle sold stress to the public and the medical profession through force of will rather than through an accumulated body of verifiable research.
His strategy worked. Harrington notes that, “As early as 1956, one commentator opined that Seyle’s ideas had ‘permeated medical thinking and influenced medical research in every land, probably more rapidly and more intensely than any other theory of disease ever proposed’” (ibid: 151-52). His ideas also had a profound impact beyond medicine. For example, the Merriam Webster Collegiate Dictionary definition of stress changed from an engineering-based definition referring to the strain caused by external forces in 1949 to a human-centered definition in the 1965 edition. The later definition referred to physical, chemical, and emotional states that can cause bodily or mental tension and may even result in disease (see Young 1980: 133). Today Seyle’s notion of a universal non-specific reaction to an external common factor is accepted in most forms of human discourse in the West and many fields of study, such as epigenetics, psychoneuroimmunology, and psychology, use it as a unifying concept (Viner 1999: 391).
Aside from Seyle’s media campaign, why was the stress model so readily accepted in science and popular culture? Seyle’s earliest allies were physicians, psychiatrists, and psychologists interested in psychosomatic medicine (Viner 1999: 395). They embraced his work, despite his failure to adequately integrate social, emotional, and psychological factors into his experiments and his mechanistic, biological model of stress. Military researchers in the 1950s and 1960s did more than any other group to expand its application from the laboratory into real world circumstances (Harrington 2008: 153). These experiments involving human beings were fundamentally different from those Seyle conducted on rats. Military and other stress studies on human subjects rarely involved physical damage of any kind. Rather, these studies involved psychological and emotional hardship. Reminiscent of Cannon’s original theories, stress was transformed into a physiological response influenced by a person’s emotional and cognitive ability to cope with many different kinds of social and environmental demands.
Once Seyle’s theory entered the arena of psychosomatic research, stress as a concept became heavily psychologized (Pollock 1988). In human studies, stress shifted from a mechanical biological model to a cognitive model. Human cognition and its entanglement with emotion became the most important part of the equation, because researchers assumed that the stress response in humans was mediated through meaning and perception. People experience situations as stressful or not based on their perceptions of experiences, the meanings they attach to them, and their emotional responses. Pollock (1988: 385) calls this shift from a mechanical model of stress in biology to a cognitive model of stress in the medical, psychological, and social sciences ‘incongruous’ and ‘unfathomable’. The cognitive model of stress and its relationship to illness is fundamentally incompatible with the more concrete and mechanistic biological model developed by Seyle. Notwithstanding the incongruities, the biological model served (and continues to serve) as the underlying source of legitimacy for the social and psychological models of stress that have developed over time (Pollock 1988: 387), as well as for the relationship of stress to illnesses in humans.
The Changing Etiology of Stress
The essential difference between the biological and cognitive models of stress becomes clearer when we consider them for what they are – etiological theories. Anthropologists classify etiological theories based on the types of ultimate causes of illness identified by the theories. As discussed in Part I in this series on Stress and the Medicalization of Life, an etiological theory can usually be classified into one of four areas of causes: natural, personal, social, or supernatural. Socio-cultural groups tend to emphasize either the first two types of causes (naturalistic theories of the causes of disease) or the latter two (personalistic theories). Seyle’s biological model is a naturalistic theory. The ultimate cause of illness is physical damage due to prolonged exposure to adverse environmental conditions (like temperature extremes). The physical environment (natural cause) and biological variation (individual cause) are both naturalistic causes of pathology. When Seyle attempted to apply his model to humans and sold it to researchers interested in psychosomatic medicine, however, the ultimate cause of illness shifted, and so did the nature of the etiological theory.
In the cognitive model of stress (the one so prevalent today), illness originates in social situations that elicit the stress response – stressful life events, like divorce, job loss, and war. Physical damage is by no means a necessary ingredient in stress. Instead, the stress response is mediated by the human ability to appraise and interpret situations, emotional coping skills, and, perhaps, genetic variation. Here we see a hybrid mix of etiologies. The ultimate cause of illness due to stress is social, which makes it a personalistic etiological theory, but biological variation (individual, naturalistic factors) may also play a role in whether stress ultimately results in disease in a person. The stress etiological theory is the ‘poster child’ of mind-body dualism; stress research is the perfect venue to elaborate the mind’s influence on the body. This is one reason it is so popular.
It is vitally important that we recognize the cultural model of stress for what it is – a psychosomatic model of illness. In fact, stress is a personalistic theory of disease parading as a naturalistic theory. It is cloaked in science, but based in beliefs about contagious, indeterminate forces that can get inside of us, make us sick, and even kill us. Stress matters, not because it is a scientific ‘reality’, but because we actually live and die by our etiological theories. Such theories not only constrain perception; they are embodied and affect well-being. This is the topic of Part III of my series on Stress and the Medicalization of Life.
Harrington, Anne. 2008. The Cure Within, A History of Mind-Body Medicine. New York: W.W. Norton & Co.
Helman, Cecil G. 2014. Culture, Health and Illness, Fifth Edition. Boca Raton: CRC Press.
Pollock, Kristian. 1988. On the Nature of Social Stress: Production of a Modern Mythology. Social Science and Medicine. 26(3): 381-92.
Viner, Russell. 1999. Putting Stress in Life: Hans Seyle and the Making of Stress Theory. Social Studies of Science. 29(3): 391-410.
Young, Allan. 1980. The Discourse on Stress and the Production of Conventional Knowledge. Social Science and Medicine, 14B: 133-46.
Seyle, Hans. 1976. Forty Years of Stress Research: Principal Remaining Problems and Misconceptions. Canadian Medical Association Journal. 115: 53-7.
– 1936. A Syndrome Produced by Diverse Nocuous Agents. Nature. 138: 32.
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