Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease

Amy R. Schwartz, William Gerin, Karina W. Davidson, Thomas G. Pickering, Jos F. Brosschot, Julian F. Thayer, Nicholas Christenfeld, Wolfgang Linden

Research output: Contribution to journalArticle

266 Citations (Scopus)

Abstract

Objective: Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding. Methods: We illustrate current understanding of stress-cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature. Results: In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship. Conclusions: A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.

Original languageEnglish (US)
Pages (from-to)22-35
Number of pages14
JournalPsychosomatic medicine
Volume65
Issue number1
DOIs
StatePublished - Jan 1 2003

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Cardiovascular Models
Cardiovascular Diseases
Environmental Exposure
Psychophysiology
Molecular Epidemiology

All Science Journal Classification (ASJC) codes

  • Applied Psychology
  • Psychiatry and Mental health

Cite this

Schwartz, A. R., Gerin, W., Davidson, K. W., Pickering, T. G., Brosschot, J. F., Thayer, J. F., ... Linden, W. (2003). Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease. Psychosomatic medicine, 65(1), 22-35. https://doi.org/10.1097/01.PSY.0000046075.79922.61
Schwartz, Amy R. ; Gerin, William ; Davidson, Karina W. ; Pickering, Thomas G. ; Brosschot, Jos F. ; Thayer, Julian F. ; Christenfeld, Nicholas ; Linden, Wolfgang. / Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease. In: Psychosomatic medicine. 2003 ; Vol. 65, No. 1. pp. 22-35.
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Schwartz, AR, Gerin, W, Davidson, KW, Pickering, TG, Brosschot, JF, Thayer, JF, Christenfeld, N & Linden, W 2003, 'Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease', Psychosomatic medicine, vol. 65, no. 1, pp. 22-35. https://doi.org/10.1097/01.PSY.0000046075.79922.61

Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease. / Schwartz, Amy R.; Gerin, William; Davidson, Karina W.; Pickering, Thomas G.; Brosschot, Jos F.; Thayer, Julian F.; Christenfeld, Nicholas; Linden, Wolfgang.

In: Psychosomatic medicine, Vol. 65, No. 1, 01.01.2003, p. 22-35.

Research output: Contribution to journalArticle

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N2 - Objective: Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding. Methods: We illustrate current understanding of stress-cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature. Results: In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship. Conclusions: A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.

AB - Objective: Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding. Methods: We illustrate current understanding of stress-cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature. Results: In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship. Conclusions: A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.

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