Stress-induced breathlessness in asthma
Leiden University, Leyden, South Holland, Netherlands Psychological Medicine
(Impact Factor: 5.94).
11/1999; 29(6):1359-66. DOI: 10.1017/S0033291799008958
A majority of patients with asthma believe that psychological factors (particularly stress) can induce asthma attacks, but empirical support for actual stress-induced airways obstruction is controversial. This study tested the hypothesis that stress induces breathlessness and not airways obstruction.
Stress was induced by a frustrating computer task in 30 adolescents with asthma and 20 normal controls, aged 14-19 years. Stress measures were self-reported emotions, heart rate, blood pressure. Respiratory measures were respiratory rate (RR), end tidal CO2, deep inspirations and sighs. Asthma measures were lung function, wheeze, cough, breathlessness.
All measures confirmed high levels of negative emotions and stress. None of the participants developed airways obstruction; they had no reduction in lung function, wheeze was absent and cough negligible. However, breathlessness increased in all participants with asthma and excessively in many. The mean breathlessness was higher than during induction of actual airways obstruction with provocative agents in previous studies. End tidal CO2 showed that breathlessness could not be explained by hypocapnia.
Stress can be sufficient to induce breathlessness in patients with asthma.
Available from: Ana F Trueba
- "Depression prevalence also appears to be higher among asthma patients (Slattery and Essex 2011 ; Wong et al. 2013 ), although the literature is more variable (Opolski and Wilson 2005 ). Negative emotions or mood have been linked to reduced airway function (Ritz et al. 2013 ) or worsening of asthmatic symptoms (Rietveld et al. 1999 ), as have depression (Richardson et al. 2006 ), adverse life events (Sandberg et al. 2000 ), low socioeconomic status, and stress (Chen et al. 2010 ). "
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ABSTRACT: The effect of stress, anxiety and other affective states on inflammatory conditions such as asthma is well documented. Although several immune pathway mechanisms have been proposed and studied, they cannot fully explain the relationship. In this chapter we present a new perspective on asthma development and exacerbation that integrates findings on the role of psychological factors in asthma with the microbiome and the hygiene hypothesis in asthma development.
Available from: ncbi.nlm.nih.gov
- "Two of three film studies that showed no significant change or low effect sizes have relied on pre-post assessments only (Table 2). An additional number of studies that showed weak or no effects have also relied on discrete assessments (Miklich et al., 1973; Rietveld et al., 1999; Kang and Fox, 2000; McQuaid et al., 2000; Put et al., 2004; Aboussafy et al., 2006; von Leupoldt et al., 2006). However, emotions have been conceptualized as phasic, transient events of a short duration (Levenson, 1988). "
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ABSTRACT: Psychosocial factors have been found to impact airway pathophysiology in respiratory disease with considerable consistency. Influences on airway mechanics have been studied particularly well. The goal of this article is to review the literature on airway responses to psychological stimulation, discuss potential pathways of influence, and present a well-established emotion-induction paradigm to study airway obstruction elicited by unpleasant stimuli. Observational studies have found systematic associations between lung function and daily mood changes. The laboratory-based paradigm of bronchoconstrictive suggestion has been used successfully to elicit airway obstruction in a substantial proportion of asthmatic individuals. Other studies have demonstrated modulation of airway responses to standard airway challenges with exercise, allergens, or pharmacological agents by psychological factors. Standardized emotion-induction techniques have consistently shown airway constriction during unpleasant stimulation, with surgery, blood, and injury stimuli being particularly powerful. Findings with various forms of stress induction have been more mixed. A number of methodological factors may account for variability across studies, such as choice of measurement technique, temporal association between stimulation and measurement, and the specific quality and intensity of the stimulus material, in particular the extent of implied action-orientation. Research has also begun to elucidate physiological processes associated with psychologically induced airway responses, with vagal excitation and ventilatory influences being the most likely candidate pathways, whereas the role of specific central nervous system pathways and inflammatory processes has been less studied. The technique of emotion-induction using films has the potential to become a standardized challenge paradigm for the further exploration of airway hyperresponsiveness mediated by central nervous system processes.
Available from: Irene H Yen
- "Stress has been linked to asthma-related morbidity (Wright et al., 1998, Rietveld et al., 2000) and negative life events have been linked to poorer asthma-specific quality of life (Archea et al., 2007)¨ Wright and co-authors propose a biopsychosocial model in which environmental demands (stressors or life events) lead to negative emotional responses, then physiological responses, and, finally, an increased risk of more severe physical disease. Clinical reports have suggested connections between an individual's experiences of stress, upset, anxiety and asthma attacks (Rietveld et al., 1999, Rumbak et al., 1993). Depression is associated with increased steroid use and greater health care utilization in asthma (Eisner et al., 2005, Stein et al., 2006, Kullowatz et al., 2006). "
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ABSTRACT: We investigated whether perceived neighborhood problems (NP) predicted changes over a 2-year period in asthma-specific quality of life (QOL), physical functioning (PF), and depressive symptomology (DEP) in a longitudinal cohort of 340 adults with asthma. There is a threshold and plateau effect between NP and PF, such that NP do not affect changes in PF until the problems reach the level of Quartile 3. People who had NP scores in Quartile 3 had lower PF compared to people who reported NP in Quartiles 1 or 2 (mean difference -3.09). High NP also predicted over two-fold odds of high DEP (Center for Epidemiological Studies Depression [CES-D] score > or = 16) at follow-up (odds ratio=2.34; 95% confidence interval: 1.09-5.00). NP did not predict decline in QOL. Analyses adjusted for demographics, asthma severity, and baseline value of the health outcome.
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