Published online before print
December 24, 2007, 10.1097/PSY.0b013e31815c1b71
Psychosomatic Medicine 70:102-116 (2008)
© 2008 American Psychosomatic Society
A Bidirectional Relationship Between Psychosocial Factors and Atopic Disorders: A Systematic Review and Meta-Analysis
Yoichi Chida, MD, PhD,
Mark Hamer, PhD and
Andrew Steptoe, DPhil
From the Psychobiology Group, Department of Epidemiology and Public Health, University College, London.
Address correspondence and reprint requests to Yoichi Chida, Psychobiology Group, Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom. E-mail: y.chida{at}ucl.ac.uk
 |
ABSTRACT
|
|---|
Objective: There is growing epidemiological literature focusing on the bidirectional association between psychosocial factors and atopic disorders, but no efforts to quantify the relationship systematically have been published.
Methods: We searched Medline, PsycINFO, Web of Science, and PubMed up to June 2007. The studies included were prospective cohort studies investigating the influence of psychosocial factors on atopic disorders and the effect of atopic disorders on mental health. Two investigators independently extracted data and determined study quality.
Results: There were 43 studies (in 22 articles), of which 34 evaluated the effect of psychosocial factors on atopic disorders and 9 evaluated the effect of atopic disorders on mental health. The major atopic disease assessed in these studies was asthma (90.7%) with allergic rhinitis, 4.7%; atopic dermatitis, 2.3%; and food allergies, 2.3%. The overall meta-analysis exhibited a positive association between psychosocial factors and future atopic disorder (correlation coefficient (r) as combined size effect .024; 95% confidence interval, 0.014–0.035; p < .001) as well as between atopic disorders and future poor mental health (r = .044, 95% confidence interval, 0.021–0.067, p < .001). More notably, the subgroup meta-analysis on the healthy and atopic disorder populations showed psychosocial factors had both an etiological and prognostic effect on atopic disorders.
Conclusions: The current review revealed a robust relationship between psychosocial factors and atopic disorders. This supports the use of psychological in addition to conventional physical and pharmacological interventions, in the successful prevention and management of atopic disorders.
Key Words: allergy • anxiety and depression • psychoneuroimmunology • psychosocial stress • social support • meta-analysis
Abbreviations: 95% CI = 95% confidence interval; r = correlation coefficient.
|
INTRODUCTION
|
|---|
Atopy can be considered to be a genetically and environmentally determined predisposition to a number of clinically expressed disorders including allergic rhinitis, atopic dermatitis or eczema, and allergic asthma, regulated through immune phenomena in which many cells (ie, mast cells, eosinophils, and T lymphocytes) and associated cytokines, chemokines, and neuropeptides play a role. Mechanisms of inflammation central to the pathophysiology of these atopic disorders overlap and involve a cascade of events that include the release of immunologic mediators triggered by both immunoglobulin E (IgE)-dependent and independent mechanisms (1). The prevalence of atopic disorders has continued to escalate worldwide in the past three to four decades, especially in the highly developed Westernized societies, where as many as one in three individuals suffer from some form of atopic disorders (2,3). The remarkable change in external environments such as allergens, deficient antigen exposure in early life (hygiene hypothesis), climate, environmental pollution, and tobacco smoke exposure may partly explain the atopic epidemic, because genetics alone cannot account for the sudden and significant rise in atopic disorder that has seen prevalence rates triple in less than 40 years (2,3).
In parallel with the increase in atopic prevalence is a documented increase in many psychosocial stresses in various socioeconomic populations (4,5). Historically, many clinicians have considered atopic disorders to be "psychosomatic." Before the underlying inflammatory basis of atopic disorders was discovered, atopic disorders were among the disorders believed to be purely psychogenic in origin. Alexander (1950) mentioned atopic dermatitis and bronchial asthma among the seven classic psychosomatic disorders (6). Recently, there have been a growing number of epidemiological studies designed to examine the effect of psychosocial factors on the expression of atopic disorders (7). However, their results are conflicting.
The mechanisms relating psychological stress, personality, and emotion to atopic disease also continue to be investigated. Hormones and neuropeptides released into the circulation when individuals experience stress are thought to be involved in regulating both immune-mediated and neurogenic inflammatory processes (1). Dysregulation of normal homeostatic neural, endocrine, and immunologic mechanisms can occur in the face of chronic stress, leading to chronic hyperarousal or hyporesponsiveness that may affect disease expression (7,8). These responses may in turn have an influence on mood and well being. Therefore, it is also important to clarify to what degree atopic diseases affect psychological state.
We conducted a systematic review and meta-analysis of prospective cohort studies to better explore and quantify the putative bidirectional relationship between psychosocial factors and atopic disease.
|
METHODS
|
|---|
Data Sources and Searches
We developed a protocol using a widely recommended method for systematic reviews of observational studies (9,10). We searched general bibliographic databases: Medline (1966 to June 2007); PsycINFO (1872 to June 2007); Web of Science (1900 to June 2007); PubMed (1950 to June 2007), and scrutinized reference lists from relevant reviews and articles. The main search strategy was ("allerg*" or "atop*" or "asthma") and ("psych*" or "stress" or "depress*" or "anxiety" or "social support") and ("prospective" or "longitudinal").
Study Selection
To better explore and quantify a putative bidirectional relationship between psychosocial factors and atopic disease, we limited the current systematic review and meta-analysis to prospective cohort studies, because cross-sectional and retrospective case-control studies are subject to recall bias and cannot conclusively detect a causal association between predictive and outcome variables. Psychosocial stress can be generally considered to be a combination of exposure to a stressor, the emotional and behavioral response to it, and the use of social supports (8,11). We therefore investigated three types of psychosocial factors in this review, namely, a) stressor exposures such as negative life event and daily stress, b) psychological distress (internalizing, anxious, or depressive symptom, stress-related personality, immature coping skills, etc.), and c) poor social support (social isolation, impoverished social relationships, etc.). In the case of cohorts containing infants or children (0–17 years old), we also included family-related distress such as caregiver stress, maternal panic disorder or depression, and family conflict, because these have been reported to exert strong immunological effects on younger subjects (12). The analyses of the impact of atopic disorders on mental health included studies of psychological distress, anxiety, panic disorder, and internalizing symptoms in children. Criteria for inclusion were as follows: a) English language full-length publication in a peer-reviewed journal; b) prospective cohort study; c) investigating a longitudinal association between psychosocial factors and the incidence or severity of atopic disease, or a longitudinal association between atopic disorders on the incidence or severity of psychological distress; d) the articles evaluating low socioeconomic status as a source of psychosocial distress were excluded, because almost all articles used this factor as a controlled covariate but not an explanatory variable; e) if a cohort overlapped across articles, the article with shorter follow-up or poorer study quality was excluded; f) if more than one kind of atopic disorders or psychosocial factors were assessed in one article, the samples were included separately.
Data Extraction and Quality Assessment
A manual was prepared for coding the studies. The manual was revised during the coding to incorporate important aspects of the located studies. The final list of variables is shown in Tables 1 and 2. The selected studies were categorized into three groups: a) a healthy population without outcome atopic disease or psychological distress at the beginning of observation, b) a population with outcome atopic disease or psychological distress at the beginning of observation, and c) a community-based population including subjects with and without atopic disease or psychological distress. This design enabled us to examine an etiological effect of explanatory variables on outcome diseases, and a prognostic effect of explanatory variables on outcome diseases.
We assessed all manuscripts that met the selection criteria for quality. Our quality items were based on existing protocols (9). We considered a study to be of good quality if it used consecutive or random recruitment of participants or representative sampling, ascertainment of explanatory or outcome variables by validated instruments or clinical examination, and control for possible covariates including smoking and socioeconomic status. We classified studies arbitrarily into high or low quality categories by whether or not they fulfilled three or more of these criteria.
One author (Y.C.) conducted and another (M.H.) verified study inclusion and data extractions. At least two reviewers independently assessed quality and validity. Disputes were settled by consensus. On occasion, we attempted to obtain supplementary information directly from the authors by E-mail or from another published report.
Data Synthesis and Analysis
We followed meta-analytic procedures that have been previously described elsewhere (13). Briefly, an effect size was calculated as a correlation coefficient (r) from the difference in atopic outcome at follow-up (the last time point assessed) across psychosocial factor levels at the baseline, or the difference in psychological distress outcome at follow-up across atopic status at the baseline. Therefore, the data in each study had to include either a zero-order r or information that could be converted to an r effect size (e.g., t tests, F tests, means and SDs, and chi-squares). If a study did not report an r effect size, we computed one from descriptive statistics, t statistics, F ratios, and tables of counts (14). If no relevant convertible statistics were presented, other than a p value, we calculated the t statistic from the p value and an r-sub (equivalent) (15). When an article reported p < .05, p < .10, or ns, we computed r-sub (equivalent) with p values of .025, .050, .50 (one-tailed), respectively, which likely yielded a highly conservative estimate of the effect size.
Weighted average effect sizes were computed as r values by proportionally weighting each study’s observed effect size according to its degrees of freedom. The advantages of reporting meta-analytic results as r values as opposed to other effect size indicators (e.g., Cohen’s d and Hedge’s g) have been discussed by Rosenthal (14). Because we compared the effect of a wide range of stress, we decided to use random effects modeling (DerSimonian-Laird method) overall (16). Random effects models take into account the amount of variance caused by differences between studies as well as differences among subjects within studies. Provided there was sufficient information, we aimed to perform sensitivity analyses according to the characteristics of cohort population, sample size, type of psychosocial factor, study quality score, and type of atopic disorder. We simultaneously used the Q-test for homogeneity between studies, which tests whether there was variability within the set of effect sizes. Finally, to detect publication biases, we examined measured the degree of asymmetry by using Begg’s asymmetry method (17). All analyses were performed using the Meta-Analysis program (18).
|
RESULTS
|
|---|
Figure 1 shows details of exclusion and inclusion of articles. Appendix Table A1 details the articles that were excluded from detailed evaluation (n = 20). Tables 1 and 2 summarize the characteristics of 34 studies investigating the effect of psychosocial factors on atopic disease and those of 9 studies investigating the effect of atopic disorders on mental health, respectively.
View larger version (18K):
[in this window]
[in a new window]
|
Figure 1. Flow diagram of systematic review (QUOROM statement flow diagram). (A) Healthy population, (B) Atopic disease population or psychological distress population, and (C) Community-based population include the subjects without outcome atopic disorders or psychological distress at the beginning of observation, the subjects with outcome atopic disease or psychological distress at the beginning of observation, and subjects with and without atopic disorders or psychological distress at the beginning of observation, respectively.
|
|
Effect of Psychosocial Factors on Atopic Disorders
Study Characteristics and Quality
Across the 17 cohorts, sample sizes ranged from n = 32 to 20,854, with a mean of 3352 (median, 411). Follow-up periods averaged 4.7 years with a median of 2.0 years. A range of psychosocial factors was assessed, which were categorized as a) stress exposure (20.6%, 7 of 34 studies), b) psychological distress (41.2%, 14 of 34 studies), or c) poor social support (38.2%, 13 of 34 studies). Regarding clinical atopic disease outcomes, almost all studies assessed asthma except for one in which atopic dermatitis was measured (Table 1, No. 9b). Fifteen studies (44.1%) were classified as high quality (quality score 
3); in detail, consecutive or random recruitment of participants, 23 studies (67.6%); satisfactory ascertainment of explanatory variables by validated instruments or clinical examination, 26 studies (76.5%); satisfactory ascertainment of outcome variables by validated instruments or clinical examination, 14 studies (41.2%); and control for possible covariates including smoking and socioeconomic status, 19 studies (55.9%).
Study Results and Meta-Analysis
More than half the studies (55.9%, 19 of 34 studies) demonstrated a detrimental effect of psychosocial factors on atopic disorders, with the odds ratios or the relative risks ranging from 1.15 to 8.95 (Table 1). As shown in Table 3, combined effect size for 34 studies was 0.024 (95% confidence interval (95% CI), 0.014–0.035). More intriguingly, the subgroup meta-analyses on the studies with healthy populations and atopic populations showed effects of 0.015 (95% CI, 0.005–0.024) and 0.046 (95% CI, 0.021–0.074) respectively (Figure 2), which indicates that psychosocial factors may have an aggravating effect on both the onset and clinical course of atopic disorders. Effects remained significant when children and adult populations were analyzed separately, and associations remained significant for both high and low methodological quality studies. We also carried out separate meta-analyses of moderate (N 500) and very large (N 5000) studies. Both were significant, though effect sizes were reduced in the very large sample studies.
View larger version (31K):
[in this window]
[in a new window]
|
Figure 2. Meta-analysis about the effect of stress on atopic disorders. Higher positive correlation coefficients (r) indicate a more detrimental role of stress in atopic disease.
|
|
We were able to carry out separate meta-analyses on stress exposure, psychological distress and poor social support, and groupings within these categories. As shown in Table 3, psychological distress had the most significant effects on atopic outcome (r = .043; 95% CI, 0.020–0.066), though associations with poor social support were also significant. Both depression or anxiety and parental psychological distress had robust effects on atopic disease (r = .029; 95% CI, 0.010–0.067; and r = .058; 95% CI, 0.001–0.115). The test for heterogeneity between studies did not show statistical significance (p < .05) in any categories, except for an overall analysis (p = .016).
The Effect of Atopic Disorders on Mental Health
Study Characteristics and Quality
Across the six cohorts, sample sizes averaged 1344 with a median of 478, ranging from 91 to 3430. Three cohorts contained children and three adults. Two cohorts (Table 2, No.4, 6) measured the influence of two or more types of atopic disorders in each cohort. Mean follow-up period of nine studies was 7.6 years (median, 4.0 years). Three types of atopic disorders were assessed, namely asthma (66.7%, 6 of 9 studies), allergic rhinitis (22.2%, 2 of 9 studies), and food allergies (11.1%, 1 of 9 studies). Outcome variables of psychological distress were all related to excessive symptoms of anxiety, such as panic disorder, although internalizing symptoms further included depressive symptoms. Two studies were classified as high quality (quality score 3); the breakdown was consecutive or random recruitment of participants, six studies (66.7%); satisfactory ascertainment of explanatory variables by validated instruments or clinical examination, none (0%); satisfactory ascertainment of outcome variables by validated instruments or clinical examination, all studies (100%); and control for possible covariates including smoking and socioeconomic status, two studies (22.2%).
Study Results and Meta-Analysis
Two thirds of the studies (6 of 9 studies) showed that atopic disorders impaired mental health, with the odds ratios ranging from 1.90 to 4.50. Combined effect size for 9 studies was 0.044 (95% CI, 0.021–0.067) (Table 3). In addition, the subgroup meta-analyses showed that asthma was significantly associated with the development of psychological distress in healthy populations with a combined effect size of 0.040 (95% CI, 0.017–0.063). In the only study that examined the effect of atopic disorders in a population that was already distressed (boys with problem behavior), no effects on psychological outcome were observed (r = .052, 95% CI, –0.050–0.153) (Figure 3). Associations between atopic disorders and future poor mental health were significant in separate analyses of children and adults, and in studies of asthmatic samples (Table 3). The test for heterogeneity between studies did not show statistical significance (p < .05) in any categories.
View larger version (12K):
[in this window]
[in a new window]
|
Figure 3. Meta-analysis about the effect of atopic disorders on mental health. Higher positive correlation coefficients (r) indicate a more detrimental role of atopic disease in mental health.
|
|
|
DISCUSSION
|
|---|
To our knowledge, this is the first systematic review to statistically confirm a bidirectional relationship between psychosocial factors and atopic disorders. The subgroup meta-analyses found that psychosocial factors were deleteriously involved in both the development and prognosis of atopic disorders. Additionally, the effect of atopic disease on future mental health was stronger than that of psychosocial factors on atopic disease development and progression. This suggests that greater clinical attention should be paid to mental health outcomes in patients with atopic conditions so as to break the vicious cycle of psychological distress-atopic disease.
Possible Underlying Mechanisms
The reciprocal relationship between psychosocial factors and atopic disorders might be mediated via behavioral and socioeconomic pathways. For example, stress might cause some atopic disease-exacerbating behaviors such as poor diet, lack of exercise, sleep disturbance, frequent smoking, substance abuse, unhygienic living environment, and poor medical adherence or compliance. In contrast, atopic diseases theoretically could have an adverse impact on mental health via chronic and unstable symptoms, consistent unsuccessful treatment and cumulative medical cost, and social functioning impairment at home, school, or workplace (7). Our review could not address all of these behavioral pathways. However, several studies demonstrated positive results even after controlling for important covariates such as smoking and socioeconomic status. This suggests that direct physiological pathways could also be involved. The hypothalamic-pituitary-adrenal axis, the sympathoadrenomedullary system, peripheral nonadrenergic noncholinergic nerves, and the sensory input from peripheral atopic inflammation might mediate a close interaction between the central nervous system and atopic disorders (7,41–43). In addition to the central role of the helper T cells (TH1–TH2) paradigm, recent studies have argued that other possible mechanisms are involved in the stress-atopic disease relationship, such as oxidative stress, glucocorticoid resistance, nerve-mast cell interactions, and intestinal dysbiosis (1,42). Investigation of a broader range of cytokines and neuropeptides produced by cells both within and outside the immune system might better delineate the true complexity of the mechanisms underlying the effect of atopic disorder on the central nervous system (7,44).
Issues Arising From the Sensitivity Analyses
The separate meta-analyses of the three types of psychosocial factor found that psychological distress and poor social support, but not exposure to stressors that included life events or daily stress, had a significant adverse impact on atopic disorders. In line with this finding, previous studies have shown that individual variation in vulnerability to stress-related diseases among people with similar life experiences is determined largely by the way stressors are perceived and the quality of social support (8). Furthermore, it implies that managing human cognition, appraisal, coping and emotional reaction to adversity, and organizing social support might be rather more important than preventing stress exposure in relation to atopic disorders. In addition, it should be noted that not all psychological distress results from psychosocial stress and adversity, because preexisting mood differences that are partly genetically determined may be present even in the absence of stressor exposure (45,46). Interestingly, data from twin studies suggest a genetic link between atopy and psychological distress (47), which could in some extent account for the present finding of a robust association between atopic disease and psychological distress including depression or anxiety and parental psychological distress.
The analyses of children and adult populations indicate that the relationship between psychosocial factors and atopic disorders was more robust in children. Recent evidence has suggested that for most children who develop atopic disorders, the polarization of their immune system into an atopic phenotype likely begins before birth (12). Moreover, gestational exposures to maternal stress can alter the development of humoral immunocompetence in offspring. The absence of maternal care has also been shown to cause some immune responses to go awry and to impair emotional stability (12). Therefore, it is plausible that these prenatal and postnatal stresses might accelerate an association between stress and atopic disorders.
Limitations and Guidelines for Future Studies
Our review was limited to evaluation of results in published articles. There was some evidence of publication bias, but only in 4 of the 25 subanalyses. This may imply a positive result bias, if authors are more likely to submit, or editors accept, positive than null (negative or inconclusive) results. The meta-analysis of the prognostic effect of atopic disorders on mental health included only one cohort study. More notably, because almost all studies assessed asthma status, the present findings may not extend to a more general relationship between psychosocial factors and atopic disorders. However, given that many cross-sectional, retrospective, or trial studies have demonstrated that atopic dermatitis, allergic rhinitis, and food and chemical allergies are strongly associated with stress (48–50), it is feasible that prospective studies would also detect a longitudinal relationship between psychosocial factors and other atopic diseases besides asthma.
Psychosocial factors had smaller effects on atopic disease in the studies with very large sample sizes. This finding was driven primarily by a recent high-quality British study of more than 20,000 adults, in which effects were significant but small (19). This suggests that Rosenthal’s method (15) of calculating correlation coefficients from sample size (N) and p values (r = 
t2/(t2 – N – 2), t value with the degrees of freedom is based on the p value) might cause effect sizes to become less as the studies have larger sample sizes. It is also worth noting that the method of grouping psychosocial factor levels was inconsistent across studies, with some using binary divisions, others tertiles or quartiles, or established cutoff scores. We evaluated the validity of psychosocial factor measurement in each study as a quality score, but clearly the meta-analysis is limited when such different methodologies are used to operationalize the main exposure on interest. Undoubtedly, it would be helpful in the future to standardize the measures of psychosocial factors used.
Asthma was the main disease investigated, with many studies using self-report measures of respiratory symptoms (e.g., wheezing and cough) or physician’s diagnosis. These relatively vague indicators might be contaminated with other respiratory diseases such as infectious bronchitis and emphysema, and be affected by participants’ recall bias, although previous studies have reported that asthma based on self-report of physician’s diagnosis had high agreement with clinical diagnosis (51,52). Not all asthma can be categorized as allergic, but detailed scrutiny of allergy-related patient characteristics was missing from many studies. In addition to the conventional skin-prick test or radioallergosorbent test, in vitro T-cell response patterns are associated with atopy, further identifying its underlying immunophenotypes (53). This new immunoepidemiological approach may provide a more objective measurement of clinical atopic outcomes, and help delineate the precise role of psychosocial factors.
Many of the studies identified in the literature did not provide sufficient data for calculating hazard ratios or relative risk ratios, which are readily interpretable clinically as well as being conventional in epidemiological prospective cohort studies. This is why we used r as effect size in this study, even though this indicator is difficult to interpret clinically, especially when the r is very small. However, our provisional meta-analysis of the studies with sufficient data revealed that psychosocial factors were associated with a 41% increase in atopic disease incidence (number of studies = 12; combined hazard ratio = 1.41; 95% CI, 1.21–1.64; p < .001; no significant publication bias). It is desirable to publish hazard ratios or relative risk ratios so that sample size estimations can be made for future studies.
Additional prospective research is needed to extend findings to other atopic diseases (particularly, atopic dermatitis and allergic rhinitis) apart from asthma, to control for all putative behavioral and socioeconomic covariates such as smoking, drinking, sleep disturbance, body mass index, physical activity, medical adherence, history of atopic disorders and psychological distress, income, and social functioning, to objectively evaluate clinical outcomes of atopic disorders, and to present appropriate outcome indicators such as hazard ratio.
|
CONCLUSION
|
|---|
The current meta-analysis revealed a bidirectional relationship between psychosocial factors and atopic disorders. This suggests that successful management of atopic disorders might involve a multipronged approach, including psychological interventions as well as conventional physical and pharmacological therapies.
We are grateful to colleagues in many research centers for providing the additional data required for meta-analysis.
|
Contributors
|
|---|
Y. C. was responsible for concept and design, retrieved and screened papers against inclusion criteria, abstracted data from papers, appraised quality of papers, and performed analyses and interpretation. M. H. verified study inclusion and data extractions, appraised quality of papers, and commented on the analysis and interpretation. A. S. provided general advice and contributed to writing up.
|
APPENDIX
|
|---|
|
NOTES
|
|---|
Received for publication April 4, 2007; revision received July 24, 2007.
This research was funded by the British Heart Foundation and Sumitomo Life Social Welfare Services Foundation.
DOI:10.1097/PSY.0b013e31815c1b71
|
REFERENCES
|
|---|
- Wright RJ, Cohen RT, Cohen S. The impact of stress on the development and expression of atopy. Curr Opin Allergy Clin Immunol 2005;5:23–9.[Medline]
- Asher M, Montefort S, Björkstén B, Lai CKW, Strachan DP, Weiland SK, Williams H; ISAAC Phase Three Study Group. Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases one and three repeat multicountry cross-sectional surveys. Lancet 2006;368:733–43.[CrossRef][Medline]
- Nelson HS. Advances in upper airway diseases and allergen immunotherapy. J Allergy Clin Immunol 2005;115:676–84.[CrossRef][Medline]
- Turner RJ, Wheaton B, Lloyd DA. The epidemiology of social stress. Am Social Rev 1995;60:104–25.[CrossRef]
- Evans GW. The built environment and mental health. J Urban Health 2003;80:536–55.[Medline]
- Alexander F. Psychosomatic medicine. New York: Norton; 1950.
- Marshall GD, Roy SR. Stress and allergic diseases. In: Ader R, editor. Psychoneuroimmunology. Amsterdam: Academic Press; 2007:799–824.
- McEwen BS. Protective and damaging effects of stress mediators. N Engl J Med 1998;338:171–9.[Free Full Text]
- Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD, Rennie D, Moher D, Becker BJ, Sipe TA, Thacker SB. Meta-analysis of observational studies in epidemiology: a proposal for reporting. JAMA 2000;283:2008–12.[Abstract/Free Full Text]
- Moher D, Cook DJ, Eastwood S, Olkin I, Rennie D, Stroup DF, for the QUOROM group. Improving the quality of reports of meta-analyses of randomized controlled trials: the QUOROM statement. Lancet 1999;354:1896–900.[CrossRef][Medline]
- Garssen B. Psychological factors and cancer development: evidence after 30 years of research. Clin Psychol Rev 2004;24:315–38.[CrossRef][Medline]
- Coe CL, Lubach GR. Mother-infant interactions and the development of immunity from conception through weaning. In: Ader R, editor. Psychoneuroimmunology. Amsterdam: Academic Press; 2007:455–74.
- Lyubomirsky S, King L, Diener E. The benefits of frequent positive affect: does happiness lead to success? Psychol Bull 2005;131:803–55.[CrossRef][Medline]
- Rosenthal R. Meta-analytic procedure for social research. 2nd ed. Newbury Park, CA: Sage; 1991.
- Rosenthal R, Rubin DB. requivalent: a simple effect size indicator. Psychol Methods 2003;8:492–6.[CrossRef][Medline]
- DerSimonian R, Laird N. Metaanalysis in clinical-trials. Control Clin Trials 1986;7:177–88.[CrossRef][Medline]
- Begg CB, Berlin JA. Publication bias and dissemination of clinical research. J Natl Cancer Inst 1989;151:419–63.
- Masui K. Meta-analysis software user’s guide. In: Masui K, editor. Kokokara-hajimeru meta-analysis. Tokyo: Shinko-Koueki Medical Press; 2003:91–121.
- Wainwright NWJ, Surtees PG, Wareham NJ, Harrison BDW. Psychosocial factors and incident asthma hospital admissions in the EPIC-Norfolk cohort study. Allergy 2007;62:554–60.[CrossRef][Medline]
- Alati R, O’Callaghan M, Najman JM, Williams GM, Bor W, Lawlor DA. Asthma and internalizing behavior problems in adolescence: a longitudinal study. Psychosom Med 2005;67:462–70.[Abstract/Free Full Text]
- Calam R, Gregg L, Simpson A, Simpson B, Woodcock A, Custovic A. Behavior problems antecede the development of wheezing in childhood. Am J Respir Crit Care Med 2005;171:323–7.[Abstract/Free Full Text]
- Stevenson J, ETAC Study Group. Relationship between behavior and asthma in children with atopic dermatitis. Psychosom Med 2003;65:971–5.[Abstract/Free Full Text]
- Wright RJ, Cohen S, Carey V, Weiss SR, Gold DR. Parental stress as a predictor of wheezing in infancy. Am J Respir Crit Care Med 2002;165:358–65.[Abstract/Free Full Text]
- Huovinen E, Kaprio J, Koskenvuo M. Asthma in relation to personality traits, life satisfaction, and stress: a prospective study among 11000 adults. Allergy 2001;56:971–7.[CrossRef][Medline]
- Klinnert MD, Nelson HS, Price MR, Adinoff AD, Leung DYM, Mrazek DA. Onset and persistence of childhood asthma: predictors from infancy. Pediatrics 2001;108:e69.[Abstract/Free Full Text]
- Mrazek DA, Klinnert M, Mrazek PJ, Brower A, McCormick D, Rubin B, Ikle D, Kastner W, Larsen G, Harbeck R, Jones J. Prediction of early-onset asthma in genetically at-risk children. Pediatr Pulmonol 1999;27:85–94.[CrossRef][Medline]
- Jonas B, Wagener D, Lando J, Feldman J. Symptoms of anxiety and depression as risk factors for development of asthma. J Appl Biobehav Res 1999;4:91–119.[CrossRef]
- Gustafsson PA, Björkstén B, Kjellman NI. Family dysfunction in asthma: a prospective study of illness development. Behav Pediatr 1994;125:493–8.
- Wright RJ, Mitchell H, Visness CM, Cohen S, Stout J, Evans R, Gold DR. Community violence and asthma morbidity: the inner-city asthma study. Am J Public Health 2004;94:625–32.[Abstract/Free Full Text]
- Schmaling KB, McKnight PE, Afari N. A prospective study of the relationship of mood and stress to pulmonary function among patients with asthma. J Asthma 2002;39:501–10.[CrossRef][Medline]
- Bartlett S, Kolodner K, Butz AM, Eggleston P, Malveaux FJ, Rand CR. Maternal depressive symptoms and emergency department use among inner-city children with asthma. Arch Pediatr Adolesc Med 2001;155:347–53.[Abstract/Free Full Text]
- Sandberg S, McCann DC, Ahola S, Oja H, Paton JY, McGuinness D. The role of acute and chronic stress in asthma attacks in children. Lancet 2000;356:982–7.[CrossRef][Medline]
- Weil CM, Wade SL, Bauman LJ, Lynn H, Mitchell H, Lavigne J. The relationship between psychosocial factors and asthma morbidity in inner-city children with asthma. Pediatrics 1999;104:1274–80.[Abstract/Free Full Text]
- Feldman JM, Ortega AN, McQuaid EL, Canino G. Comorbidity between asthma attacks and internalizing disorders among Puerto Rican children at one-year follow-up. Psychosomatics 2006;47:333–9.[Abstract/Free Full Text]
- Hasler G, Gergen PJ, Ajdacic V, Gamma A, Eich D, Rössler W, Angst J. Asthma and body weight change: a 20-year prospective community study of young adults. Int J Obesity 2006;30:1111–8.[CrossRef][Medline]
- Hasler G, Gergen PJ, Kleinbaum DG, Ajdacic V, Gamma A, Eich D, Rössler W, Angst J. Asthma and panic in young adults. Am J Respir Crit Care Med 2005;171:1224–30.[Abstract/Free Full Text]
- Romans S, Belaise C, Martin J, Morris E, Raffi A. Childhood abuse and later medical disorders in women. Psychother Psychosom 2002;71:141–50.[CrossRef][Medline]
- Goodwin RD, Eaton WW. Asthma and the risk of panic attacks among adults in the community. Psychol Med 2003;33:879–85.[CrossRef][Medline]
- Craske MG, Poulton R, Tsao JCI, Plotkin D. Paths to panic disorder/agoraphobia: an exploratory analysis from age 3 to 21 in an unselected birth cohort. J Am Acad Child Adolesc Psychiatry 2001;40:556–63.[CrossRef][Medline]
- Hart EL, Lahey BB, Hynd GW, Loeber RL, McBurnett K. Association of chronic overanxious disorder with atopic rhinitis in boys: a four-year longitudinal study. J Clin Child Psychol 1995;24:332–7.[CrossRef]
- Chrousos GP. Stress, chronic inflammation, and emotional and physical well-being: concurrent effects and chronic sequelae. J Allergy Clin Immunol 2000;106:S275–91.[CrossRef][Medline]
- Wright RJ. Stress and atopic disorders. J Allergy Clin Immunol 2005;116:1301–6.[CrossRef][Medline]
- Chida Y, Sudo N, Sonoda J, Hiramoto T, Kubo C. Childhood psychological stress exacerbates adult mouse asthma by hypothalamus-pituitary-adrenal axis. Am J Respir Crit Care Med 2007;175:316–22.[Abstract/Free Full Text]
- Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends Immunol 2006;27:24–31.[CrossRef][Medline]
- Roy-Byrne PP, Craske MG, Stein MB. Panic disorder. Lancet 2006;368:1023–32.[CrossRef][Medline]
- Ebmeier KP, Donaghey C, Steele JD. Recent development and current controversies in depression. Lancet 2006;367:153–67.[CrossRef][Medline]
- Wamboldt MZ, Hewitt FK, Schmitz S, Wamboldt FS, Rasanen M, Koskenvuo M, Romanov K, Varjonen J, Kaprio J. Familial association between allergic disorders and depression in adult Finnish twins. Am J Med Genet 2000;96:146–53.[CrossRef][Medline]
- Kodama A, Horikawa T, Suzuki T, Ajiki W, Takashima T, Harada S, Ichihashi M. Effect of stress on atopic dermatitis: investigation in patients after the Great Hanshin Earthquake. J Allergy Clin Immunol 1999;104:173–6.[CrossRef][Medline]
- Friedman AH, Morris TL. Allergies and anxiety in children and adolescents: a review of the literature. J Clin Psychol Med Settings 2006;13:323–35.
- Chida Y, Steptoe A, Hirakawa N, Sudo N, Kubo C. The effect of psychological intervention on atopic dermatitis. Int Arch Allergy Immunol 2007;144:1–9.[CrossRef][Medline]
- Toren K, Brisman J, Jarvholm B. Asthma and asthma-like symptoms in adults assessed by questionnaires. A literature review. Chest 1993;104:600–8.[CrossRef][Medline]
- Jenkins MA, Clarke JR, Carlin JB, Robertson CF, Hopper JL, Dalton MF, Holst DP, Choi K, Giles GG. Validation of questionnaire and bronchial hyper responsiveness against respiratory physician assessment in the diagnosis of asthma. Int J Epidemiol 1996;25:609–16.[Abstract/Free Full Text]
- Heaton T, Rowe J, Turner S, Aalberse RC, de Klerk N, Suriyaarachchi D, Serralha M, Holt BJ, Hollams E, Yerkovich S, Holt K, Sly PD, Goldblatt J, Le Souef P, Holt PG. An immunoepidemiological approach to asthma: identification of in vitro T-cell response patterns associated with different wheezing phenotypes in children. Lancet 2005;365:142–9.[CrossRef][Medline]
This article has been cited by other articles:
|
|
|
|
 
P. Magin, D. Sibbritt, and K. Bailey
The Relationship Between Psychiatric Illnesses and Skin Disease: A Longitudinal Analysis of Young Australian Women
Arch Dermatol,
August 1, 2009;
145(8):
896 - 902.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. F. Suglia, M. B. Enlow, A. Kullowatz, and R. J. Wright
Maternal Intimate Partner Violence and Increased Asthma Incidence in Children: Buffering Effects of Supportive Caregiving
Arch Pediatr Adolesc Med,
March 1, 2009;
163(3):
244 - 250.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. M. Scott, M. Von Korff, J. Alonso, M. C. Angermeyer, C. Benjet, R. Bruffaerts, G. de Girolamo, J. M. Haro, R. C. Kessler, V. Kovess, et al.
Childhood Adversity, Early-Onset Depressive/Anxiety Disorders, and Adult-Onset Asthma
Psychosom Med,
November 1, 2008;
70(9):
1035 - 1043.
[Abstract]
[Full Text]
[PDF]
|
|
|
TOP
ABSTRACT
INTRODUCTION
