Prevention of Asthma
Prevention of Asthma
The social environment, in which a child is exposed to, may also contribute to the development and severity of asthma. Lower SES has been shown to associate with higher asthma prevalence rates and hospitalizations. Still to be answered is whether early life lower SES increases vulnerability for asthma later in life. Most studies on the topic are cross-sectional, and find associations between current SES and numerous child health outcomes. Higher levels of parental stress, related to the lower SES, may also relate to increases in the risk of infant wheezing. Prenatal maternal stress has also been found to associate with elevated cord blood IgE as well as childhood wheeze, asthma, eczema and allergic rhinitis. Additionally, maternal distress that persisted from birth to early school age was associated with an increased risk for asthma in the child. These relationships are not explained by an increased level of stress in the child leading Wright et al., to propose an impact of the hypothalamic-pituitary-adrenal axis on fetal immune developmental processes. Consistent with this, we have shown a lower cortisol response to a stressor among school aged children with asthma who had been exposed to persistent maternal stress in early life.
The connection of asthma with psychosocial aspects seems logical because data showing a connection between stress and immune-related Th cells. One murine model looked at the impact of perceived stress and learned helplessness on airway inflammation. Mice that experienced uncontrollable stress also experienced more narrowing of airways and goblet cell hyperplasia, features of asthma pathogenesis, than those mice in the control group. After an ovalbumin (OVA) challenge, Deshmukh et al., reported a lymphocyte population highly saturated with CD4+ T cells, indicative of increases in IL-4, IL-13 and lack of IFN-γ production. Mice that experienced control over the stressful situation were able to dampen inflammatory disease by limiting CD4+ T cells and production of cytokines related to Th2 cells. Helpless mice, however, were unable to do this and, in fact, had increased levels of B cells and eosinophils.
Research supporting this model has found an association between lower levels of family support and higher levels of nighttime asthma symptoms, lower pulmonary functioning in the morning and higher eosinophil and IL-4. Likewise, in a sample of 15,357 adults, increasing numbers of adverse childhood experiences related to a 70% increase in risk for hospitalization with Th1, 80% increase in risk for hospitalization with Th2 and 100% increased risk for rheumatic disease.
Psychosocial Factors
The social environment, in which a child is exposed to, may also contribute to the development and severity of asthma. Lower SES has been shown to associate with higher asthma prevalence rates and hospitalizations. Still to be answered is whether early life lower SES increases vulnerability for asthma later in life. Most studies on the topic are cross-sectional, and find associations between current SES and numerous child health outcomes. Higher levels of parental stress, related to the lower SES, may also relate to increases in the risk of infant wheezing. Prenatal maternal stress has also been found to associate with elevated cord blood IgE as well as childhood wheeze, asthma, eczema and allergic rhinitis. Additionally, maternal distress that persisted from birth to early school age was associated with an increased risk for asthma in the child. These relationships are not explained by an increased level of stress in the child leading Wright et al., to propose an impact of the hypothalamic-pituitary-adrenal axis on fetal immune developmental processes. Consistent with this, we have shown a lower cortisol response to a stressor among school aged children with asthma who had been exposed to persistent maternal stress in early life.
The connection of asthma with psychosocial aspects seems logical because data showing a connection between stress and immune-related Th cells. One murine model looked at the impact of perceived stress and learned helplessness on airway inflammation. Mice that experienced uncontrollable stress also experienced more narrowing of airways and goblet cell hyperplasia, features of asthma pathogenesis, than those mice in the control group. After an ovalbumin (OVA) challenge, Deshmukh et al., reported a lymphocyte population highly saturated with CD4+ T cells, indicative of increases in IL-4, IL-13 and lack of IFN-γ production. Mice that experienced control over the stressful situation were able to dampen inflammatory disease by limiting CD4+ T cells and production of cytokines related to Th2 cells. Helpless mice, however, were unable to do this and, in fact, had increased levels of B cells and eosinophils.
Research supporting this model has found an association between lower levels of family support and higher levels of nighttime asthma symptoms, lower pulmonary functioning in the morning and higher eosinophil and IL-4. Likewise, in a sample of 15,357 adults, increasing numbers of adverse childhood experiences related to a 70% increase in risk for hospitalization with Th1, 80% increase in risk for hospitalization with Th2 and 100% increased risk for rheumatic disease.
Source...