The Editors' Choice

Abstract

The racial divide: Asthma severity in blacks and whitesHigh body weight during infancy might protect against asthmaInconsistent findings have been observed regarding the risk of asthma in overweight children. One possible reason is that overweight status attained at different ages could have different effects on disease development, especially during early childhood, the crucial and dynamic time period for growth. As reported by Zhang et al (p 1157), early versus late onset of overweight status was associated with opposite effects on physician-diagnosed asthma at ages 6 and 8 years. The study used data from the Childhood Origin of Asthma cohort, which comprises 289 full-term newborns with at least 1 asthmatic/atopic parent. The results showed that being overweight at age 1 year was associated with a decreased risk of asthma and better lung function at ages 6 and 8 years. However, being overweight beyond infancy did not have any protective effect. In fact, children who were overweight at age 5 years only but not at age 1 year had an increased risk of asthma. These findings provide evidence of an age-dependent relationship between overweight status and asthma: early weight gain might promote lung development, whereas excessive weight gain after age 1 year might increase asthma risk.Food allergy herbal formula 2 inhibits mast cell and basophil number and IgE-mediated activationFAHF-2 reduced the number of peripheral basophils and peritoneal mast cells.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Why do mutations in forkhead box protein 3 cause immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome?Only F373A had a diminished capacity to suppress responder CD4+ T-cell proliferation.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Increased skin pH might promote colonization by Staphylococcus aureusWestern immunoblot showing expression levels of S aureus proteins.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Does acetaminophen use early in life cause childhood asthma?Epidemiologic evidence has been accumulating to suggest a link between the use of acetaminophen in pregnancy and infancy and childhood asthma. It is important to find out whether this link is causal because there is a high prevalence of both acetaminophen use and asthma in Western populations, and hence there might be important scope for asthma prevention. As reported in this issue, Shaheen et al (p 1141) have continued their study of acetaminophen use in early life and childhood asthma in a population-based birth cohort in the United Kingdom, the Avon Longitudinal Study of Parents and Children. They found evidence to suggest that certain antioxidant gene polymorphisms (nuclear erythroid 2 p45-related factor 2 and glutathione S-transferase M1 and T1) in the mother, which might be expected to influence acetaminophen toxicity, might modify the effect of prenatal exposure on asthma risk. In contrast, child gene variants did not modify the association between infant exposure and asthma, a relation that was restricted to children who wheezed in infancy. The interactions observed with maternal genes strengthen evidence suggesting that the effects of prenatal acetaminophen exposure on asthma risk might be causal. Ultimately, however, this can be confirmed only through randomized trials in pregnancy. The racial divide: Asthma severity in blacks and whites High body weight during infancy might protect against asthmaInconsistent findings have been observed regarding the risk of asthma in overweight children. One possible reason is that overweight status attained at different ages could have different effects on disease development, especially during early childhood, the crucial and dynamic time period for growth. As reported by Zhang et al (p 1157), early versus late onset of overweight status was associated with opposite effects on physician-diagnosed asthma at ages 6 and 8 years. The study used data from the Childhood Origin of Asthma cohort, which comprises 289 full-term newborns with at least 1 asthmatic/atopic parent. The results showed that being overweight at age 1 year was associated with a decreased risk of asthma and better lung function at ages 6 and 8 years. However, being overweight beyond infancy did not have any protective effect. In fact, children who were overweight at age 5 years only but not at age 1 year had an increased risk of asthma. These findings provide evidence of an age-dependent relationship between overweight status and asthma: early weight gain might promote lung development, whereas excessive weight gain after age 1 year might increase asthma risk. Inconsistent findings have been observed regarding the risk of asthma in overweight children. One possible reason is that overweight status attained at different ages could have different effects on disease development, especially during early childhood, the crucial and dynamic time period for growth. As reported by Zhang et al (p 1157), early versus late onset of overweight status was associated with opposite effects on physician-diagnosed asthma at ages 6 and 8 years. The study used data from the Childhood Origin of Asthma cohort, which comprises 289 full-term newborns with at least 1 asthmatic/atopic parent. The results showed that being overweight at age 1 year was associated with a decreased risk of asthma and better lung function at ages 6 and 8 years. However, being overweight beyond infancy did not have any protective effect. In fact, children who were overweight at age 5 years only but not at age 1 year had an increased risk of asthma. These findings provide evidence of an age-dependent relationship between overweight status and asthma: early weight gain might promote lung development, whereas excessive weight gain after age 1 year might increase asthma risk. Food allergy herbal formula 2 inhibits mast cell and basophil number and IgE-mediated activation Why do mutations in forkhead box protein 3 cause immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome? Increased skin pH might promote colonization by Staphylococcus aureus Does acetaminophen use early in life cause childhood asthma?Epidemiologic evidence has been accumulating to suggest a link between the use of acetaminophen in pregnancy and infancy and childhood asthma. It is important to find out whether this link is causal because there is a high prevalence of both acetaminophen use and asthma in Western populations, and hence there might be important scope for asthma prevention. As reported in this issue, Shaheen et al (p 1141) have continued their study of acetaminophen use in early life and childhood asthma in a population-based birth cohort in the United Kingdom, the Avon Longitudinal Study of Parents and Children. They found evidence to suggest that certain antioxidant gene polymorphisms (nuclear erythroid 2 p45-related factor 2 and glutathione S-transferase M1 and T1) in the mother, which might be expected to influence acetaminophen toxicity, might modify the effect of prenatal exposure on asthma risk. In contrast, child gene variants did not modify the association between infant exposure and asthma, a relation that was restricted to children who wheezed in infancy. The interactions observed with maternal genes strengthen evidence suggesting that the effects of prenatal acetaminophen exposure on asthma risk might be causal. Ultimately, however, this can be confirmed only through randomized trials in pregnancy. Epidemiologic evidence has been accumulating to suggest a link between the use of acetaminophen in pregnancy and infancy and childhood asthma. It is important to find out whether this link is causal because there is a high prevalence of both acetaminophen use and asthma in Western populations, and hence there might be important scope for asthma prevention. As reported in this issue, Shaheen et al (p 1141) have continued their study of acetaminophen use in early life and childhood asthma in a population-based birth cohort in the United Kingdom, the Avon Longitudinal Study of Parents and Children. They found evidence to suggest that certain antioxidant gene polymorphisms (nuclear erythroid 2 p45-related factor 2 and glutathione S-transferase M1 and T1) in the mother, which might be expected to influence acetaminophen toxicity, might modify the effect of prenatal exposure on asthma risk. In contrast, child gene variants did not modify the association between infant exposure and asthma, a relation that was restricted to children who wheezed in infancy. The interactions observed with maternal genes strengthen evidence suggesting that the effects of prenatal acetaminophen exposure on asthma risk might be causal. Ultimately, however, this can be confirmed only through randomized trials in pregnancy.