Background

Obesity and asthma have increased in westernised countries. Maternal obesity may increase childhood asthma risk. If this relation is causal, it may be mediated through factors associated with maternal adiposity, such as fetal development, pregnancy complications or infant adiposity. We investigated the relationships of maternal body mass index (BMI) and fat mass with childhood wheeze, and examined the influences of infant weight gain and childhood obesity.

Methods

Maternal prepregnancy BMI and estimated fat mass (from skinfold thicknesses) were related to asthma, wheeze and atopy in 940 children. Transient or persistent/late wheeze was classified using questionnaire data collected at ages 6, 12, 24 and 36 months and 6 years. At 6 years, skin-prick testing was conducted and exhaled nitric oxide and spirometry measured. Infant adiposity gain was calculated from skinfold thickness at birth and 6 months.

Results

Greater maternal BMI and fat mass were associated with increased childhood wheeze (relative risk (RR) 1.08 per 5 kg/m², p=0.006; RR 1.09 per 10 kg, p=0.003); these reflected associations with transient wheeze (RR 1.11, p=0.003; RR 1.13, p=0.002, respectively), but not with persistent wheeze or asthma. Infant adiposity gain was associated with persistent wheeze, but not significantly. Adjusting for infant adiposity gain or BMI at 3 or 6 years did not reduce the association between maternal adiposity and transient wheeze. Maternal adiposity was not associated with offspring atopy, exhaled nitric oxide, or spirometry.

Discussion

Greater maternal adiposity is associated with transient wheeze but not asthma or atopy, suggesting effects upon airway structure/function but not allergic predisposition.

ConclusionsBuccal mucosa sampling is a reliable method for detecting changes in gene expression in patients with asthma. This non‐invasive technique may serve as a valuable tool for diagnosing asthma and evaluating therapeutic response. (Source: Pediatric Allergy and Immunology)

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