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Over the past several decades, longitudinal studies, and especially more recent birth cohorts, have made landmark contributions toward clarifying the association between obesity and asthma. Several possible biological mechanisms have been suggested and the consistency of the association with the temporal and dose-response link have been replicated in a wide variety of settings, including different age groups, cultural, ethnic, socioeconomic and geographic backgrounds. Nowadays, it is largely recognised that obesity is implicated in asthma development,1 but the road to the identification of environmental and behavioural modifiable risk factors and quantification of health benefits related to obesity prevention is still steep and long.
As asthma is a complex and heterogeneous disease that usually begins in early childhood, and in line with ‘fetal origins’ hypothesis,2 the current research has moved the interest to exposures during prenatal and early postnatal period, and in particular to fetal and infant weight and growth. It was reasonable to assume that biologically plausible mechanisms proposed for childhood and adulthood obesity1 could be extended also to the effect of fetal and infant weight on lung development and its later function. These include inflammatory and immune responses, obesity-related reductions in pulmonary compliance and limitations in airflow, and, more recently, disrupted microbiota.1
Almost 30 years ago, Barker et al 3 reported low birth weight to be associated with reduced adult lung function, and since then this association has been replicated in children and in adults. Low birth weight, which is the most commonly used proxy of intrauterine growth restriction and a strong predictor of fast postnatal growth, is a well-established risk factor for childhood and adulthood respiratory morbidity. However, some disagreement still exists on how much of this association is explained by gestational age.4 5 Interestingly, current evidence supporting the associations of fetal growth …
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; externally peer reviewed.
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