Developmental origins of disease: Effects of parental diet on asthma

Asthma is a predisposition to chronic inflammation of the lungs, often presenting with reversible airway obstruction, but with irreversible reduction in lung function. Asthma has typically been described to have a heritable genetic component, in which various environmental exposures exacerbate asthma in early childhood or later in li fe. Interestingly, there is growing interest
that prenatal exposure influences the susceptibility of developing various diseases later in life. Rising rates of allergic disease in early infancy, together with pre-symptomatic differences in immune function at birth, suggests antenatal events play a predisposing role in the development of disease. The Barker hypothesis of foetal programming proposes that adverse modifications in nutritional or environmental conditions in utero results in altered developmental programming of organs, thus stimulates the tendency to develop disease later in life. Environmental factors, deficiencies in dietary supplements and psychological factors may all contribute to the predisposition to various diseases such as asthma, lower respiratory tract disease and type I diabetes. In utero foetal programming has a high association with the field of epigenetics, which refers to heritable changes in phenotype or gene expression without alteration of the underlying DNA sequence. Of the various epigenetic mechanisms, DNA methylation, predominantly in cytosine phosphate guanine (CpG) dinucleotides and post-translational modifications, particularly acetylation and deacetylation of core histones, are the most well-defined. Such epigenetic modifications alter chromatin structure and thus regulate gene transcription. Here we discuss epigenetic programming during development and how transgenerational
changes may influence the development of asthma.