NUTRIENT INTAKE, EPIGENETICS AND ASTHMA

Asthma is described as a complex chronic inflammatory airway disorder of variable severity and intensity, inflicting over 300 million people worldwide of all ages, residing in both developed and undeveloped countries. It has been estimated that an additional 100 million people will suffer from asthma by the year 2025. There are wide geographical variations in asthma prevalence and severity, with prevalence dominating in high-income countries and asthma-related mortality in low- to middle-income countries. Secular trends show that asthma incidence and prevalence are higher in children, up to 20% in English-fluent countries versus (vs.) 4% in adults. Despite advances in pharmacotherapy, asthma control is suboptimal in children and associated with a higher rate of exacerbations, hospital admissions, pediatric emergency visits, school absenteeism, poor academic performance, and an impaired quality of life. Asthma causes considerable morbidity along with an economic burden for the individual, family, and healthcare system due to increased medical costs, work absenteeism, and loss of productivity days. Therefore, it is of utmost global public health importance that the etiology of asthma induction and progression is fully understood. Unequivocally, asthma is caused by the complex interaction of genetic and environmental exposures, including atmospheric pollution, cigarette smoke, upper respiratory infections, pet hair, cold weather, high humidity, dampness, obesity, and diet, which trigger immunological and inflammatory mechanisms, subsequently leading to symptoms of wheeze, cough, shortness of breath, and chest tightness. Multiple immune cells are involved in the inception of asthma including T cells, macrophages, dendritic cells, eosinophils, neutrophils, mast cells, and basophils.

More specifically, macrophage (M1) polarization stimulates the expression of CD80, CD86, TLR4 (Toll-receptor 4), and inducible nitric oxide synthase (iNOS), further producing T-helper 1 (Th1)-associated cytokines (TNFa, IL-1b, IL-2, IL-6, and IL-12), Th17 associated cytokines (IL-23 and IL-27), monocyte chemotactic protein- (MCP-) 1, reactive oxygen species (ROS), and chemokines (CXCL9, CXCL10, CXCL11, CXCL16, CCL2, CCL5, and CCL8). Combined with the imbproduction of IgE, mucus secretion, hyperplasia of goblet cells, and airway hyperresponsive. Altogether, this contributes to asthma progression and the manifestation of symptoms. The growing awareness that genetics can only partially explain the rapid rise in allergic disease and the fact that asthma has a strong environmental component, as illustrated by country variations in asthma prevalence as well as the critical role of early-life exposures as determinants of asthma in later life, has stemmed great interest in epigenetic processes and respiratory disorders, including asthma. Epigenetics, a budding science, is defined as the study of heritable changes of a phenotype (involving gene expression and chromatin organization) without causing structural alterations to the underlying DNA sequence (genetic code). Investigating epigenetic alterations by using -omics analysis may uncover asthma etiology, noninvasive biomarkers, and molecular pathways involved in disease pathogenesis.

The purpose of this narrative review is to provide an overview of the latest scientific evidence on the role of epigenetics in asthma inception, dietary influences on gene expression/DNA methylation in relation to asthma etiology, and uncover potential epigenetic traits and possible molecular targets for the development of future primary preventive strategies and personalized treatment of this disease. Understanding how these mechanisms impact asthma will allow for better asthma care in patients, reduce the burden of asthma, improve the quality of life, and decrease individual and societal costs.

Read more below
1. Papamichael 2024 TOLLEFSBOL_Epigenetics ebook Ch 18 MP