Food allergies and intolerances are a major issue affecting children and adults. It is a fact that environmental and nutritional changes in recent decades have led to an increase in their global prevalence, but accurate epidemiological data are lacking. The symptoms of food allergies can be fatal, while those of food intolerances are clearly milder. Their diagnosis is based on a combination of methods to avoid a false positive or negative result, while there is currently no cure for these adverse reactions. They are managed through a diet that excludes the guilty allergens from the daily diet of individuals.
It is known that two of the strongest risk factors for the outbreak of food allergies and intolerances are genetic and environmental factors, but also the interaction between them. Genome-wide studies (GWAS) and mapping of genetic variants throughout the genome, usually single nucleotide polymorphisms (SNPs), have made it possible to identify and pave the way for understanding the involvement of these susceptible genes. The HLA, STAT6, SERPINB, SPINK5, FOXP3, IL-10 and FLG genes are the best studied genes associated with food allergies, which will be analyzed in the present dissertation, while the counterparts of food intolerances are LCT, HLA, DAO, ALDOB and CYP1A2.
Given that most diet-related diseases are polygenic, it is easily understood that there are many gaps in genetics that need to be filled. Future studies should consider the environment, genetics and epigenetics, as risk factors in order to clarify the multifaceted etiology and biological mechanisms of food allergies. The genetic information that will be made known in conjunction with the existing knowledge in the science of nutrition will significantly enhance the ability of health professionals to individually design the most appropriate and complete models of prevention and treatment that will greatly improve overall patients’ care.