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En los últimos diez años, se ha incrementado notablemente el número de personas con alergias e intolerancias alimentarias. Esto se hace patente en nuestra vida diaria, pues ahora los menús de los restaurantes siempre indican con toda claridad los alérgenos de cada plato, cosa que hace unos años no se veía con tanta frecuencia. Pero, ¿cuál es el motivo? Aunque no existe ninguna hipótesis totalmente contrastada, sí sabemos que nuestra dieta cambia rápidamente, avanzando hacia el consumo de alimentos ultraprocesados, con multitud de conservantes, saborizantes, colorantes, etc.

Esto, junto con la sobreexposición a ciertos alimentos, como la leche o el trigo, son dos factores que determinan un índice creciente de alergias e intolerancias alimentarias. En este artículo vamos a ver en qué consisten, cuál es la genética que hay tras ellas, y cómo puede ayudarnos el viaje único que emprendemos con ADNTRO y nuestra prueba de ADN

Definition of food allergy and intolerance and the difference between them

The allergy is the immune response that occurs when the body comes into contact with a foreign agent or a certain food (which is called an allergen), which is safe for the normal population. This immune response consists of an inflammatory process triggered by the production of IgE-type antibodies, and causes symptoms of varying severity, ranging from minor irritation to respiratory problems and anaphylactic shock. 

The food intolerancesinstead, they are non-immune adverse reactions produced when the body is not able to process or digest a certain food compound, which can cause digestive problems of varying severity, the most frequent being abdominal pain, gas and diarrhea. Depending on what causes them, we distinguish intolerances of metabolic or enzymatic type, pharmacological and of undetermined cause. 

Therefore, the main difference between allergy and food intolerance is that the former activates an immune response, and the latter does not. 

In addition, in both cases the ingestion of the food in question (allergen) is responsible for the subsequent symptoms, but in the case of intolerances, many of those affected can tolerate small amounts of the food without causing great discomfort. The reactions that are triggered when an intolerant to a certain substance ingests it are dose-dependent, since the symptoms become more evident the higher the ingested dose is. 

food intolerances

Genetics of allergies and food intolerances 

Allergic processes present a family accumulation, which means that a significant number of allergic patients have a family history of allergy. This suggests, therefore, the existence of a genetic predisposition to allergy. However, it has been observed that the inheritance of allergy does not follow a clear Mendelian pattern, since its appearance is determined by several genes with additive effects (polygenic) that also interact with environmental factors. 

Regarding intolerances, each of them must be considered separately, since, although there is a genetic component in all of them, this will be different depending on the type of intolerance that we analyze (metabolic, pharmacological, etc.). 

What nutritional aspects can we discover from what we carry in our DNA? 

The journey we embark on with ADNTRO gives us information about our greater or lesser predisposition to develop allergies to peanuts (and very soon also to shellfish and egg) and lactose, fructose and gluten food intolerances. But how is this predisposition calculated?

nutritional aspects with additive

To explain, let's take the example of lactose intolerance. Lactose intolerance is the main example of metabolic intolerance and is caused by a deficiency of the enzyme lactase, responsible for breaking down lactose into galactose and glucose. 

The first step is to locate within a given gene the position of the genetic variants involved in the development of lactose intolerance. To do this, association studies (better known as GWAS, by its English acronym Genome-wide association study) included in the NHGRI catalog (National Human Genome Research Institute). 

The GWAS-type studies they are based on comparing the genotype of family nuclei that present a certain trait or pathology (in our example, lactose intolerance) with the genotype of the control population. In this way, it is possible to locate genetic variants whose frequency is higher in patients (with intolerance) than in controls. 

Once the prevalent genetic variants in people with intolerances have been located, the next step is to analyze a person's genotype. In doing so, we will look at the variant associated with lactose intolerance (identified thanks to the GWAS studies) and we will verify whether that person has the prevalent variant in the group of patients or the prevalent variant in the control population. That's how we can determine your greater or lesser genetic predisposition, respectively, to develop said food intolerance. 

A type of genetic variant widely used in GWAS-type studies are the SNPs (single nucleotide polymorphisms), which are single base genetic variants. Continuing with our example of lactose intolerance, at ADNTRO we analyzed two SNPs located in the gene MCM6, which is responsible for regulating the amount of lactase generated by the body. People whose genotype matches the SNPs associated with intolerance will have a greater predisposition to suffer it than those whose genotype does not match. 

Fructose intolerance or fructosemia, on the other hand, consists of a genetic disorder present from birth, caused by a deficiency of hepatic fructose-1-phosphate aldolase, also called the enzyme aldolase B. The gene that codes for this enzyme is called ALDOB, and the presence of variants in its sequence allows to identify people with fructose intolerance.

The case of gluten intolerance or celiac disease is more complex, since it is a permanent condition, whose development is influenced by genetic, environmental and immunological factors, and therefore it is not entirely correct to classify it as a food intolerance. 

Since our relationship with food is very important and special, and knowing that our genes control the way we digest, absorb and use nutrients, we invite you to come on board and start this journey with us. 

Bibliography

  • Dr Francisco Arasa and Dr. Santiago García Tornel. Most common food intolerances. Pediatrics Service. Sant Joan de Déu Hospital. 
  • Ballesta F. Genetics and allergy. Vol. 26 No. 3, pages 81-119 (May 1998)
  • Hong X. et al, Genome-wide association study identifies peanut allergy-specific loci and evidence of epigenetic mediation in US children. DOI: 10.1038 / ncomms7304
  • Dzialanski Z. et al, Lactase persistence versus lactose intolerance: Is there an intermediate phenotype? DOI: https://linkinghub.elsevier.com/retrieve/pii/S0009912015005081
  • Hereditary fructose intolerance. Medline Plus. 
  • Uitterlinden AG An Introduction to Genome-Wide Association Studies: GWAS for Dummies. Semin Reprod Med 2016; 34: 196–204
  • Ana Zugasti Murillo†. Alimentary intolerance. Unit of Clinical Nutrition and Dietetics. Virgen del Camino Hospital. Pamplona. Navarre. Spain
  • Ruiz Sánchez JG. [A global vision of adverse reactions to foods: food allergy and food intolerance].

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