The concept of lactose intolerance is based on evidence that intestinal lactase activity persist into later childhood and throughout life in only a minority of the world’s population. Lactose is the major carbohydrate found in mammalian milk, and lactose powder is widely used as an ingredient by the food industry. Lactose is hydrolyzed by lactase, an endo-enzyme present in the brush border membrane of the small intestine, which is encoded by LCT gene that maps on chromosome 2 (2q21). In most humans, lactase activity reaches a maximum in late pregnancy but declines after 2–3 years of age and reaches a stable low level at age 5–10 years (lactase non-persistence). Only about 35% of the human population can digest lactose beyond the age of about seven or eight, notably northern European-derived populations (lactase persistence). About two thirds of the world’s population undergoes a genetically programmed decrease in lactase synthesis after weaning. In Europe, the persistence or not persistence of the expression of lactase is predominantly associated with so-called point polymorphism C/T 13910. For many years, it was thought that lactase persistence (LP) in humans was the “wild-type” pattern but is now considered to be rather novel for humans and probably adaptative for particular circumstances, whereas the lactase non-persistence ((LNP) is the ancestral type. Lactase persistence is a recent human adaptation and its geographic distribution correlates with the importance of dairying in different human populations. The kinetics of the reduction and the amount of residual lactase has considerable variability between different ethnic groups and even between individuals.Both, lactase persistence and non-persistence (leading to lactose malabsorbtion) are thus normal phenotypes. However, the reduction up to 50% of lactose is sufficient to ensure effective digestion of lactose. When the low lactase activity does not cause symptoms, it is called “lactose malabsorbtion”. Lactose intolerance occurs when the malabsorption causes symptoms.Lactose is a key nutrient which provides about half of an infant’s energy needs, but is also a bifidogenic factor and may be involved in promoting innate immunity. The role of lactose in life-long human health may change with age, with key periods being infancy, growth and development, the reproductive years and later life. Nowadays milk and dairy products are often assumed to be the cause of gastrointestinal symptoms and inappropriate avoidance can lead to nutritional inadequacy, particularly for calcium intake and vitamin D status.If the lactase enzyme activity is inadequate, the unabsorbed lactose is fermented by gut microflora with a production of short fatty acids (SCFA) and gases, thus increasing colonic distention and accelerating the oro-cecal transit time. The variable ability of the colonic microflora to ferment lactose in subjects with intolerance may explain why different subjects have different levels of tolerance. Fermentation of milk improves tolerance to lactose because of the pre...
Dietary side effects represent an increasingly prevalent public health issue worldwide. The proper illustration of the differences between food allergies, which involve immunological mechanisms, either IgE or non-IgE mediated, and food intolerances, which appear without immune involvement, is critical for establishing subsequent diagnostic and therapeutic options. Current medical research aims to study the pathogenesis of food allergies in order to develop new therapeutic tools.The existence of an abundance of modulating environmental factors, which act upon a genetic substrate entail a wide phenotypic variability of allergic reactions that leads to complex clinical manifestations. A comprehensive and correct diagnosis followed by prompt, adequate preventive measures, an adequate therapeutic approach, allow the maintaining of a proper nutritional status and psycho-behavioural development, the goal being to establish good quality of life for these patients.Food allergies are a major public health problem. Statistic data concerning the incidence and prevalence of food allergies in children vary. They depend on multiple parameters, such as age, sex, diet, existing comorbidities, genetic factor, socioeconomic factors, geographical area etc. In the general population, food allergies have a medically documented incidence of 10.8%, affecting around 8% of children and 3.7% of adults [1]. Approximately 6%–8% of children under the age of 2 will develop this disorder [2], which in 80% of cases will recede until school age [3]. The vast majority of proteic food allergies (60%) are IgE mediated. In most cases, these appear with exposure to a single type of food and in 35% of cases multiple food allergies are noted [1]. The most frequent type of food allergy in the first years of life is milk protein allergy, which affects 21.1% of children with documented food allergies [1].The trigger of the allergic reaction involves the interaction between food allergen, gastrointestinal barrier and immune system. Gastrointestinal tract is a complex ecosystem, its functions and components ensuring the absorption of nutrients from the ingested food. Furthermore, it is involved in the intestinal immune activity by averting pathogenic agents from entering the body. The intestinal immune components consist of gut-associated lymphoid tissue (GALT), mucosa associated lymphoid tissue (MALT), secretory IgA, effector immune cells (helper and suppressor T cells, macrophages, plasmocytes). Payer’s patches, the enterocytes and the intercellular junctions have the role of macromolecular passageway [6]. The non-immunologic barrier consists of: gastric pH, intestinal mucus, commensal microflora, lactoferrin etc. These components are underdeveloped in infants and toddlers. Therefore, enzymatic activity is reduced and the IgA secretion rate reaches normal values around the age of 4 years, features that determine a high prevalence of food allergies in these age groups [4]. The most significant risk factors involved in developing food allergies are immaturity...
Conclusions Studies showed that in children with chronic gastritis, Epstein-Barr virus markers are detected in the blood with high frequency. There is a relationship between the presence of the Epstein-Barr virus in the gastric mucosa and histological signs of gastritis.
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