Nestle Nutrition workshop series. Paediatric programme最新文献

Around 2.5% of neonates experience hypersensitivity reactions to cow's milk protein during the first year of life, which is highly associated with early exposure to cow's milk. To prevent early allergy development, cow's milk proteins in infant formulas were modified by hydrolyzation processes for use in children at high atopic risk who need milk supplementation in the first months of life. Dependent on the degree of modification, hydrolyzed cow's milk formulas are differentiated into extensively and partially hydrolyzed whey or casein hydrolysates (pHF, eHF). However, their allergy-preventive potential seems not only to dependent on the degree but also on the process of hydrolysis. pHF and eHF can be used for primary prevention of allergy in infants at high atopic risk, while only eHFs are indicated for secondary prevention in patients with manifest cow's milk allergy. In clinical trials a consistent trend to a reduction in atopy, mainly atopic eczema and food allergy, by certain pHFs and eHFs could be demonstrated in children with a familial risk of atopy until the age of 6 years. Because more than 50% of allergic children do not have a family history of atopy, it would be worthwhile to consider primary allergy prevention with hydrolysates for all children who need supplementation to breastfeeding.

The human gastrointestinal tract is colonized by 100 trillion microorganisms, including both beneficial and potentially pathogenic species. A zwitterionic polysaccharide (PSA) from the gastrointestinal microorganism Bacteroides fragilis has been shown to be the archetypal molecule of commensal bacteria that mediates development of the host immune system. PSA stimulates the normal balance of Th1 and Th2 CD4+ T cells and can correct histologic defects in the spleen and thymus of germ-free mice. PSA stimulates the innate immune system as a ligand for Toll-like receptor 2 and thereby promotes interactions with the adaptive immune system that are required for T-cell activation. PSA protects animals from colitis induced by Helicobacter hepaticus, a commensal with pathogenic potential. In animals harboring a B. fragilis mutant that does not express PSA, H. hepaticus colonization leads to disease and proinflammatory cytokine production in colonic tissues. Purified PSA administered to animals suppresses the production of the proinflammatory cytokine interleukin-17 by intestinal immune cells. PSA protects animals from inflammatory disease through a functional requirement for interleukin-10-producing CD4+ T cells. Thus polysaccharides of the bacterial microbiota can mediate the critical balance between health and disease in the host. As evidence accumulates, this concept is being accepted as an important feature of the immune repertoire.

The focus here is on research involving long-term calorie restriction (CR) to prevent or delay the incidence of the metabolic syndrome with age. The current societal environment is marked by overabundant accessibility of food coupled with a strong trend to reduced physical activity, both leading to the development of a constellation of disorders including central obesity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome). Prolonged CR has been shown to extend median and maximal lifespan in a variety of lower species (yeast, worms, fish, rats, and mice). Mechanisms of this lifespan extension by CR are not fully elucidated, but possibly involve alterations in energy metabolism, oxidative damage, insulin sensitivity, and functional changes in neuroendocrine systems. Ongoing studies of CR in humans now makes it possible to identify changes in 'biomarkers of aging' to unravel some of the mechanisms of its anti-aging phenomenon. Analyses from controlled human trials involving long-term CR will allow investigators to link observed alterations from body composition down to changes in molecular pathways and gene expression, with their possible effects on the metabolic syndrome and aging.

The epidemiological characteristics of chronic non-communicable diseases (NCD) are fast changing. The prevalence has risen to unprecedented levels, and the young and the underprivileged are increasingly affected. The classic view of the etiology of NCD consists of a genetic susceptibility which is precipitated by aging and modern lifestyle. In a virtual absence of any methods to tackle genetic susceptibility, the preventive approach has so far been focused on the control of lifestyle factors in those at high risk (old, and those with positive family history and elevated risk factors). Such an approach might help high risk individuals, but is unlikely to curtail the burgeoning epidemic of obesity and diabetes. Recent research has suggested that susceptibility to NCD originates in early life through non-genetic mechanisms (fetal programming). Tackling these may offer an exciting opportunity to control the NCD epidemic by influencing the susceptibility in a more durable manner than only controlling the lifestyle factors in adult life. The imperative is to address the life cycle rather than concentrate on the end stages.

Over the last 30 years, the nutritional status of Chinese children has greatly improved due to economic development and improved incomes. In this review, the status of childhood malnutrition and obesity in China is evaluated based on the National Nutrition and Health Survey of 2002 (NNHS2002) and the survey on National Student Health and Physical Fitness in China of 2005. Compared with the NNHS1992 survey, the body weights and heights of preschool children in urban and rural areas have significantly improved, and the prevalence of malnutrition (underweight and stunting) has been significantly reduced. However, micronutrient deficiencies, including calcium, zinc, vitamin A, vitamins B1 and B2, are still common in preschool and school children. These data show that the growth and development of Chinese children are under our expectations. On the other hand, the national averaged prevalences of overweight and obesity in the children under 6 years of age are 3.4 or 2.0% as estimated by the Chinese or WHO standards, respectively. We are now facing double challenges: to prevent malnutrition and the increase in overweight and obesity in children.

Two adaptive homeostatic mechanisms normally preserve mucosal integrity: (i) immune exclusion mediated by secretory antibodies to inhibit penetration of potentially dangerous microorganisms and proteins, and (ii) immunosuppression to counteract hypersensitivity against innocuous antigens. The latter mechanism is called 'oral tolerance' when induced via the gut. Similar mechanisms are suppressive against commensal bacteria. Such two-layered anti-inflammatory defense explains why persistent allergy to dietary proteins is not more common, with the exception of gluten intolerance (celiac disease) where abrogation of mucosal homeostasis is overt. Thus, mucosally induced tolerance is generally a robust adaptive mechanism in view of the fact that a ton of food may pass annually through the gut of an adult - regularly giving rise to uptake of intact dietary antigens in the nanogram range after a meal. However, the immunoregulatory network and the epithelial barrier are poorly developed in the neonatal period, which therefore is critical with regard to priming for allergy. Notably, the postnatal development of mucosal immune homeostasis depends on appropriate microbial colonization. In this process, antigen-presenting cells are 'decision makers', linking innate and adaptive immunity. Their microbe-sensing function is influenced by both microbial products and dietary constituents, including vitamin A and lipids such as polyunsaturated n-3 fatty acids.

Here we explore whether there is any evidence that the rapid development of the obesity epidemic in emerging nations, and its unusual coexistence with malnutrition, may have evolutionary origins that make such populations especially vulnerable to the obesogenic conditions accompanying the nutrition transition. It is concluded that any selection of so-called 'thrifty genes' is likely to have affected most races due to the frequency and ubiquity of famines and seasonal food shortages in ancient populations. Although it remains a useful stimulus for research, the thrifty gene hypothesis remains a theoretical construct that so far lacks any concrete examples. There is currently little evidence that the ancestral genomes of native Asian or African populations carry particular risk alleles for obesity. Interestingly, however, there is evidence that a variant allele of the FTO gene that favors leanness may be less active in Asians or Africans. There is also some evidence that Caucasians may be less prone to developing type 2 diabetes mellitus than other races suggesting that there has been recent selection of protective alleles. In the near future, recently developed statistical methods for comparing genome-wide data across populations are likely to reveal or refute the presence of any thrifty genes and might indicate mechanisms of vulnerability.

The nutrition transition relates to broad patterns of diet, activity and body composition that have defined our nutritional status in various stages of history. The world is rapidly shifting from a dietary period in which the higher income countries were dominated by patterns of nutrition-related non-communicable diseases (NR-NCDs; while the lower and middle world were dominated by receding famine) to one in which the world is increasingly being dominated by NR-NCDs. Dietary changes appear to be shifting universally toward a diet dominated by higher intakes of caloric sweeteners, animal source foods, and edible oils. Activity patterns at work, leisure, travel, and in the home are equally shifting rapidly toward reduced energy expenditure. Large-scale declines in food prices (e.g., beef prices), increased access to supermarkets, and urbanization of urban and rural areas are key underlying factors.

Whether diet may influence autoimmunity has been the subject of many unsolved debates. Interestingly, growing evidence indicates a large overlap between the mechanisms controlling tolerance to dietary antigens and autoimmunity. To discuss these links, we will focus on two model human diseases. The first one is IPEX syndrome due to mutations in the X-linked foxp3 gene. Studies of this disease underscore the role of regulatory FOXP3+ T cells in controlling the reactivity against self antigens and the response to dietary proteins in humans. The second is celiac disease, a complex poly-genic disease where exposure to dietary wheat proteins can trigger an autoimmune-like attack of the intestine frequently associated with the onset of extra-digestive autoimmune disorders. In the later disease, recent work shed light on the mechanisms that drive the intestinal inflammatory response to gluten and suggests impairment of immunoregulatory mechanisms that control intestinal tolerance and autoimmunity. Yet the exact role of gluten in the pathogenesis of extra-intestinal autoimmunity has not been elucidated. Interestingly, recent work indicates that dietary factors, including vitamin A and breast milk feeding, can protect against the development of harmful responses to dietary proteins. It is unclear whether this protection can apply to the prevention of autoimmunity.

Probiotics were originally used to influence human health through intestinal microbiota alterations. At present, probiotics and their effects on human health have been demonstrated both within different food matrices and as single or mixed culture preparations. The health-promoting properties are known to be strain-dependent. Thus, strain identification and characterization are important: only well-characterized strains identified with modern techniques are acceptable, especially if health claims are desired. Linking the strain to a specific health effect as well as to enable accurate surveillance and epidemiological studies are important targets. Currently there are specific strains which have demonstrated beneficial in vitro properties and clinically proven health benefits. Such specific probiotics have been included in recommendations on pediatric nutrition. The model is the microbiota of the healthy breastfed infant. Molecular methods in microbiota assessment enable more specific probiotics and prebiotics to be identified for infants with aberrancies in intestinal microbiota. Probiotic products require information on the concentration and viability of the strain(s) in the product as well as data on required dosages. Continuous control of probiotic strains or strain combinations is a must as small changes in production process or growth media may significantly affect the properties of a strain or strain combination.