Nestle Nutrition workshop series. Paediatric programme最新文献

As a proportion of all deaths in India, cardiovascular disease (CVD) will be the largest cause of disability and death, by the year 2020. At the present stage of India's health transition, an estimated 53% of deaths and 44% of disability-adjusted life-years lost are contributed to chronic diseases. India also has the largest number of people with diabetes in the world, with an estimated 19.3 million in 1995 and projected 57.2 million in 2025. The prevalence of hypertension has been reported to range from 20 to 40% in urban adults and 12-17% among rural adults. The number of people with hypertension is expected to increase from 118.2 million in 2000 to 213.5 million in 2025, with nearly equal numbers of men and women. Over the coming decade, until 2015, CVD and diabetes will contribute to a cumulative loss of USD237 billion for the Indian economy. Much of this enormous burden is already evident in urban as well as semi-urban and slum dwellings across India, where increasing lifespan and rapid acquisition of adverse lifestyles related to the demographic transition contribute to the rising prevalence of CVDs and its risk factors such as obesity, hypertension, and type 2 diabetes. The underlying determinants are sociobehavioral factors such as smoking, physical inactivity, improper diet and stress. The changes in diet and physical activity have resulted largely from the epidemiological transition that is underway in most low income countries including India. The main driving forces of these epidemiological shifts are the globalized world, rapid and uneven urbanization, demographic shifts and inter- and intra-country migrations--all of which result in alterations in dietary practices and decreased physical activity. While these changes are global, India has several unique features. The transitions in India are uneven with several states in India still battling the ill effects of undernutrition and infectious diseases, while in other states with better indices of development, chronic diseases including diabetes are emerging as a major area of concern. Regional and urban-rural differences in the occurrence of CVD are the hallmark. All these differences result in a differing prevalence of CVD and its risk factors. Therefore while studying nutrition and physical activity shifts in India, the marked heterogeneity and secular changes in dietary and physical activity practices should be taken into account. This principle should also apply to strategies, policies and nutrition and physical activity guidelines so that they take the regional differences into account.

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.