Nestle Nutrition workshop series. Paediatric programme最新文献

The World Health Organization estimates that since 1980 the prevalence of obesity has increased more than threefold throughout much of the world, and this increase is not limited to developed nations. Indeed, the incidence of obesity is increasing most rapidly among rapidly industrializing countries raising the spectre of a burgeoning epidemic in obesity-associated diseases, including diabetes, dyslipidemia, nonalcoholic fatty liver disease and atherosclerosis. Reducing the rates of obesity and its attendant complications will require both coordinated public health policy and a better understanding of the pathophysiology of obesity. Obesity is associated with low grade chronic inflammation, a common feature of many complications of obesity that appears to emanate in part from adipose tissue. In obese individuals and rodents adipose tissue macrophage accumulation is a critical component in the development of obesity-induced inflammation. The macrophages in adipose tissue are bone marrow-derived and their number is strongly correlated with bodyweight, body mass index and total body fat. The recruited macrophages in adipose tissue express high levels of inflammatory factors that contribute to systemic inflammation and insulin resistance. Interventions aimed at either reducing macrophage numbers or decreasing their inflammatory characteristics improves insulin sensitivity and decreases inflammation. Macrophage accumulation and adipose tissue inflammation are dynamic processes under the control of multiple mechanisms. Investigating the role of macrophages in adipose tissue biology and the mechanisms involved in their recruitment and activation in obesity will provide useful insights for developing therapeutic approaches to treating obesity-induced complications.

Undernutrition continues to be high in many regions of the developing world. Birthweight, a common proxy measure of intrauterine growth, is influenced by nutritional, environmental and lifestyle factors during pregnancy and, in turn, affects immediate survival and function, and is a determinant of later life risk of chronic diseases. Maternal pre-pregnancy weight and height are independently associated with birthweight and also modify the effects of pregnancy weight gain and interventions during pregnancy on birthweight and perinatal mortality. Other prenatal factors commonly known to impact birthweight include maternal age, parity, sex, and birth interval, whereas lifestyle factors such as physical activity and maternal stress, as well as environmental toxicants have variable influences. Tobacco and other substance use and infections, specifically ascending reproductive tract infections, malaria, and HIV, can cause intrauterine growth restriction (IUGR). Few studies have examined the contribution of prenatal factors including low birthweight to childhood wasting and stunting. Studies that have examined this, with adequate adjustment for confounders, have generally found odds ratios associated with low birthweight ranging between 2 and 5. Even fewer studies have examined birth length or maternal nutritional status as risk factors. More research is needed to determine the proportion of childhood under-nutrition attributable to IUGR so that interventions can be targeted to the appropriate life stages.

Dietary elimination of causative food ingredients, usually food proteins, is the basis of treating food hypersensitivity. Proper diagnostic assessment is essential to avoid burdening children with unnecessary dietary restrictions with potential adverse effects. Diagnosis requires a detailed history, allergen elimination, and re-challenge with suspected foods. Complete elimination of causative food components depends on professional counseling and training of the patient and family, and transparent labeling of food products. Elimination diets carry the risk of inducing insufficient supplies of critical nutrients with adverse effects on health and wellbeing, particularly in children with exclusion of foods that provide a major part of dietary supply and patients with multiple food allergies. Infants and young children with cow's milk allergy, who have not been fully breastfed, require milk substitutes based on extensively hydrolyzed protein or amino acids. Elimination diets must be supervised and monitored to a similar degree as drug treatments, and the need for continued dietary elimination should be reviewed on a regular basis and re-challenges considered.

Obesity and nutrition-related chronic disorders are fast rising in developing countries. But undernutrition--stunting, underweight, wasting and micronutrient deficiencies--still affect millions of preschool children in both rural and urban settings increasing the risks of morbidity and mortality, impairing cognitive development, reducing productivity and increasing the risk of chronic diseases in later life. In addition undernutrition has a transgenerational effect. Here I review the evidence for a synergistic effect of inadequate nutrition (breastfeeding, complementary feeding), infection, and inappropriate mother-child interactions on growth and nutritional deficiencies. Underlying socioeconomic, environmental and genetic factors are also explored. Finally some perspectives on how urbanization and globalization may affect the prevalence and distribution of undernutrition are discussed. Fighting child under-nutrition is still an urgent necessity and a moral imperative.

Food allergy may be life-threatening and its management continues to consist of avoiding relevant allergens and, in the case of accidental ingestion, initiation of appropriate emergency therapy. The purpose of this review is to highlight the most promising novel approaches for treating food allergy using allergens. The use of specific immunotherapy for food allergy treatment is described. Clinical trials of immunotherapy have been published in the past. However, randomized, placebo-controlled studies are needed, including the evaluation of immune mechanisms. Immunotherapy is mainly indicated for persistent food allergy after the usual age of recovery. Reactive dose and symptoms of food allergy are less defined to indicate immunotherapy. Several procedures have been described: subcutaneous with constant adverse effects; oral tolerance induction with efficacy in a third of the cases, and sublingual which seems promising. The significance of the immunotherapy effect, persistent or transitory, or increasing the tolerated dose need to be defined.

The intestinal microbiota plays an important role in immune development and may play a role in the development of allergic disorders. Manipulation of the intestinal microbiota may therefore offer an approach to the prevention or treatment of allergic diseases. Probiotics and prebiotics, used alone or together (synbiotics), can influence the intestinal microbiota and modulate immune responses in vitro and in vivo. Clinical studies suggest a potential role for selected probiotics (alone or in combination with prebiotics) in the prevention of atopic eczema. A prenatal component of treatment appears important for beneficial effects. Effects are dependent upon the specific bacteria and characteristics of the study population. One study reported beneficial effects for prebiotics in the prevention of eczema in high-risk infants, however, further studies are required to confirm this. The use of probiotics in the treatment of allergic disease is less promising. A Cochrane meta-analysis concluded that probiotics are not effective for the treatment of atopic dermatitis. Probiotic effects in the treatment of asthma and allergic rhinitis are conflicting. Probiotics, prebiotics and synbiotics offer potential treatments for the prevention of atopic eczema; however, there is currently insufficient evidence to recommend their use in clinical practice. Studies to clarify the optimal dose, bacterial species/strains, whether there is added benefit with synbiotics, the optimal timing for intervention, and the patient populations who would benefit most from such therapies are warranted.

Most extremely low birthweight (ELBW; <1,000 g) infants will survive if cared for at a tertiary neonatal intensive care unit, and should be given optimal nutrition for brain development. Human milk confers nutritional and non-nutritional advantages over infant formula, and is started during the first hours of life. In Sweden, most ELBW infants are fed individually with mother's own milk (preferred) and banked milk, with supplementary parenteral nutrition. There is an enormous variation particularly in the fat and protein content of milk between mothers, during the day and the course of lactation. Infrared macronutrient analyses on 24-hour collections of mother's milk are performed once a week allowing for optimal protein and energy intakes. All banked milk is analyzed, and the most protein-rich milk is given to a newborn ELBW infant. After 2 weeks, the milk may be fortified if the protein or energy intakes need to be further increased, and fortification is continued throughout the tube-feeding period. Parenteral nutrition is continued until the enteral intake constitutes 75-80% of the total volume intake. Protein markers, e.g. serum urea and transthyretin, are assessed, and growth is monitored by measurements of weight, crown-heel length and head circumference.

It is estimated that over 51 million people in Brazil live in slums, areas where a high prevalence of malnutrition is also found. In general, the population of 'slum dwellers' is growing at a faster rate than urban populations. This condition is associated with poor sanitation, unhealthy food habits, low birthweight, and stunting. Stunting is of particular concern as longitudinal and cross-sectional studies of stunted adolescents have shown a high susceptibility to gain central fat, lower fat oxidation, and lower resting and postprandial energy expenditure. In addition, higher blood pressure, higher plasma uric acid and impaired flow-mediated vascular dilation were all associated with a higher level of hypertension in low birthweight and stunted children. In particular, stunted boys and girls also showed lower insulin production by pancreatic beta cells. All these factors are linked with a higher risk of chronic diseases later in life. Among stunted adults, alterations in plasma lipids, glucose and insulin have also been reported. However, adequate nutritional recovery with linear catch-up growth, after treatment in nutritional rehabilitation centers, can moderate the alterations in body composition, bone density and insulin production.

The coexistence of intrauterine and neonatal malnutrition and the development of obesity, type 2 diabetes and related comorbidities have been confirmed in a number of studies in humans and animal models. Data from studies in animals suggest that epigenetic changes as a result of altered methylation of the genomic DNA may be responsible for such metabolic patterning. Methionine, an essential amino acid, plays a critical role in the methyltranferases involved in the methylation by providing the one-carbon units via the methionine transmethylation cycle. Because of its interaction with a number of vitamins (B12, folate, pyridoxine), its regulation by hormones, i.e. insulin and glucagon, and by the changes in redox state, methionine metabolism is effected by nutrient and environmental influences and by altered physiological states. In the present review the impact of human pregnancy, dietary protein restriction and fatty liver disease on methionine metabolism is discussed. The role of methionine in metabolic programming in a commonly used model of intrauterine growth retardation and in propagation of fatty liver disease is briefly described.

Within the last decades a dramatic increase in allergic diseases has been recognized in the Westernized societies, leading to the fact that meanwhile 25-30% of the population is afflicted by allergic disorders. Besides a hereditary disposition, other factors, including a reduced microbial contact early in life or changes in nutrition, might also have influenced this epidemiological development. So far the only causative treatment against type-I allergies is specific immunotherapy. In young and monosensitized patients this treatment is highly efficacious, while there are clear limitations in older or multisensitized patients. Allergy research therefore aims at establishing new and more efficacious treatment strategies in prophylactic as well as therapeutic settings. Our research programs focus on the development of novel allergy vaccines based on the induction of mucosal tolerance. In different mouse models of respiratory allergy mucosal treatment with genetically engineered allergen constructs proved to prevent the development of allergic mono- and multisensitivities. The additional use of mucosal adjuvants seems particularly important to improve therapeutic treatment approaches. Recent studies on the inverse relation of certain parasite infections and the development of allergy prompted us to search for selected parasitic molecules with immunosuppressive properties as potential adjuvant systems for novel allergy vaccines. An overview of our recent studies will be given.