In December 2016, a panel of experts in microbiology, nutrition and clinical research was convened by the International Scientific Association for Probiotics and Prebiotics to review the definition and scope of prebiotics. Consistent with the original embodiment of prebiotics, but aware of the latest scientific and clinical developments, the panel updated the definition of a prebiotic: a substrate that is selectively utilized by host microorganisms conferring a health benefit. This definition expands the concept of prebiotics to possibly include non-carbohydrate substances, applications to body sites other than the gastrointestinal tract, and diverse categories other than food. The requirement for selective microbiota-mediated mechanisms was retained. Beneficial health effects must be documented for a substance to be considered a prebiotic. The consensus definition applies also to prebiotics for use by animals, in which microbiota-focused strategies to maintain health and prevent disease is as relevant as for humans. Ultimately, the goal of this Consensus Statement is to engender appropriate use of the term 'prebiotic' by relevant stakeholders so that consistency and clarity can be achieved in research reports, product marketing and regulatory oversight of the category. To this end, we have reviewed several aspects of prebiotic science including its development, health benefits and legislation

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Alongside its immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of health in the offspring during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on the offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes and asthma. Maternal obesity may also lead to poorer cognitive performance in the offspring and an increased risk of neurodevelopmental disorders including cerebral palsy. Preliminary evidence suggests potential implications for immune and infectious disease related outcomes. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, mediated at least in part through changes in epigenetic processes including alternations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight prior Authors' contributionsAll authors each drafted parts of the Series paper, which were subsequently integrated by KMG and RMR. The final version of the manuscript was corrected where needed and approved by all authors. Europe PMC Funders Group

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Food allergy can have significant effects on morbidity and quality of life and can be costly in terms of medical visits and treatments. There is therefore considerable interest in generating efficient approaches that may reduce the risk of developing food allergy. This guideline has been prepared by the European Academy of Allergy and Clinical Immunology's (EAACI) Taskforce on Prevention and is part of the EAACI Guidelines for Food Allergy and Anaphylaxis. It aims to provide evidence-based recommendations for primary prevention of food allergy. A wide range of antenatal, perinatal, neonatal, and childhood strategies were identified and their effectiveness assessed and synthesized in a systematic review.Based on this evidence, families can be provided with evidence-based advice about preventing food allergy, particularly for infants at high risk for development of allergic disease. The advice for all mothers includes a normal diet without restrictions during pregnancy and lactation. For all infants, exclusive breastfeeding is recommended for at least first 4-6 months of life. If breastfeeding is insufficient or not possible, infants at high-risk can be recommended a hypoallergenic formula with a documented preventive effect for the first 4 months. There is no need to avoid introducing complementary foods beyond 4 months, and currently, the evidence does not justify recommendations about either withholding or encouraging exposure to potentially allergenic foods after 4 months once weaning has commenced, irrespective of atopic heredity. There is no evidence to support the use of prebiotics or probiotics for food allergy prevention. 590Food allergy can have a significant effect on people's morbidity and quality of life and can be costly in terms of medical visits and treatments. Given the morbidity resulting from food allergy, there is considerable scientific, professional, and lay interest in approaches that may reduce the risk of developing food allergy. This guideline has been prepared by the European Academy of Allergy and Clinical Immunology's (EAACI) Taskforce on Prevention and is part of the EAACI Guidelines for Food Allergy and Anaphylaxis. This guideline aims to provide evidence-based recommendations for the primary prevention of food allergy. The primary audience is allergists throughout Europe, but this guideline is also likely to be of relevance to all other healthcare professionals (e.g., doctors, nurses, and pharmacists) in hospitals' primary care and other ambulatory settings.The causes of food allergy are likely to reflect an interaction between genetic factors and environmental exposure. Genetic factors are currently not modifiable, so strategies to prevent food allergy have tended to focus on early likely exposures to the food proteins most likely to be involved in its pathogenesis. These strategies may be implemented before birth or during breastfeeding, by focusing on the maternal diet, or it may directly target infant nutrition. In addition, there has been a focus on other nutritional f...

While food allergies and eczema are among the most common chronic non-communicable diseases in children in many countries worldwide, quality data on the burden of these diseases is lacking, particularly in developing countries. This 2012 survey was performed to collect information on existing data on the global patterns and prevalence of food allergy by surveying all the national member societies of the World Allergy Organization, and some of their neighbouring countries. Data were collected from 89 countries, including published data, and changes in the health care burden of food allergy. More than half of the countries surveyed (52/89) did not have any data on food allergy prevalence. Only 10% (9/89) of countries had accurate food allergy prevalence data, based on oral food challenges (OFC). The remaining countries (23/89) had data largely based on parent-reporting of a food allergy diagnosis or symptoms, which is recognised to overestimate the prevalence of food allergy. Based on more accurate measures, the prevalence of clinical (OFC proven) food allergy in preschool children in developed countries is now as high as 10%. In large and rapidly emerging societies of Asia, such as China, where there are documented increases in food allergy, the prevalence of OFC-proven food allergy is now around 7% in pre-schoolers, comparable to the reported prevalence in European regions. While food allergy appears to be increasing in both developed and developing countries in the last 10–15 years, there is a lack of quality comparative data. This survey also highlights inequities in paediatric allergy services, availability of adrenaline auto-injectors and standardised National Anaphylaxis Action plans. In conclusion, there remains a need to gather more accurate data on the prevalence of food allergy in many developed and developing countries to better anticipate and address the rising community and health service burden of food allergy.

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Food allergy is a substantial and evolving public health issue, recently emerging over the last 10-15 yr as a 'second wave' of the allergy epidemic. It remains unclear why this new phenomenon has lagged decades behind the 'first wave' of asthma, allergic rhinitis and inhalant sensitization. In regions like Australia, which lead the respiratory epidemic, challenge-proven IgE-mediated food allergy now affects up to 10% of infants. Although their parents were among the first generation to experience the large-scale rise in allergic diseases, disorders of oral tolerance were previously uncommon. Of further concern, this new generation appears less likely to outgrow food allergy than their predecessors with long-term implications for disease burden. Allergic disease has been linked to the modern lifestyle including changing dietary patterns, changing intestinal commensal bacteria and vehicular pollution. It is not yet known whether the rise in food allergy is a harbinger of earlier and more severe effects of these progressive environmental changes or whether additional or unrelated lifestyle factors are implicated. New studies suggest environmental factors can produce epigenetic changes in gene expression and disease risk that may be potentially heritable across generations. The rising rates of maternal allergy, a strong direct determinant of allergic risk, could also be amplifying the effect of environmental changes. Preliminary evidence that non-Caucasian populations may be even more susceptible to the adverse effects of 'westernisation' has substantial global implications with progressive urbanization of the more populous regions in the developing world. Unravelling the environmental drivers is critical to curtail a potential tsunami of allergic disease.