Primary schools contribute to promoting healthy eating behaviour and preventing overweight and obesity by providing nutrition education. Research highlights the importance of improving teachers’ programme implementation to enhance intervention effectiveness. An integrative approach has been suggested to reduce time barriers that teachers currently experience in teaching nutrition. This scoping review explores use and effectiveness of integrative teaching in primary-school-based nutrition education programmes. Six databases were searched for primary-school-based interventions on nutrition education. Papers reporting on integration of nutrition topics within core curriculum were included. Abstracts and full texts of potentially relevant articles were screened to determine eligibility. Next, data were extracted and tabulated. Findings were collated and summarised to describe intervention characteristics, subject integration and effectiveness of the included programmes. Data describing integration of nutrition into the primary school curriculum were extracted from 39 eligible papers. Nutrition education programmes often involve lessons about food groups and are frequently embedded within the mathematics, science or literacy syllabus. Although articles report on the integration of nutrition, the use of this approach was not commonly described in detail. Only seven papers discussed student outcomes related to the integration of nutrition education within core subjects. The ability to draw strong conclusions about school-based nutrition intervention effectiveness is limited by the current lack of programme description and methodological issues. Hence, more research is warranted to inform evidence on effectiveness of integrative nutrition education for both teacher and student outcomes. Future studies that include greater detail regarding the integrative approach are needed.

Abstract Strong epidemiological data exists implicating anthropometric risk factors in breast cancer aetiology. In premenopausal women the risk of breast cancer increases with increased height, yet decreases with increasing weight and BMI. Although the evidence is not strong, a counter-intuitive positive relationship between central adiposity and premenopausal breast cancer risk is emerging. In post-menopausal women an increased risk in breast cancer has been found for all anthropometric measures: height, weight, BMI, measures of central adiposity (waist:hip ratio and waist circumference) and weight gain, with breast size being a possible additional risk factor. Weight loss as a strategy for reducing breast cancer risk seems to offer a viable prophylaxis in obese post-menopausal women, although data are limited. The evidence for anthropometric measures in relation to breast cancer risk is consistently stronger for post-menopausal women compared with premenopausal women and seems to be dependent on age. A number of possible biological mechanisms have been offered to explain the link between breast cancer risk and anthropometric measures. It has been hypothesised that obesity, especially central fat deposits, linked to insulin resistance, increases circulating hormones such as oestrogens, androgens, insulin, insulin-like growth factor-1 (IGF-1), and decreased levels of hormone-binding proteins such as steroid hormone-binding globulin and IGF-1 binding protein-1. Thus there are resulting increased concentrations of bioavailable sex hormones, which have been linked to increased breast cancer risk. As obesity is an important modifiable risk factor, which has been linked to increased post-menopausal breast cancer, public health recommendations to maintain ideal weight throughout life are warranted.

To inform programmes and policies that promote health equity, it is essential to monitor the distribution of nutritional problems among young individuals. Common nutritional problems include overall low diet quality, the underconsumption and overconsumption of certain dietary components, unhealthy meal and snack patterns, problematic feeding practices and disordered eating. The objective of the present narrative review was to summarise recent evidence of disparities among US children (2–19 years) according to age, sex, socio-economic status, ethnicity/race and rural–urban location. Searches in PubMed® and MEDLINE® were completed to identify peer-reviewed research studies published between January 2009 and January 2019. Findings from the ninety-nine reviewed studies indicate adolescent females, young individuals from lower socio-economic households and individuals who identify as non-Hispanic Black race are particularly vulnerable populations for whom targeted strategies should be developed to address evidence of increased risk with regards to multiple aspects of nutritional wellbeing. Limitations of the existing evidence relate to the accuracy of self-reported dietary data; the need for consistent definitions of disordered eating; the focus on individual dietary components v. patterns; the complexities of categorising socio-economic status, ethnicity/race, and rural and urban areas; and the cross-sectional, observational nature of most research designs. There is an urgent need for research to address these limitations and fill a large gap in evidence on rural–urban differences in nutritional problems. It will further be important for future studies to build greater understanding of how nutritional problems cluster among population groups.

Alcohol intake at levels posing an acute heath risk is common amongst teenagers. Alcohol abuse is the second most common mental disorder worldwide. The incidence of smoking is decreasing in the Western world but increasing in developing countries and is the leading cause of preventable death worldwide. Considering the longstanding history of alcohol and tobacco consumption in human societies, it might be surprising that the molecular mechanisms underlying alcohol and smoking dependence are still incompletely understood. Effective treatments against the risk of relapse are lacking. Drugs of abuse exert their effect manipulating the dopaminergic mesocorticolimbic system. In this brain region, alcohol has many potential targets including membranes and several ion channels, while other drugs, for example nicotine, act via specific receptors or binding proteins. Repeated consumption of drugs of abuse mediates adaptive changes within this region, resulting in addiction. The high incidence of alcohol and nicotine co-abuse complicates analysis of the molecular basis of the disease. Gene expression profiling is a useful approach to explore novel drug targets in the brain. Several groups have utilised this technology to reveal drug-sensitive pathways in the mesocorticolimbic system of animal models and in human subjects. These studies are the focus of the present review.

CVD are the leading cause of death in women globally, with ageing associated with progressive endothelial dysfunction and increased CVD risk. Natural menopause is characterised by raised non-fasting TAG concentrations and impairment of vascular function compared with premenopausal women. However, the mechanisms underlying the increased CVD risk after women have transitioned through the menopause are unclear. Dietary fat is an important modifiable risk factor relating to both postprandial lipaemia and vascular reactivity. Meals rich in SFA and MUFA are often associated with greater postprandial TAG responses compared with those containing n-6 PUFA, but studies comparing their effects on vascular function during the postprandial phase are limited, particularly in postmenopausal women. The present review aimed to evaluate the acute effects of test meals rich in SFA, MUFA and n-6 PUFA on postprandial lipaemia, vascular reactivity and other CVD risk factors in postmenopausal women. The systematic search of the literature identified 778 publications. The impact of fat-rich meals on postprandial lipaemia was reported in seven relevant studies, of which meal fat composition was compared in one study described in three papers. An additional study determined the impact of a high-fat meal on vascular reactivity. Although moderately consistent evidence suggests detrimental effects of high-fat meals on postprandial lipaemia in postmenopausal (than premenopausal) women, there is insufficient evidence to establish the impact of meals of differing fat composition. Furthermore, there is no robust evidence to conclude the effect of meal fatty acids on vascular function or blood pressure. In conclusion, there is an urgent requirement for suitably powered robust randomised controlled trials to investigate the impact of meal fat composition on postprandial novel and established CVD risk markers in postmenopausal women, an understudied population at increased cardiometabolic risk.

Macular pigment (MP) confers potent antioxidant and anti-inflammatory effects at the macula, and may therefore protect retinal tissue from the oxidative stress and inflammation associated with ocular disease and ageing. There is a body of evidence implicating oxidative damage and inflammation as underlying pathological processes in diabetic retinopathy. MP has therefore become a focus of research in diabetes, with recent evidence suggesting that individuals with diabetes, particularly type 2 diabetes, have lower MP relative to healthy controls. The present review explores the currently available evidence to illuminate the metabolic perturbations that may possibly be involved in MP’s depletion. Metabolic co-morbidities commonly associated with type 2 diabetes, such as overweight/obesity, dyslipidaemia, hyperglycaemia and insulin resistance, may have related and independent relationships with MP. Increased adiposity and dyslipidaemia may adversely affect MP by compromising the availability, transport and assimilation of these dietary carotenoids in the retina. Furthermore, carotenoid intake may be compromised by the dietary deficiencies characteristic of type 2 diabetes, thereby further compromising redox homeostasis. Candidate causal mechanisms to explain the lower MP levels reported in diabetes include increased oxidative stress, inflammation, hyperglycaemia, insulin resistance, overweight/obesity and dyslipidaemia; factors that may negatively affect redox status, and the availability, transport and stabilisation of carotenoids in the retina. Further study in diabetic populations is warranted to fully elucidate these relationships.

The early hominids and their successors, the nomadic hunter–gatherers, were evolutionarily adapted to an omnivorous diet. Their food was well balanced nutritionally and they acquired adequate supplies with relatively little expenditure of energy. The complete change to a fixed agricultural lifestyle (the Neolithic revolution) took place only some 12 000 years ago and was the most momentous event in human history. Being tied to the land that they worked led eventually to the city states and the great civilisations of history, which brought with them wars and epidemics of infectious diseases. Much more serious were the insidious effects of the new cereal-based diet which persisted until the twentieth century. Not only was it labour intensive, but also for the bulk of the population it was often deficient in vitamins, minerals and energy, particularly at certain times of the year. Time-series analysis reveals a regular short wavelength oscillation in the grain supply that persisted for at least 350 years and dominated the population dynamics of pre-industrial England. In addition to reducing fertility, it acted primarily via its effects on the nutrition of the pregnant woman. Malnutrition during one of the critical trimesters of pregnancy could have far-reaching effects not only on the health of the fetus and neonate but also on the illnesses of later, adult life. These consequences were insidiously and inevitably carried forward to the subsequent generations. Girls who were born with a low birth weight produced daughters and granddaughters of low birth weight, irrespective of their nutrition during childhood. These intergenerational, knock-on effects established a vicious circle from which there was little chance of escape.

At the crossroad between nutrient supply and requirements, the liver plays a central role in partitioning nitrogenous nutrients among tissues. The present review examines the utilisation of amino acids (AA) within the liver in various physiopathological states in mammals and how the fates of AA are regulated. AA uptake by the liver is generally driven by the net portal appearance of AA. This coordination is lost when demands by peripheral tissues is important (rapid growth or lactation), or when certain metabolic pathways within the liver become a priority (synthesis of acute-phase proteins). Data obtained in various species have shown that oxidation of AA and export protein synthesis usually responds to nutrient supply. Gluconeogenesis from AA is less dependent on hepatic delivery and the nature of nutrients supplied, and hormones like insulin are involved in the regulatory processes. Gluconeogenesis is regulated by nutritional factors very differently between mammals (glucose absorbed from the diet is important in single-stomached animals, while in carnivores, glucose from endogenous origin is key). The underlying mechanisms explaining how the liver adapts its AA utilisation to the body requirements are complex. The highly adaptable hepatic metabolism must be capable to deal with the various nutritional/physiological challenges that mammals have to face to maintain homeostasis. Whereas the liver responds generally to nutritional parameters in various physiological states occurring throughout life, other complex signalling pathways at systemic and tissue level (hormones, cytokines, nutrients, etc.) are involved additionally in specific physiological/nutritional states to prioritise certain metabolic pathways (pathological states or when nutritional requirements are uncovered).

Diet, nutritional status and lifestyle practices are significant determinants of the risk of certain cancers. In 1997 The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) developed a series of evidence-based recommendations to help reduce the population and individual risk of cancer. However, guidance for evaluating concordance or compliance with these recommendations is limited. To illustrate the challenges in evaluation, four publications were reviewed that explored the task of creating operative criteria from which to assess concordance with the tenets of the WCRF/AICR recommendations. Three documents dealt with secondary analysis, whereas one was a prospective inquiry, with procedures and instruments designed to obtain responses to WCRF/AICR cancer-prevention specification. One considered only population-goal criteria, and two dealt implicitly or explicitly with criteria at both population and individual levels. The assessment approaches used by the authors were compared with alternative semantic and conceptual interpretations of the WCRF/AICR population goals and individual guidelines. Attempts to develop operative criteria for assessment of concordance (reflecting either a more superficial or more in-depth parsing of recommendations) have been inconsistent. The results indicate that the language of the WCRF/AICR leaves a certain degree of semantic ambiguity for evaluation purposes. Future design of prospective studies for analyses of behaviours and relevant exposures (including those reported in the 2007 WCRF/AICR report) should carefully consider evaluation criteria and fully document detailed methodology.

The present paper provides a comprehensive review of the literature pertaining to the impact of alcohol intake on cardiovascular disease. Both cross-sectional and prospective studies have disclosed a negative association between moderate intake of alcoholic beverages and cardiovascular disease. The relationship appears to be present for both wine, beer and spirits. Effects of alcohol itself and also the role of different cardio-protective substances in alcoholic beverages are discussed. Alcohol has been suggested to beneficially affect the blood lipid profile, as it increases plasma HDL-cholesterol level. Furthermore, it may inhibit thrombogenesis by reducing thromboxan formation and decreasing the plasma level of fibrinogen. However, high blood concentrations of alcohol may impair fibrinolysis by increasing plasma plasminogen activator inhibitor-1 level. This action could contribute to explaining the ‘U’-shaped association between alcohol intake and cardiac events. Alcohol seems to promote abdominal fat distribution, but the importance of this effect in non-obese individuals is uncertain. Wine in particular, but also beer, contains polyphenols which act as antioxidants. Their action could maintain the integrity of the endothelial function by reducing the formation of superoxide. Moreover, these antioxidants may protect against LDL oxidation and modulate the macrophage attack on the endothelium. Although the cardio-protective effect of alcohol can hardly be addressed in healthy individuals by intervention studies with hard end points, there are many observational and experimental findings indicating that moderate alcohol drinking possesses properties preventive of cardiovascular disease.

Diet is an important factor in the causation of cancer. Previous systematic reviews of one-to-one interventions to encourage dietary change have found that such interventions can achieve modest improvements in diet. However, such interventions are resource intensive and unlikely to be good value for money at a population level. Interventions that address groups, communities or whole populations may be less resource intensive and effect change in a wider population. We report a systematic review of such interventions. We set wide inclusion criteria, including before-and-after studies and studies with a non-randomized comparison group as well as randomized trials. We found eighteen studies based in the community, seventeen based on worksites, five based in churches and one based in a supermarket. Interventions which targeted fruit and vegetable intake were most likely to be successful, particularly in worksites and churches. There was also evidence of small positive effects on reducing fat intake in worksites and churches. Overall the community-based interventions showed little effect. The studies included in the present review were generally poorly reported. Dietary changes are reported in the relatively short-term studies reviewed here but may not be sustained in the long term. The effects that we have identified are small but the reach is potentially very wide, in some cases as wide as a whole country. The cost effectiveness of such strategies remains to be evaluated.

The optimisation of nutritional support for the growing number of older individuals does not usually take into account medication. Paracetamol (acetaminophen; APAP) is the first intention treatment of chronic pain that is highly prevalent and persistent in the elderly. Detoxification of APAP occurs in the liver and utilises sulfate and glutathione (GSH), both of which are issued from cysteine (Cys), a conditionally indispensable amino acid. The detoxification-induced siphoning of Cys could reduce the availability of Cys for skeletal muscle. Consequently, APAP could worsen sarcopenia, an important component of the frailty syndrome leading to dependency. The present review provides the rationale for the potential pro-sarcopenic effect of APAP then recent results concerning the effect of chronic APAP treatment on muscle mass and metabolism are discussed. The principal findings are that chronic treatments with doses of APAP comparable with the maximum posology for humans can increase the requirement for sulfur amino acids (SAA), reduce Cys availability for muscle, reduce muscle protein synthesis and aggravate sarcopenia in animals. One clinical study is in favour of an enhanced SAA requirement in the older individual under chronic treatment with APAP. Few clinical studies investigated the effect of chronic treatment with APAP combined with exercise, in nutritional conditions that probably did not affect Cys and GSH homeostasis. Whether APAP can aggravate sarcopenia in older individuals with low protein intake remains to be tested. If true, nutritional strategies based on enhancing Cys supply could be of prime interest to cut down the pro-sarcopenic effect of chronic treatment with APAP.

The amino acid arginine and one of its metabolites NO have gathered broad attention in the last decade. Although arginine is regarded as a conditionally essential amino acid in disease, L-arginine supplementation in severe illness has not found its way into clinical practice. This might be due to the invalid interpretation of results from studies with immune-enhancing diets containing L-arginine amongst other pharmaconutrients. However, not much attention is given to research using L-arginine as a monotherapy and the possibility of the alternative hypothesis: that L-arginine supplementation is beneficial in disease. The present review will discuss data from studies in healthy and diseased animals and patients with monotherapy of L-arginine to come to an objective overview of positive and negative aspects of L-arginine supplementation in disease with special emphasis on sepsis, cancer, liver failure and wound healing.