Beneficial effects of probiotic, prebiotic and polyphenol-rich interventions on fasting lipid profiles have been reported, with changes in the gut microbiota composition believed to play an important role in lipid regulation. Primary bile acids, which are involved in the digestion of fats and cholesterol metabolism, can be converted by the gut microbiota to secondary bile acids, some species of which are less well reabsorbed and consequently may be excreted in the stool. This can lead to increased hepatic bile acid neo-synthesis, resulting in a net loss of circulating low-density lipoprotein. Bile acids may therefore provide a link between the gut microbiota and cardiovascular health. This narrative review presents an overview of bile acid metabolism and the role of probiotics, prebiotics and polyphenol-rich foods in modulating circulating cardiovascular disease (CVD) risk markers and bile acids. Although findings from human studies are inconsistent, there is growing evidence for associations between these dietary components and improved lipid CVD risk markers, attributed to modulation of the gut microbiota and bile acid metabolism. These include increased bile acid neo-synthesis, due to bile sequestering action, bile salt metabolising activity and effects of short-chain fatty acids generated through bacterial fermentation of fibres. Animal studies have demonstrated effects on the FXR/FGF-15 axis and hepatic genes involved in bile acid synthesis (CYP7A1) and cholesterol synthesis (SREBP and HMGR). Further human studies are needed to determine the relationship between diet and bile acid metabolism and whether circulating bile acids can be utilised as a potential CVD risk biomarker.

A low-glycaemic diet is crucial for those with diabetes and cardiovascular diseases. Information on the glycaemic index (GI) of different ingredients can help in designing novel food products for such target groups. This is because of the intricate dependency of material source, composition, food structure and processing conditions, among other factors, on the glycaemic responses. Different approaches have been used to predict the GI of foods, and certain discrepancies exist because of factors such as inter-individual variation among human subjects. Besides other aspects, it is important to understand the mechanism of food digestion because an approach to predict GI must essentially mimic the complex processes in the human gastrointestinal tract. The focus of this work is to review the advances in various approaches for predicting the glycaemic responses to foods. This has been carried out by detailing conventional approaches, their merits and limitations, and the need to focus on emerging approaches. Given that no single approach can be generalised to all applications, the review emphasises the scope of deriving insights for improvements in methodologies. Reviewing the conventional and emerging approaches for the determination of GI in foods, this detailed work is intended to serve as a state-of-the-art resource for nutritionists who work on developing low-GI foods.

The increasing prevalence of non-alcoholic fatty liver disease (NAFLD) poses a growing challenge in terms of its prevention and treatment. The ‘multiple hits’ hypothesis of multiple insults, such as dietary fat intake, de novo lipogenesis, insulin resistance, oxidative stress, mitochondrial dysfunction, gut dysbiosis and hepatic inflammation, can provide a more accurate explanation of the pathogenesis of NAFLD. Betaine plays important roles in regulating the genes associated with NAFLD through anti-inflammatory effects, increased free fatty oxidation, anti-lipogenic effects and improved insulin resistance and mitochondrial function; however, the mechanism of betaine remains elusive.

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.

Undernutrition is a growing public health challenge affecting growth and development during adolescence in many low- and middle-income countries. This scoping review maps the evidence on adolescent undernutrition (stunting, thinness and micronutrient deficiencies) in South Asia and highlights gaps in knowledge. Using Arksey and O’Malley’s framework and the Joanna Briggs Institute Reviewers’ Manual, the search included electronic bibliographic databases (Medline (OVID), Embase, Cochrane Library, Web of Science, CINAHL, PsycInfo, and Scopus) as well as various grey literature sources published up to March 2019. In total, 131 publications met the inclusion criteria of this review. All the included evidence used quantitative data and 115 publications used a cross-sectional design. Nearly 70% (n = 86) of the included publications were conducted in India. Prevalence of undernutrition was reported based on different growth references and cut-offs. Evidence is divided into publications that included an intervention component (n = 12) and publications that did not include an intervention component (n = 116), and presented in a narrative synthesis. This scoping review provides a wide range of publications on adolescent undernutrition in South Asia and identifies future research priorities in the field.

This narrative review provides mechanistic insight into the biological link between smoking and/or chronic excess alcohol consumption, and increased risk of developing sarcopenia. Although the combination of excessive alcohol consumption and smoking is often associated with ectopic adipose deposition, this review is focused on the context of a reduced caloric intake (leading to energy deficit) that also may ensue due to either lifestyle habit. Smoking is a primary cause of periodontitis and chronic obstructive pulmonary disease that both induce swallowing difficulties, inhibit taste and mastication, and are associated with increased risk of muscle atrophy and mitochondrial dysfunction. Smoking may contribute to physical inactivity, energy deficit via reduced caloric intake, and increased systemic inflammation, all of which are factors known to suppress muscle protein synthesis rates. Moreover, chronic excess alcohol consumption may result in gut microbiota dysbiosis and autophagy-induced hyperammonemia, initiating the up-regulation of muscle protein breakdown and down-regulation of muscle protein synthesis via activation of myostatin, AMPK and REDD1, and deactivation of IGF-1. Future research is warranted to explore the link between oral healthcare management and personalised nutrition counselling in light of potential detrimental consequences of chronic smoking on musculoskeletal health outcomes in older adults. Experimental studies should investigate the impact of smoking and chronic excess alcohol consumption on the gut–brain axis, and explore biomarkers of smoking-induced oral disease progression. The implementation of behavioural change interventions and health policies regarding smoking and alcohol intake habits may mitigate the clinical and financial burden of sarcopenia on the healthcare system.

Cow’s milk is a naturally nutrient-dense foodstuff. A significant source of many essential nutrients, its inclusion as a component of a healthy balanced diet has been long recommended. Beyond milk’s nutritional value, an increasing body of evidence illustrates cow’s milk may confer numerous benefits related to health. Evidence from adult populations suggests that cow’s milk may have a role in overall dietary quality, appetite control, hydration and cognitive function. Although evidence is limited compared with the adult literature, these benefits may be echoed in recent paediatric studies. This article, therefore, reviews the scientific literature to provide an evidence-based evaluation of the associated health benefits of cow’s milk consumption in primary-school-aged children (4–11 years). We focus on seven key areas related to nutrition and health comprising nutritional status, hydration, dental and bone health, physical stature, cognitive function, and appetite control. The evidence consistently demonstrates cow’s milk (plain and flavoured) improves nutritional status in primary-school-aged children. With some confidence, cow’s milk also appears beneficial for hydration, dental and bone health and beneficial to neutral concerning physical stature and appetite. Due to conflicting studies, reaching a conclusion has proven difficult concerning cow’s milk and cognitive function; therefore, a level of caution should be exercised when interpreting these results. All areas, however, would benefit from further robust investigation, especially in free-living school settings, to verify conclusions. Nonetheless, when the nutritional-, physical- and health-related impact of cow’s milk avoidance is considered, the evidence highlights the importance of increasing cow’s milk consumption.

There is mounting evidence that microbiome composition is intimately and dynamically connected with host energy balance and metabolism. The gut microbiome is emerging as a novel target for counteracting the chronically positive energy balance in obesity, a disease of pandemic scale which contributes to >70 % of premature deaths. This scoping review explores the potential for therapeutic modulation of gut microbiota as a means of prevention and/or treatment of obesity and obesity-associated metabolic disorders. The evidence base for interventional approaches which have been shown to affect the composition and function of the intestinal microbiome is summarised, including dietary strategies, oral probiotic treatment, faecal microbiota transplantation and bariatric surgery. Evidence in this field is still largely derived from preclinical rodent models, but interventional studies in obese populations have demonstrated metabolic improvements effected by microbiome-modulating treatments such as faecal microbiota transplantation, as well as drawing attention to the unappreciated role of microbiome modulation in well-established anti-obesity interventions, such as dietary change or bariatric surgery. The complex relationship between microbiome composition and host metabolism will take time to unravel, but microbiome modulation is likely to provide a novel strategy in the limited armamentarium of effective treatments for obesity.

Fasting has been a practice among followers of different religions for many years. Christian Orthodox Church (COC) fasting is a periodic vegetarian-type diet in which seafood and snails are allowed on most fasting days. The present scoping review aimed to present available data regarding the benefits of COC fasting on metabolic syndrome (MetS) risk factors. Databases were searched for available studies. Twenty publications, with a total of 1226 fasting participants, provided data on the effects on different variables of MetS, including blood pressure, blood lipids and anthropometric measurements. Fasters’ diet is characterised by low saturated and trans fat intake, high complex carbohydrate and fibre consumption, due to permissible foods. COC fasting has no deficiency in essential amino acid intake since seafood and snails are allowed on fasting days. Fasters have healthier blood lipid profiles during and after COC fasting periods, and total cholesterol, LDL-cholesterol, systolic blood pressure, body weight and BMI are reduced after a fasting period. Due to restricted or forbidden intake of specific foods during the COC fasting periods, one might expect that fasters have reduced intake of macro- and micronutrients, but as shown in the available literature, there are no deficiencies. Future research on COC fasting is needed in areas not investigated at all, like MetS, before reaching definite conclusions.

Cigarette smoke (CS) is likely the most common preventable cause of human morbidity and mortality worldwide. Consequently, inexpensive interventional strategies for preventing CS-related diseases would positively impact health systems. Inhaled CS is a powerful inflammatory stimulus and produces a shift in the normal balance between antioxidants and oxidants, inducing oxidative stress in both the respiratory system and throughout the body. This enduring and systemic pro-oxidative state within the body is reflected by increased levels of oxidative stress and inflammation biomarkers seen in smokers. Smokers might benefit from consuming antioxidant supplements, or a diet rich in fruit and vegetables, which can reduce the CS-related oxidative stress. This review provides an overview of the plasma profile of antioxidants observable in smokers and examines the heterogeneous literature to elucidate and discuss the effectiveness of interventional strategies based on antioxidant supplements or an antioxidant-rich diet to improve the health of smokers. An antioxidant-rich diet can provide an easy-to-implement and cost-effective preventative strategy to reduce the risk of CS-related diseases, thus being one of the simplest ways for smokers to stay in good health for as long as possible. The health benefits attributable to the intake of antioxidants have been observed predominantly when these have been consumed within their natural food matrices in an optimal antioxidant-rich diet, while these preventive effects are rarely achieved with the intake of individual antioxidants, even at high doses.

The aim of this review is to explore how metabolic changes induced by diets high in saturated fat (HFD) affect nucleus accumbens (NAc) dopamine neurotransmission and food intake, and to explore how stress and inflammation influence this process. Recent evidence linked diet-induced obesity and HFD with reduced dopamine release and reuptake. Altered dopamine neurotransmission could disrupt satiety circuits between NAc dopamine terminals and projections to the hypothalamus. The NAc directs learning and motivated behaviours based on homeostatic needs and psychological states. Therefore, impaired dopaminergic responses to palatable food could contribute to weight gain by disrupting responses to food cues or stress, which impacts type and quantity of food consumed. Specifically, saturated fat promotes neuronal resistance to anorectic hormones and activation of immune cells that release proinflammatory cytokines. Insulin has been shown to regulate dopamine neurotransmission by enhancing satiety, but less is known about effects of diet-induced stress. Therefore, changes to dopamine signalling due to HFD warrant further examination to characterise crosstalk of cytokines with endocrine and neurotransmitter signals. A HFD promotes a proinflammatory environment that may disrupt neuronal endocrine function and dopamine signalling that could be exacerbated by the hypothalamic–pituitary–adrenal and κ-opioid receptor stress systems. Together, these adaptive changes may dysregulate eating by changing NAc dopamine during hedonic versus homeostatic food intake. This could drive palatable food cravings during energy restriction and hinder weight loss. Understanding links between HFD and dopamine neurotransmission will inform treatment strategies for diet-induced obesity and identify molecular candidates for targeted therapeutics.

Circadian rhythms, metabolic processes and dietary intake are inextricably linked. Timing of food intake is a modifiable temporal cue for the circadian system and may be influenced by numerous factors, including individual chronotype – an indicator of an individual’s circadian rhythm in relation to the light–dark cycle. This scoping review examines temporal patterns of eating across chronotypes and assesses tools that have been used to collect data on temporal patterns of eating and chronotype. A systematic search identified thirty-six studies in which aspects of temporal patterns of eating, including meal timings; meal skipping; energy distribution across the day; meal frequency; time interval between meals, or meals and wake/sleep times; midpoint of food/energy intake; meal regularity; and duration of eating window, were presented in relation to chronotype. Findings indicate that, compared with morning chronotypes, evening chronotypes tend to skip meals more frequently, have later mealtimes, and distribute greater energy intake towards later times of the day. More studies should explore the difference in meal regularity and duration of eating window amongst chronotypes. Currently, tools used in collecting data on chronotype and temporal patterns of eating are varied, limiting the direct comparison of findings between studies. Development of a standardised assessment tool will allow future studies to confidently compare findings to inform the development and assessment of guidelines that provide recommendations on temporal patterns of eating for optimal health.

Non-alcoholic fatty liver disease (NAFLD) was defined in 1980 and has the same histological characteristics as alcoholic liver disease except for alcohol consumption. After 40 years, the understanding of this disease is still imperfect. Without specific drugs available for treatment, the number of patients with NAFLD is increasing rapidly, and NAFLD currently affects more than one-quarter of the global population. NAFLD is mostly caused by a sedentary lifestyle and excessive energy intake of fat and sugar. To ameliorate or avoid NAFLD, people commonly replace high-fat foods with high-carbohydrate foods (especially starchy carbohydrates) as a way to reduce caloric intake and reach satiety. However, there are few studies that concentrate on the effect of carbohydrate intake on liver metabolism in patients with NAFLD, much fewer than the studies on fat intake. Besides, most of these studies are not systematic, which has made identification of the mechanism difficult. In this review, we collected and analysed data from studies on human and animal models and, surprisingly, found that carbohydrates and liver steatosis could be linked by inflammation. This review not only describes the effects of carbohydrates on NAFLD and body lipid metabolism but also analyses and predicts possible molecular pathways of carbohydrates in liver lipid synthesis that involve inflammation. Furthermore, the limitations of recent research and possible targets for regulating inflammation and lipogenesis are discussed. This review describes the effects of starchy carbohydrates, a nutrient signal, on NAFLD from the perspective of inflammation.

The negative impact of stunting and severe underweight on cognitive neurodevelopment of children is well documented; however, the effect of overweight/obesity is still unclear. The 2018 Global Nutrition Report reported that stunting and overweight concurrently affect 189 million children worldwide. As existing reviews discuss undernutrition and overweight/obesity separately, this scoping review aims to document the impact of mild/moderate and severe underweight, stunting, and overweight/obesity among children aged 0–60 months on their cognitive neurodevelopmental trajectories. Twenty-six articles were analysed to extract significant information from literature retrieved from PubMed and Cochrane databases published from 1 January 2009 to 31 October 2019. Length gain is associated with cognitive neurodevelopment in normo-nourished and stunted children aged under 24 months. Among stunted children, it seems that cognitive and neurodevelopmental deficits can potentially be recovered before 8 years of age, particularly in those whose nutritional status has improved. The impact of overweight/obesity on cognitive neurodevelopment appears to be limited to attention, gross motor skills and executive control. Parental education level, birth weight/length, breastfeeding duration, and sanitation level are some identifiable factors that modify the impact of undernutrition and overweight/obesity on cognitive and neurodevelopment. In conclusion, underweight, stunting and overweight/obesity have a significant impact on cognitive neurodevelopment. Multidimensional approaches with various stakeholders should address all issues simultaneously, such as improving sanitation levels, assuring parental job security and adequate social welfare, and providing access to adequate nutrients for catch-up growth among underweight or stunted children and to affordable healthy foods for those who are overweight/obese and from low socio-economic status.

Intestinal stem cells, which are capable of both self-renewal and differentiation to mature cell types, are responsible for maintaining intestinal epithelial homeostasis. Recent evidence indicates that these processes are mediated, in part, through nutritional status in response to diet. Diverse dietary patterns including caloric restriction, fasting, high-fat diets, ketogenic diets and high-carbohydrate diets as well as other nutrients control intestinal stem cell self-renewal and differentiation through nutrient-sensing pathways such as mammalian target of rapamycin and AMP-activated kinase. Herein, we summarise the current understanding of how intestinal stem cells contribute to intestinal epithelial homeostasis and diseases. We also discuss the effects of diet and nutrient-sensing pathways on intestinal stem cell self-renewal and differentiation, as well as their potential application in the prevention and treatment of intestinal diseases.

Tremendous progress has been made in the field of ferroptosis since this regulated cell death process was first named in 2012. Ferroptosis is initiated upon redox imbalance and driven by excessive phospholipid peroxidation. Levels of multiple intracellular nutrients (iron, selenium, vitamin E and coenzyme Q10) are intimately related to the cellular antioxidant system and participate in the regulation of ferroptosis. Dietary intake of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) regulates ferroptosis by directly modifying the fatty acid composition in cell membranes. In addition, amino acids and glucose (energy stress) manipulate the ferroptosis pathway through the nutrient-sensitive kinases mechanistic target of rapamycin complex 1 (mTORC1) and AMP-activated protein kinase (AMPK). Understanding the molecular interaction between nutrient signals and ferroptosis sensors might help in the identification of the roles of ferroptosis in normal physiology and in the development of novel pharmacological targets for the treatment of ferroptosis-related diseases.

Aspirin (acetylsalicylic acid, ASA) is inexpensive and is established in preventing cardiovascular disease (CVD) and colorectal adenomas. Omega-3 (n3) polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have also shown benefit in preventing CVD. The combination could be an effective preventative measure in patients with such diseases. ASA and n3 PUFA reduced the risk of CVD in ASA-resistant or diabetic patients. EPA- and DHA-deficient patients also benefited the most from n3 PUFA supplementation. Synergistic effects between ASA and EPA and DHA are ‘V-shaped’ such that optimal ASA efficacy is dependent on EPA and DHA concentrations in blood. In colorectal adenomas, ASA (300 mg/d) and EPA reduced adenoma burden in a location- and subtype-specific manner. Low doses of ASA (75–100 mg/d) were used in CVD prevention; however, ultra-low doses (30 mg/d) can also reduce thrombosis. EPA-to-DHA ratio is also important with regard to efficacy. DHA is more effective in reducing blood pressure and modulating systemic inflammation; however, high-dose EPA can lower CVD events in high-risk individuals. Although current literature has yet to examine ASA and DHA in preventing CVD, such combination warrants further investigation. To increase adherence to ASA and n3 PUFA supplementation, combination dosage form may be required to improve outcomes.