Non-alcoholic fatty liver disease (NAFLD) is now the most common cause of chronic liver disease, worldwide. The molecular pathogenesis of NAFLD is complex, involving numerous signalling molecules, including microRNAs (miRNAs). Dysregulation of miRNA expression is associated with hepatic inflammation, fibrosis and hepatocellular carcinoma. Although miRNAs are also critical to the cellular response to vitamin D, mediating regulation of the vitamin D receptor and vitamin D’s anti-cancer effects, the role of vitamin-D-regulated miRNAs in NAFLD pathogenesis has been relatively unexplored. Therefore, this review aims to critically assess the evidence for a potential subset of miRNAs that are both dysregulated in NAFLD and modulated by vitamin D. Comprehensive review of eighty-nine human studies identified twenty-five miRNAs found dysregulated in more than one NAFLD study. In contrast, only seventeen studies, including a protocol for a trial in NAFLD, had examined miRNAs in relation to vitamin D status, response to supplementation, or vitamin D in the context of the liver. This paper summarises these data and reviews the biological roles of six miRNAs (miR-21, miR-30, miR-34, miR-122, miR-146, miR-200) found dysregulated in multiple independent NAFLD studies. While modulation of miRNAs by vitamin D has been understudied, integration of the data suggests seven vitamin-D-modulated miRNAs (miR-27, miR-125, miR-155, miR-192, miR-223, miR-375, miR-378) potentially relevant to NAFLD pathogenesis. Our summary tables provide a significant resource to underpin future hypothesis-driven research, and we conclude that the measurement of serum and hepatic miRNAs in response to vitamin D supplementation in larger trials is warranted.

Cardiovascular disease (CVD) is the most common non-communicable disease occurring globally. Although previous literature has provided useful insights into the important role that diet plays in CVD prevention and treatment, understanding the causal role of diets is a difficult task considering inherent and introduced weaknesses of observational (e.g. not properly addressing confounders and mediators) and experimental research designs (e.g. not appropriate or well designed). In this narrative review, we organised current evidence linking diet, as well as conventional and emerging physiological risk factors, with CVD risk, incidence and mortality in a series of diagrams. The diagrams presented can aid causal inference studies as they provide a visual representation of the types of studies underlying the associations between potential risk markers/factors for CVD. This may facilitate the selection of variables to be considered and the creation of analytical models. Evidence depicted in the diagrams was systematically collected from studies included in the British Nutrition Task Force report on diet and CVD and database searches, including Medline and Embase. Although several markers and disorders linked to conventional and emerging risk factors for CVD were identified, the causal link between many remains unknown. There is a need to address the multifactorial nature of CVD and the complex interplay between conventional and emerging risk factors with natural and built environments, while bringing the life course into the spotlight.

Consumption of edible insects has been widely suggested as an environmentally sustainable substitute for meat to reduce greenhouse gas emissions. However, the novel research field for edible insects relies on the content of bioactive ingredients and on the ability to induce a functional effect in humans. The goal of this manuscript is to review the available body of evidence on the properties of edible insects in modulating oxidative and inflammatory stress, platelet aggregation, lipid and glucose metabolism and weight control. A search for literature investigating the functional role of edible insects was carried out in the PubMed database using specific keywords. A total of 55 studies, meeting inclusion criteria after screening, were divided on the basis of the experimental approach: in vitro studies, cellular models/ex vivo studies or in vivo studies. In the majority of the studies, insects demonstrated the ability to reduce oxidative stress, modulate antioxidant status, restore the impaired activity of antioxidant enzymes and reduce markers of oxidative damage. Edible insects displayed anti-inflammatory activity reducing cytokines and modulating specific transcription factors. Results from animal studies suggest that edible insects can modulate lipid and glucose metabolism. The limited number of studies focused on the assessment of anti-coagulation activity of edible insects makes it difficult to draw conclusions. More evidence from dietary intervention studies in humans is needed to support the promising evidence from in vitro and animal models about the functional role of edible insect consumption.

Zinc (Zn) deficiency is a worldwide problem, and this review presents an overview of the magnitude of Zn deficiency with a particular emphasis on present global challenges, current recommendations for Zn intake, and factors that affect dietary requirements. The challenges of monitoring Zn status are clarified together with the discussion of relevant Zn bioaccessibility and bioavailability issues. Modern lifestyle factors that may exacerbate Zn deficiency and new strategies of reducing its effects are presented. Biofortification, as a potentially useful strategy for improving Zn status in sensitive populations, is discussed. The review proposes potential actions that could deliver promising results both in terms of monitoring dietary and physiological Zn status as well as in alleviating dietary Zn deficiency in affected populations.

Poor nutritional intake is common among older adults. Given that nutrition knowledge is an important determinant of eating behaviour and nutritional status, understanding areas of inadequate knowledge can guide educational interventions to reduce risk of nutritional deficiencies and promote healthy ageing. This review investigated tools assessing general nutritional knowledge of older adults and their carers. Following the Joanna Briggs for Scoping Reviews guidelines, 4 databases (MEDLINE, CINAHL, Global Health and Embase) and grey literature were searched. Studies of any type containing general nutrition knowledge assessment tools for older adults or their carers were included. In total, 6934 articles were identified, of which 24 met the eligibility criteria, and 23 unique nutrition knowledge assessment tools were included. Of these tools, 14 were original, 6 were modified from other tools and 3 used dietary-related responses from national dietary survey questions. 6 tools were developed for carers (mostly nurses) and 17 tools for older adults. Tools had between 4 and 110 items. The most common topics for general nutrition knowledge questions were related to nutrients and roles, food sources of nutrients, and diet–disease relationships. 8 tools were developed prior to 2000. Most studies did not specify or assess psychometric properties of the tool, with only 9 (38 %) and 6 (26 %) studies testing for reliability and validity, respectively, and only 1 tool was considered reliable. Additional research for the development of reliable and validated tools or the validation of existing tools to assess nutrition knowledge of older adults and their carers is needed across different healthcare settings.

Adequate protein intake is essential for the maintenance of whole-body protein mass. Different methodological approaches are used to substantiate the evidence for the current protein recommendations, and it is continuously debated whether older adults require more protein to counteract the age-dependent loss of muscle mass, sarcopenia. Thus, the purpose of this critical narrative review is to outline and discuss differences in the approaches and methodologies assessing the protein requirements and, hence, resulting in controversies in current protein recommendations for healthy older adults. Through a literature search, this narrative review first summarises the historical development of the Food and Agriculture Organization/World Health Organization/United Nations University setting of protein requirements and recommendations for healthy older adults. Hereafter, we describe the various types of studies (epidemiological studies and protein turnover kinetic measurements) and applied methodological approaches founding the basis and the different recommendations with focus on healthy older adults. Finally, we discuss important factors to be considered in future studies to obtain evidence for international agreement on protein requirements and recommendations for healthy older adults. We conclude by proposing future directions to determine ‘true’ protein requirements and recommendations for healthy older adults.

The term ‘epigenetics’ refers to a series of meiotically/mitotically inheritable alterations in gene expression, related to environmental factors, without disruption on DNA sequences of bases. Recently, the pathophysiology of autoimmune diseases (ADs) has been closely linked to epigenetic modifications. In fact, epigenetic mechanisms can modulate gene expression or repression of targeted cells and tissues involved in autoimmune/inflammatory conditions acting as keys effectors in regulation of adaptive and innate responses. ADs, as systemic lupus erythematosus (SLE), a rare disease that still lacks effective treatment, is characterised by epigenetic marks in affected cells. Taking into account that epigenetic mechanisms have been proposed as a winning strategy in the search of new, more specific and personalised therapeutics agents, pharmacology and pharmaco-epigenetic studies about epigenetic regulations of ADs may provide novel individualised therapies. Focusing on possible implicated factors on development and predisposition of SLE, diet is feasibly one of the most important factors since it is linked directly to epigenetic alterations and these epigenetic changes may augment or diminish the risk of SLE. Nevertheless, several studies have suggested that dietary therapy could be promising to SLE patients via prophylactic actions deprived of side effects of pharmacology, decreasing co-morbidities and improving lifestyle of SLE sufferers. Herein, we review and discuss the cross-link between epigenetic mechanisms on SLE predisposition and development, as well as the influence of dietary factors on regulation of epigenetic modifications that may eventually make a positive impact on SLE patients.

Currently, there is considerable emphasis on the relationship between dietary sugar consumption and various health outcomes, with some countries and regions implementing national sugar reduction campaigns. This has resulted in significant efforts to quantify dietary sugar intakes, to agree on terms to describe dietary sugars and to establish associated recommendations. However, this information is infrequently collated on a global basis and in a regularised manner. The present review provides context regarding sugar definitions and recommendations. It provides a global review of the available data regarding dietary sugar intake, considering forms such as total, free and added sugars. A comprehensive breakdown of intakes is provided by age group, country and sugar form. This analysis shows that free sugar intakes as a percentage of total energy (%E) are the highest for children and adolescents (12–14%E) and the lowest for older adults (8%E). This trend across lifecycle stages has also been observed for added sugars. The available data also suggest that, while some reductions in sugar intake are observed in a few individual studies, overall intakes of free/added sugars remain above recommendations. However, any wider conclusions are hampered by a lack of detailed high-quality data on sugar intake, especially in developing countries. Furthermore, there is a need for harmonisation of terms describing sugars (ideally driven by public health objectives) and for collaborative efforts to ensure that the most up-to-date food composition data are used to underpin recommendations and any estimates of intake or modelling scenarios.

The coronavirus disease 2019 (COVID-19) pandemic has generated high interest in factors modulating risk of infection, disease severity and recovery. Vitamin D has garnered interest since it is known to modulate immune function and vitamin D deficiency is associated with increased risk of respiratory infections and adverse health outcomes in severely ill patients. There are no population representative data on the direct relationship between vitamin D status and severe acute respiratory syndrome coronavirus 2 infection risk and severity of COVID-19. Data from intervention studies are limited to four studies. Here we summarise findings regarding vitamin D status and metabolism and their alterations during severe illness, relevant to COVID-19 patients. Further, we summarise vitamin D intervention studies with respiratory disease outcomes and in critically ill patients and provide an overview of relevant patient and population guidelines. Vitamin D deficiency is highly prevalent in hospitalised patients, particularly when critically ill, including those with COVID-19. Acute and critical illness leads to pronounced changes in vitamin D metabolism and status, suggestive of increased requirements. This needs to be considered in the interpretation of potential links between vitamin D status and disease risk and severity and for patient management. There is some evidence that vitamin D supplementation decreases the risk of respiratory tract infections, while supplementation of intensive care unit patients has shown little effect on disease severity or length of treatment. Considering the high prevalence of deficiency and low risks associated with supplementation, pro-actively applying current population and patient management guidelines to prevent, monitor and correct vitamin D deficiency is appropriate.

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.

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.

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.

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.

Dietary intake and tissue levels of carotenoids have been associated with a reduced risk of several chronic diseases, including cardiovascular diseases, type 2 diabetes, obesity, brain-related diseases and some types of cancer. However, intervention trials with isolated carotenoid supplements have mostly failed to confirm the postulated health benefits. It has thereby been speculated that dosing, matrix and synergistic effects, as well as underlying health and the individual nutritional status plus genetic background do play a role. It appears that our knowledge on carotenoid-mediated health benefits may still be incomplete, as the underlying mechanisms of action are poorly understood in relation to human relevance. Antioxidant mechanisms – direct or via transcription factors such as NRF2 and NF-κB – and activation of nuclear hormone receptor pathways such as of RAR, RXR or also PPARs, via carotenoid metabolites, are the basic principles which we try to connect with carotenoid-transmitted health benefits as exemplified with described common diseases including obesity/diabetes and cancer. Depending on the targeted diseases, single or multiple mechanisms of actions may play a role. In this review and position paper, we try to highlight our present knowledge on carotenoid metabolism and mechanisms translatable into health benefits related to several chronic diseases.

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.

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.

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.

The global COVID-19 (coronavirus disease 2019) pandemic has become a complex problem that overlaps with a growing public health problem, obesity. Obesity alters different components of the innate and adaptive immune responses, creating a chronic and low-grade state of inflammation. Nutritional status is closely related to a better or worse prognosis of viral infections. Excess weight has been recognised as a risk factor for COVID-19 complications. In addition to the direct risk, obesity triggers other diseases such as diabetes and hypertension, increasing the risk of severe COVID-19. The present review explains the diets that induce obesity and the importance of different foods in this process. We also review tissue disruption in obesity, leading to impaired immune responses and the possible mechanisms by which obesity and its co-morbidities increase COVID-19 morbidity and mortality. Nutritional strategies that support the immune system in patients with obesity and with COVID-19 are also discussed in light of the available data, considering the severity of the infection. The discussions held may contribute to combating this global emergency and planning specific public health policy.