The cardiometabolic syndrome (MetS) is a clustering of related metabolic abnormalities including abdominal adiposity, insulin resistance, hypertension, dyslipidaemia and increased inflammatory and thrombotic markers, which is linked to increased risk of type 2 diabetes, CVD and overall mortality. Several cross-sectional and prospective studies have shown an association between low vitamin D status, as indicated by concentrations of serum 25-hydroxyvitamin D (s25(OH)D), and increased prevalence of the MetS and individual CVD risk factors. These epidemiological observations are supported by mechanistic studies but experimental data are limited. The available data from intervention studies are largely confounded as most vitamin D supplementation trials were mainly carried out to explore the role of Ca in CVD and include Ca in the treatment arms. Inadequate consideration of seasonal effects on s25(OH)D concentrations is also a common design flaw in most studies. Further complications arise from shared risk factors such as adiposity and ageing, which predispose individuals to exhibit both a more pronounced risk profile and relatively lower s25(OH)D concentrations. In conclusion, while epidemiological associations are promising and a rationale for low vitamin D status as a potentially modifiable risk factor for CVD is supported by mechanistic data, suitable experimental data from appropriately designed trials are just beginning to emerge. As yet, this body of literature is too immature to draw firm conclusions on the role of vitamin D in CVD prevention. Carefully controlled vitamin D trials in well-described population groups using intervention doses that are titrated against target s25(OH)D concentrations could yield potentially valuable outcomes that may have a positive impact on CVD risk modification.

Although stearic acid is a saturated fatty acid, its influence on plasma cholesterol acid other health variables is neutral; possibly owing in part to poor absorption. Reduced absorption of stearic acid from particular triacylglycerols, cocoa butter and novel fats formulated with short- and long-chain acid triacylglycerol molecules (Salatrims) has been attributed to high intakes. However, the circumstances and causes of poor stearic acid digestion from triacylglycerols are unclear; published data were therefore collected and analysed, with emphasis on human studies. Of twenty-eight studies conducted in adults, most are in men (>90%). The assertion that reduced absorption is due to a high intake of stearoyl groups is not supported: dietary intakes of stearoyl of 0·05–0·65 g stearic acid equivalent/kg body weight (cf typical intake of 0·2 g stearic acid equivalent/kg body weight in the Western diet) indicate that the ‘true’ digestibility of stearoyl is 0·98 (SE 0·01) g/g, with apparent digestibility less than this value at low intakes owing to endogenous stearic acid excretion and to inter-publication variation of unidentified cause. The neutral health impact of stearic acid must be due to factors other than availability. Exceptions include cocoa butter, Salatrims and tristearin, for which digestibility is an additional factor. The efficiency with which human subjects digest stearoyl from cocoa butter still remains uncertain, while the digestion of total long-chain fat from this source is 0·89–0·95 g/g, high in comparison with 0·33 g/g for Salatrim 23CA and 0·15 g/g for tristearin in their prepared states. Salatrims contain the highest proportion of long-chain fatty acids that are stearic acid-rich other than tristearin, which is the main component of fully-hydrogenated soyabean and rapeseed oil. Analysis shows that apparent digestibility of stearic acid is associated with stearoyl density within the triacylglycerol molecule and that, in Salatrims, the occurrence of short-chain fatty acids in place of long-chain fatty acids increases this density. Soap formation appears not to be a major factor in the reduced digestion of stearic acid from tristearin under regular dietary circumstances, but both microcrystallinity and reduced digestibility of tri-, di- and monostearoylglycerols appears to be important. Solubilisation of high-melting-point tristearin in low-melting-point oils improves the digestibility of its stearic acid, particularly when emulsified or liquidized at above melting point. However, without such artificial aids, the digestive tracts of the rat, dog and man have a low capacity for emulsifying and digesting stearic acid from tristearin. Reduced digestibility of stearic acid from Salatrim 23CA also appears to be attributable to reduced digestibility of di- and monostearoylglycerols and is particularly due to remnants with the 1- or 3-stearoylglycerol intact after initial hydrolytic cleavage. Short-chain organic acid in Salatrim 23CA, which is readily hydrolysed, leaves such remnants. Unlike tristearin, Salatrim 23CA melts at body temperature and mixing it with low-melting-point oils is not expected to cause further disruption of microcrystalline structures to aid digestibility of its stearoyl groups. The low digestibility of stearoyl in Salatrim 23CA, together with the occurrence of short-chain organic acids in this product, account for its relatively low nutritional energy value (about 20 kJ (5 kcal)/g) compared with traditional fats (37 kJ (9 kcal)/g) and low fat value (<20:37 kJ/kJ; <5:9 kcal/kcal) relative to traditional fats. In part these differences are because of minor effects of Salatrim 23CA on the excretion of other fat and protein, due to the bulking properties of this poorly-digestible fat.

Iodine deficiency affects an estimated 241 million school-aged children in the world. Little is known about iodine deficiency in relation to auditory function, except for the fact that deaf–mutism is one of the features of cretinism. In the present review, we documented the scientific knowledge on the role of iodine and hypothyroidism in the auditory system. We found that ear development and hearing function depend on thyroid hormones. Multiple pathways are involved in this, including both inner ear morphology as well as neurological processes. Conductive as well as sensorineural hearing loss is found in studies with animals that were rendered hypothyroidic. In humans, auditory impairment is reported frequently in relation to hypothyroidism, ranging from mild disturbances to severe handicap. Auditory impairment has been related more explicitly to congenital hypothyroidism than to acquired hypothyroidism. The critical period for thyroid function-related hearing maturation is the first and second trimesters of pregnancy. Although only a limited number of studies have directly investigated the relationship between iodine deficiency and auditory function, most studies point toward an association. However, evidence from good randomised controlled trials is lacking. Inclusion of auditory outcomes in iodine supplementation studies is therefore to be recommended, especially for trials in pregnancy. Hearing deficit is an invisible abnormality, but has major consequences for educational and social skills if not detected. In view of this, auditory impairment should be mapped in iodine-deficient areas in order to realistically estimate the magnitude of the problem.

Parkinson’s disease (PD) is the second most common neurodegenerative disorder. It is characterised by the progressive degeneration of dopaminergic (DA) neurons. The cause of degeneration is not well understood; however, both genetics and environmental factors, such as nutrition, have been implicated in the disease process. Deficiencies in one-carbon metabolism in particular have been associated with increased risk for PD onset and progression, though the precise relationship is unclear. The aim of the present review is to determine the role of one-carbon metabolism and elevated levels of homocysteine in PD onset and pathology and to identify potential mechanisms involved. A search of PubMed, Google Scholar and Web of Science was undertaken to identify relevant human and animal studies. Case–control, prospective cohort studies, meta-analyses and non-randomised trials were included in the present review. The results from human studies indicate that polymorphisms in one-carbon metabolism may increase risk for PD development. There is an unclear role for dietary B-vitamin intake on PD onset and progression. However, dietary supplementation with B-vitamins may be beneficial for PD-affected individuals, particularly those on l-DOPA (levodopa or l-3,4-dihydroxyphenylalanine) treatment. Additionally, one-carbon metabolism generates methyl groups, and methylation capacity in PD-affected individuals is reduced. This reduced capacity has an impact on expression of disease-specific genes that may be involved in PD progression. During B-vitamin deficiency, animal studies report increased vulnerability of DA cells through increased oxidative stress and altered methylation. Nutrition, especially folates and related B-vitamins, may contribute to the onset and progression of PD by making the brain more vulnerable to damage; however, further investigation is required.

Epidemiological evidence consistently shows that diets high in fresh fruit and vegetables significantly lower cancer risk. Given the postulated role of oxidative DNA damage in carcinogenesis, the assumption has been made that it is the antioxidant properties of food constituents, such as vitamin C, E and carotenoids, which confer protection. However, epidemiological studies with specific antioxidants, either singly or in combination, have not, on the whole, supported this hypothesis. In contrast, studies examining the in vitro effect of antioxidants upon oxidative DNA damage have generally been supportive, in terms of preventing damage induction. The same, however, cannot be said for the in vivo intervention studies where overall the results have been equivocal. Nevertheless, recent work has suggested that some dietary antioxidants may confer protective properties through a novel mechanism, unrelated to their conventional free-radical scavenging abilities. Upregulation of antioxidant defence, xenobiotic metabolism, or DNA-repair genes may all limit cellular damage and hence promote maintenance of cell integrity. However, until further work has clarified whether dietary supplementation with antioxidants confers a reduced risk of cancer and the mechanism by which this effect is exerted, the recommendation for a diet rich in fruit and vegetables remains valid empirically.

Protein is important for growth, maintenance and protection of the body. Both adequacy of protein quantity and protein quality in the diet are important to guarantee obtaining all the essential amino acids. Protein–energy malnutrition is widely present in developing countries such as Nigeria and might result in stunting and wasting. Needs for protein differ depending on age and physiological status and are higher during growth, pregnancy and lactation. The present review assessed protein quantity and quality in diets of Nigerian infants, children, adolescents, and pregnant and lactating women. Literature reviews and calculations were performed to assess adequacy of Nigerian protein intake and to examine the Nigerian diet. The digestible indispensable amino acid score was used to calculate protein quality of nine Nigerian staple foods and of a mixture of foods. The Nigerian population had mostly adequate protein intake when compared with the most recent protein recommendations by the FAO (2013) and WHO/FAO/UNU (2007). An important exception was the protein intake of adolescent girls and pregnant and lactating women. Most of the assessed Nigerian plant-based staple foods were of low protein quality and predominantly lacked the amino acid lysine. The addition of animal-source foods can bridge the protein quality gap created by predominance of plant-based foods in the Nigerian diet. The methodology of this review can be applied to other low- and middle-income countries where diets are often plant-based and lack variety, which might influence protein intake adequacy.

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.

Hormesis defines an effect where exposure to a low dose of a toxic agent results in a beneficial response. It has been described in organisms exposed to low-dose radiation, heat stress, and chemicals. The effect is characterised by a J-shaped dose–response as opposed to a linear dose–response. Confirmation of the general phenomena of hormesis has proved difficult due to the lack of appropriate methodology and the absence of well-defined mechanisms to support the experimental observations. In the nutritional field there are few reports of its existence. The clearest illustration of the effect is seen in animals that are energy restricted when there is a clear benefit in the reduction of age-related disease, and an extension of maximum lifespan. DNA microarray experiments have shown that there is a down regulation of the stress-response genes that are up regulated through the ageing process. Electrophilic phytochemicals, that have been shown to have beneficial health effects at low doses, up regulate the antioxidant–electrophile response element. This probably occurs through an alteration in the redox state of the target cells which causes activation of protein kinases, the activation of the Nrf2 transcription factor and the up regulation of the phase II enzymes, similar to responses that occur under mild chemical stress. This situation might enable organisms to adapt to stress such that the effects of a subsequent exposure to a harmful challenge are reduced. There may be a permanent alteration in cellular homeostasis, or redox state, if the low level exposure is maintained. It remains to be proven if such a situation occurs in response to chronic low-dose exposure to dietary phytochemicals such that the target cells are better able to respond to a subsequent stress challenge.

Personalised nutrition is at its simplest form the delivery of dietary advice at an individual level. Incorporating response to different diets has resulted in the concept of precision nutrition. Harnessing the metabolic phenotype to identify subgroups of individuals that respond differentially to dietary interventions is becoming a reality. More specifically, the classification of individuals in subgroups according to their metabolic profile is defined as metabotyping and this approach has been employed to successfully identify differential response to dietary interventions. Furthermore, the approach has been expanded to develop a framework for the delivery of targeted nutrition. The present review examines the application of the metabotype approach in nutrition research with a focus on developing personalised nutrition. Application of metabotyping in longitudinal studies demonstrates that metabotypes can be associated with cardiometabolic risk factors and diet-related diseases while application in interventions can identify metabotypes with differential responses. In general, there is strong evidence that metabolic phenotyping is a promising strategy to identify groups at risk and to potentially improve health promotion at a population level. Future work should verify if targeted nutrition can change behaviours and have an impact on health outcomes.

There is considerable epidemiological evidence that a Western-style diet may increase the risk of certain hormone-dependent conditions in men via its effects on hormone metabolism. Experimental evidence also suggests that dietary factors may exert subtle effects on hormone metabolism. Here we review the clinical and epidemiological evidence that diet is associated with circulating sex hormone levels in men. In comparison with factors such as age and BMI, nutrients do not appear to be strong determinants of sex hormone levels. Dietary intervention studies have not shown that a change in dietary fat and/or dietary fibre intake is associated with changes in circulating sex hormone concentrations over the short term. The data on the effects of dietary phyto-oestrogens on sex hormone levels in men are too limited for conclusions to be drawn. Observational studies between men from different dietary groups have shown that a vegan diet is associated with small but significant increases in sex-hormone-binding globulin and testosterone concentrations in comparison with meat-eaters. However, these studies have not demonstrated that variations in dietary composition have any long-term important effects on circulating bioavailable sex hormone levels in men. This lack of effect may be partly explained by the body's negative feedback mechanism, which balances out small changes in androgen metabolism in order to maintain a constant level of circulating bioavailable androgens. It appears, therefore, that future studies should look for dietary effects on the feedback mechanism itself, or on the metabolism of androgens within the target tissues.

N and S metabolisms are closely interwoven throughout both the plant and animal kingdoms. The essentiality of S relates to its participation in the structure of S-containing amino acids (SAA), to its inclusion in many sulfonated molecules, and to a myriad of metabolic and catalytic reactions of vital importance. Methionine (Met) is the indispensable SAA supplied by food proteins and its plasma homeostasis is achieved via a number of highly efficient regulatory mechanisms. In all conditions characterised by a negative body protein balance such as in dietary restriction or cytokine-induced hypercatabolic losses, N and S endogenous pools manifest parallel tissue depletion rates. Adaptive conservation of N and S body stores is reached by a functional restraint of the trans-sulfuration cascade, through the depression of cystathionine β-synthase activity. As a result, upstream accumulation of homocysteine favours its re-methylation conversion to Met which helps maintain metabolic pathways of survival value. In addition to the measurement of vitamin indices, that of plasma transthyretin, a sensitive marker of protein nutritional status, is proposed to identify the fluctuations of the total body N component accountable for the alterations of homocysteine concentrations in body fluids.

Poor diets, including excess added sugar consumption, contribute to the global burden of disease. Subsequently, many nutrition policies have been implemented to reduce added sugar intake and improve population health, including taxes, education, labelling and environmental interventions. A potential consequence of these policy actions is the substitution of added sugars with non-nutritive sweeteners (NNS) in a variety of foods and beverages. NNS are used to reduce the energy and sugar content of foods and beverages while maintaining their palatability. Evidence of the toxicological risks of NNS is inconsistent, though concerns have been raised over the potential substitution effects of ultra-processed foods containing NNS for whole foods. This review aimed to provide an overview of current NNS food supply and consumption patterns, assess added sugar-reduction policies and their impact on NNS, and determine the impact of NNS on food choice, energy intake and diet quality. NNS are widely available in a variety of products, though most commonly in carbonated beverages, dairy products, confectionery, table-top sweeteners and fruit drinks. However, the longitudinal trends of different product categories, and differences between geographies and economy-income levels, require further study. Few studies have examined NNS consumption trends globally, though an increase in NNS consumption in beverages has been observed in some regions. Research examining how the increased availability of low-sugar, NNS-containing products affects global dietary patterns is limited, particularly in terms of their potential substitution effects.

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.

In recent years there has been a rapid growth of interest in exploring the relationship between nutritional therapies and the maintenance of cognitive function in adulthood. Emerging evidence reveals an increasingly complex picture with respect to the benefits of various food constituents on learning, memory and psychomotor function in adults. However, to date, there has been little consensus in human studies on the range of cognitive domains to be tested or the particular tests to be employed. To illustrate the potential difficulties that this poses, we conducted a systematic review of existing human adult randomised controlled trial (RCT) studies that have investigated the effects of 24 d to 36 months of supplementation with flavonoids and micronutrients on cognitive performance. There were thirty-nine studies employing a total of 121 different cognitive tasks that met the criteria for inclusion. Results showed that less than half of these studies reported positive effects of treatment, with some important cognitive domains either under-represented or not explored at all. Although there was some evidence of sensitivity to nutritional supplementation in a number of domains (for example, executive function, spatial working memory), interpretation is currently difficult given the prevailing ‘scattergun approach’ for selecting cognitive tests. Specifically, the practice means that it is often difficult to distinguish between a boundary condition for a particular nutrient and a lack of task sensitivity. We argue that for significant future progress to be made, researchers need to pay much closer attention to existing human RCT and animal data, as well as to more basic issues surrounding task sensitivity, statistical power and type I error.