Oxidative stress plays a major role in the pathogenesis of diabetes mellitus, which further exacerbates damage of cardiac, hepatic and other tissues. We have recently reported that Zn supplementation beneficially modulates hyperglycaemia and hypoinsulinaemia, with attendant reduction of associated metabolic abnormalities in diabetic rats. The present study assessed the potential of Zn supplementation in modulating oxidative stress and cardioprotective effects in diabetic rats. Diabetes was induced in Wistar rats with streptozotocin, and groups of diabetic rats were treated with 5- and 10-fold dietary Zn interventions (0·19 and 0·38 g Zn/kg diet) for 6 weeks. The markers of oxidative stress, antioxidant enzyme activities and concentrations of antioxidant molecules, lipid profile, and expressions of fibrosis and pro-apoptotic factors in the cardiac tissue were particularly assessed. Supplemental Zn showed significant attenuation of diabetes-induced oxidative stress in terms of altered antioxidant enzyme activities and increased the concentrations of antioxidant molecules. Hypercholesterolaemia and hyperlipidaemia were also significantly countered by Zn supplementation. Along with attenuated oxidative stress, Zn supplementation also showed significant cardioprotective effects by altering the mRNA expressions of fibrosis and pro-apoptotic factors (by >50 %). The expression of lipid oxidative marker 4-hydroxy-2-nonenal (4-HNE) protein in cardiac tissue of diabetic animals was rectified (68 %) by Zn supplementation. Elevated cardiac and hepatic markers in circulation and pathological abnormalities in cardiac and hepatic tissue architecture of diabetic animals were ameliorated by dietary Zn intervention. The present study indicates that Zn supplementation can attenuate diabetes-induced oxidative stress in circulation as well as in cardiac and hepatic tissues.

An olive oil bioactive extract (OBE) rich in bioactive compounds like polyphenols, triterpenic acids, long-chain fatty alcohols, unsaturated hydrocarbons, tocopherols and sterols was tested (0, 0·08, 0·17, 0·42 and 0·73 % OBE) in diets fed to sea bream (Sparus aurata) (initial weight: 5·4 (sd 1·2) g) during a 90-d trial (four replicates). Fish fed diets containing 0·17 and 0·42 % OBE were 5 % heavier (61·1 (sd 1·6) and 60·3 (sd 1·1) g, respectively) than those of the control group (57·0 (sd 0·7) g), although feed conversion ratio and specific feed intake did not vary. There were no differences in lipid peroxidation (LPO) levels, catalase, glutathione reductase and glutathione S-transferase activities in the intestine and liver, although there was a tendency of lower intestinal and hepatic LPO levels in fish fed OBE diets. No differences in villus size were found among treatments, whereas goblet cell density in the control group was on average14·3 % lower than in fish fed OBE diets. The transcriptomic profiling of intestinal markers, covering different biological functions like (i) cell differentiation and proliferation, (ii) intestinal permeability, (iii) enterocyte mass and epithelial damage, (iv) IL and cytokines, (v) pathogen recognition receptors and (vi) mitochondria function, indicated that among the eighty-eight evaluated genes, twenty-nine were differentially expressed (0·17 % OBE diet), suggesting that the additive has the potential of improving the condition and defensive role of the intestine by enhancing the maturation of enterocytes, reducing oxidative stress, improving the integrity of the intestinal epithelium and enhancing the intestinal innate immune function, as gene expression data indicated.

The biohydrogenation theory of milk fat depression (MFD) attributes decreases in milk fat in cows to the formation of specific fatty acids (FA) in the rumen. Trans-10, cis-12-CLA is the only biohydrogenation intermediate known to inhibit milk fat synthesis, but it is uncertain if increased ruminal synthesis is the sole explanation of MFD. Four lactating cows were used in a 4×4 Latin square with a 2×2 factorial arrangement of treatments and 35-d experimental periods to evaluate the effect of diets formulated to cause differences in ruminal lipid metabolism and milk fat synthesis on the flow of FA and dimethyl acetal at the omasum. Treatments comprised total mixed rations based on grass silage with a forage:concentrate ratio of 35:65 or 65:35 containing 0 or 50 g/kg sunflower oil (SO). Supplementing the high-concentrate diet with SO lowered milk fat synthesis from −20·2 to −31·9 % relative to other treatments. Decreases in milk fat were accompanied by alterations in ruminal biohydrogenation favouring the trans-10 pathway and an increase in the formation of specific intermediates including trans-4 to trans-10-18 : 1, trans-8, trans-10-CLA, trans-9, cis-11-CLA and trans-10, cis-15-18 : 2. Flow of trans-10, cis-12-CLA at the omasum was greater on high- than low-concentrate diets but unaffected by SO. In conclusion, ruminal trans-10, cis-12-CLA formation was not increased on a diet causing MFD suggesting that other biohydrogenation intermediates or additional mechanisms contribute to the regulation of fat synthesis in the bovine mammary gland.

Nutrition during pregnancy can impact on the susceptibility of the offspring to CVD. Postnatal consumption of trans-fatty acids (TFA), associated with partially hydrogenated vegetable oil (PHVO), increases the risk of atherosclerosis, whereas evidence for those TFA associated with ruminant-derived dairy products and meat remain equivocal. In this study, we investigate the impact of maternal consumption of dietary PHVO (P) and ruminant milk fat (R) on the development of atherosclerosis in their offspring, using the transgenic apoE*3 Leiden mouse. Dams were fed either chow (C) or one of three high-fat diets: a diet reflecting the SFA content of a ‘Western’ diet (W) or one enriched with either P or R. Diets were fed during either pregnancy alone or pregnancy and lactation. Weaned offspring were then transferred to an atherogenic diet for 12 weeks. Atherosclerosis was assessed as lipid staining in cross-sections of the aorta. There was a significant effect of maternal diet during pregnancy on development of atherosclerosis (P=0·013) in the offspring with those born of mothers fed R or P during pregnancy displaying smaller lesions that those fed C or W. This was not associated with changes in total or lipoprotein cholesterol. Continuing to feed P during lactation increased atherosclerosis compared with that seen in offspring of dams fed P only during pregnancy (P<0·001). No such effect was seen in those from mothers fed R (P=0·596) or W (P=901). We conclude that dietary TFA have differing effects on cardiovascular risk at different stages of the lifecycle.

The incidence of type 2 diabetes mellitus (T2DM) is increasing worldwide, including in developing countries, particularly in South Asia. Intakes of foods generating a high postprandial glucose (PPG) response have been positively associated with T2DM. As part of efforts to identify effective and feasible strategies to reduce the glycaemic impact of carbohydrate-rich staples, we previously found that addition of guar gum (GG) and chickpea flour (CPF) to wheat flour could significantly reduce the PPG response to flatbread products. On the basis of the results of an exploratory study with Caucasian subjects, we have now tested the effect of additions of specific combinations of CPF with low doses of GG to a flatbread flour mix for their impacts on PPG and postprandial insulin (PPI) responses in a South-Asian population. In a randomised, placebo-controlled full-cross-over design, fifty-six healthy Indian adults consumed flatbreads made with a commercial flatbread mix (100 % wheat flour) with no further additions (control) or incorporating 15 % CPF in combination with 2, 3 or 4 % GG. The flatbreads with CPF and 3 or 4 % GG significantly reduced PPG (both ≥15 % reduction in positive incremental AUC, P<0·01) and PPI (both ≥28 % reduction in total AUC, P<0·0001) compared with flatbreads made from control flour. These results confirm the efficacy and feasibility of the addition of CPF with GG to flatbread flour mixes to achieve significant reductions in both PPG and PPI in Indian subjects.

The post-lunch dip in cognition is a well-established phenomenon of decreased alertness, memory and vigilance after lunch consumption. Lunch composition reportedly influences the post-lunch dip. Moreover, dieting is associated with cognitive function impairments. The negative effects of dieting have been reversed with nut-supplemented diets. The aims of this study were to (1) evaluate the acute effect of an almond-enriched high-fat lunch or high-carbohydrate lunch on the post-lunch decline in cognitive function, and (2) evaluate the effects of chronic almond consumption as part of an energy-restricted diet on the memory and attention domains of cognitive function. In total, eighty-six overweight and obese adults were randomised to consume either an almond-enriched diet (AED) or a nut-free control diet (NFD) over a 12-week weight loss intervention. Participants were also randomised to receive either an almond-enriched high-fat lunch (A-HFL) (>55 % energy from fat, almonds contributing 70–75 % energy) or a high-carbohydrate lunch (HCL) (>85 % energy from carbohydrates) at the beginning and end of the weight loss intervention. Memory and attention performance indices decreased after lunch consumption (P<0·001). The A-HFL group ameliorated the decline in memory scores by 57·7 % compared with the HCL group (P=0·004). Both lunch groups had similar declines in attention. Moreover, memory and attention performance indices increased after the 12-week intervention period (P<0·05) with no difference between the AED and NFD groups. In conclusion, almond consumption at a midday meal can reduce the post-lunch dip in memory. However, long-term almond consumption may not further improve cognitive function outcomes in a weight loss intervention.

TAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf>400), in partially hydrolysed remnants (Sf 20–400) and in a TAG-deplete fraction (Sf<20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf<20 fraction (70–75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf<20 fraction. However, approximately 40 % of subjects demonstrated exaggerated postprandial lipaemia specifically in response to the SFA-rich PO meal, with a transient shift to more buoyant chylomicron fractions. The latter demonstrates that heterogeneity in the magnitude and duration of hyper-remnantaemia is dependent on both the nature of the meal fatty acids ingested and possible metabolic determinants that influence chylomicron metabolism. The study findings reiterate that fasting plasma TAG is a poor indicator of atherogenic chylomicron remnant homoeostasis and emphasises the merits of considering specifically, chylomicron remnant abundance and kinetics in the context of atherogenic risk. Few studies address the latter, despite the majority of life being spent in the postprandial and absorptive state.

In this paper, we decompose the difference between the weight of a child and the weight of a reference child into the difference between the height of the child and the height of the reference child and the difference between the weight per unit height of the child and the weight per unit height of the reference child. The decomposition provides the theoretical justification to the classification of the nutritional status proposed by Svedberg and by Nandy et al. An application of the decomposition framework to the Indian data shows that the level, depth and severity of the faltering of the growth of the body mass in Indian children are primarily due to the level, depth and severity of the faltering of the ponderal growth.

I is an important mineral for health, required for the production of key thyroid hormones, which are essential for cellular metabolism, growth and physical development. Hence, adequate I is crucial at all stages of life, but imperative during pregnancy for fetal brain development and during a child’s early life for neurodevelopment. Within Ireland, limited information exists on population I intakes and status. Therefore, the purposes of the present analysis were to estimate dietary I intakes and to analyse urinary iodine (UI) status using the cross-sectional National Adult Nutrition Survey 2008–2010 and the most recent Irish Total Diet Study. Median I intakes in the total population (n 1106) were adequate with only 26 % of the population being classified as below the estimated average requirement (EAR). Milk consumption was the major source of I in the diet, contributing 45 % to total intake. Likewise, median UI concentrations (107 µg/l) indicated ‘optimal’ I nutrition according to the WHO cut-off points. In our cohort, 77 % of women of childbearing age (18–50 years) did not meet the EAR recommendation set for pregnant women. Although I is deemed to be sufficient in the majority of adult populations resident in Ireland, any changes to the current dairy practices could significantly impact intake and status. Continued monitoring should be of priority to ensure that all subgroups of the population are I sufficient.

Glycaemic index (GI) and glycaemic load (GL) are indicators of dietary carbohydrate quantity and quality and have been associated with increased risk of certain cancers and type 2 diabetes. Insulin resistance has been associated with increased melanoma risk. However, GI and GL have not been investigated for melanoma. We present the first study to examine the possible association of GI and GL with melanoma risk. We carried out a population-based, case–control study involving 380 incident cases of cutaneous melanoma and 719 age- and sex-matched controls in a northern Italian region. Dietary GI and GL were computed for each subject using data from a self-administered, semi-quantitative food frequency questionnaire. We computed the odds ratio (OR) for melanoma according to quintiles of distribution of GL and GL among controls. A direct association between melanoma risk and GL emerged in females (OR 2·38; 95 % CI 1·25, 4·52 for the highest v. the lowest quintile of GL score, Pfor trend 0·070) but not in males. The association in females persisted in the multivariable analysis after adjusting for several potential confounders. There was no evidence of an association between GI and melanoma risk. GL might be associated with melanoma risk in females.

The occurrence of thyroid disorders relies on I nutrition and monitoring of all populations is recommended. Measuring I in urine is standard but thyroglobulin in serum is an alternative. This led us to assess the reliability of studies using serum thyroglobulin compared with urinary I to assess the I nutrition level and calculate the number of participants needed in a study with repeated data sampling in the same individuals for 1 year. Diet, supplement use and life style factors were assessed by questionnaires. We measured thyroglobulin and thyroglobulin antibodies in serum and I in urine. Participants were thirty-three Caucasians and sixty-four Inuit living in Greenland aged 30–49 years. Serum thyroglobulin decreased with rising I excretion (Kendall’s τ −0·29, P=0·005) and did not differ with ethnicity. Variation in individuals was lower for serum-thyroglobulin than for urinary I (mean individual CV: 15·1 v. 46·1 %; P<0·01). It required 245 urine samples to be 95 % certain of having a urinary I excretion within 10 % of the true mean of the population. For serum-thyroglobulin the same precision required 206 samples. In an individual ten times more samples were needed to depict I deficiency when using urinary I excretion compared with serum-thyroglobulin. In conclusion, more participants are need to portray I deficiency in a population when using urinary I compared with serum-thyroglobulin, and about ten times more samples are needed in an individual. Adding serum-thyroglobulin to urinary I may inform surveys of I nutrition by allowing subgroup analysis with similar reliability.

Diet is a major modifiable lifestyle factor that may affect the components of the metabolic syndrome. We aimed to investigate the association between relative proportions of macronutrients and the components of the metabolic syndrome in a population of individuals with type 1 diabetes. In all, 791 individuals without nephropathy, with plausible energy intake and known metabolic syndrome status, taking part in the Finnish Diabetic Nephropathy Study were included in the analyses. Dietary data were collected with a diet record. The association between the relative macronutrient intake and the outcome variables were analysed using multivariable nutrient density substitution models. The relative proportions of dietary macronutrients or fatty acids were not associated with the presence of the metabolic syndrome. In men, however, favouring carbohydrates over fats was associated with lower odds of the waist component, whereas favouring either carbohydrates or fats over proteins was associated with lower odds of the blood pressure component of the metabolic syndrome. In women, substituting carbohydrates for fats was associated with lower HDL-cholesterol concentration. Substituting carbohydrates or fats for alcohol or protein was, in men, associated with lower systolic blood pressure. To conclude, the relative distribution of macronutrients may have some relevance for the metabolic syndrome.

Recently, countries at high latitudes have updated their vitamin D recommendations to ensure adequate intake for the musculoskeletal health of their respective populations. In 2010, the dietary guidelines for vitamin D for Canadians and Americans aged 1–70 years increased from 5 μg/d to 15 μg/d, whereas in 2016 for citizens of the UK aged ≥4 years 10 μg/d is recommended. The vitamin D status of Canadian children following the revised dietary guidelines is unknown. Therefore, this study aimed to assess the prevalence and determinants of vitamin D deficiency and sufficiency among Canadian children. For this study, we assumed serum 25-hydroxy vitamin D (25(OH)D) concentrations <30 nmol/l as ‘deficient’ and ≥50nmol/l as ‘sufficient’. Data from children aged 3–18 years (n 2270) who participated in the 2012/2013 Canadian Health Measures Survey were analysed. Of all children, 5·6 % were vitamin D deficient and 71 % were vitamin D sufficient. Children who consumed vitamin D-fortified milk daily (77 %) were more likely to be sufficient than those who consumed it less frequently (OR 2·7; 95 % CI 1·4, 5·0). The 9 % of children who reported taking vitamin D-containing supplements in the previous month had higher 25(OH)D concentrations (OR 6·9 nmol/l; 95 % CI 1·1, 12·7 nmol/l) relative to those who did not. Children who were older, obese, of non-white ethnicity and from low-income households were less likely to be vitamin D sufficient. To improve vitamin D status, consumption of vitamin D-rich foods should be promoted, and fortification of more food items or formal recommendations for vitamin D supplementation should be considered.

Perinatal exposure to nutrients and dietary components may affect the risk for coeliac disease (CD). We investigated the association between maternal use of vitamin D, n-3 fatty acids (FA) and Fe supplements during pregnancy and risk for CD autoimmunity (CDA) and CD in the offspring. Children at increased genetic risk were prospectively followed from birth in The Environmental Determinants of Diabetes in the Young (TEDDY) study. CDA was defined as having persistently positive tissue transglutaminase autoantibodies (tTGA). Diagnosis of CD was either biopsy-confirmed or considered likely if having persistently elevated levels of tTGA>100 AU. Of 6627 enrolled children, 1136 developed CDA at a median 3·1 years of age (range 0·9–10) and 409 developed CD at a median 3·9 years of age (range 1·2–11). Use of supplements containing vitamin D, n-3 FA and Fe was recalled by 66, 17 and 94 % of mothers, respectively, at 3–4 months postpartum. The mean cumulative intake over the entire pregnancy was 2014 μg vitamin D (sd 2045 μg), 111 g n-3 FA (sd 303 g) and 8806 mg Fe (sd 7017 mg). After adjusting for country, child’s human leucocyte antigen genotype, sex, family history of CD, any breast-feeding duration and household crowding, Cox’s proportional hazard ratios did not suggest a statistically significant association between the intake of vitamin D, n-3 FA or Fe, and risk for CDA or CD. Dietary supplementation during pregnancy may help boost nutrient intake, but it is not likely to modify the risk for the disease in the offspring.

Nutritional requirements and responses of all organisms are estimated using various models representing the response to different dietary levels of the nutrient in question. To help nutritionists design experiments for estimating responses and requirements, we developed a simulation workbook using Microsoft Excel. The objective of the present study was to demonstrate the influence of different numbers of nutrient levels, ranges of nutrient levels and replications per nutrient level on the estimates of requirements based on common nutritional response models. The user provides estimates of the shape of the response curve, requirements and other parameters and observation to observation variation. The Excel workbook then produces 1–1000 randomly simulated responses based on the given response curve and estimates the standard errors of the requirement (and other parameters) from different models as an indication of the expected power of the experiment. Interpretations are based on the assumption that the smaller the standard error of the requirement, the more powerful the experiment. The user can see the potential effects of using one or more subjects, different nutrient levels, etc., on the expected outcome of future experiments. From a theoretical perspective, each organism should have some enzyme-catalysed reaction whose rate is limited by the availability of some limiting nutrient. The response to the limiting nutrient should therefore be similar to enzyme kinetics. In conclusion, the workbook eliminates some of the guesswork involved in designing experiments and determining the minimum number of subjects needed to achieve desired outcomes.