Zn plays an important role in maintaining the anti-oxidant status within the heart and helps to counter the acute redox stress that occurs during myocardial ischaemia and reperfusion. Individuals with low Zn levels are at greater risk of developing an acute myocardial infarction; however, the impact of this on the extent of myocardial injury is unknown. The present study aimed to compare the effects of dietary Zn depletion with in vitro removal of Zn (N,N,N′,N′-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN)) on the outcome of acute myocardial infarction and vascular function. Male Sprague–Dawley rats were fed either a Zn-adequate (35 mg Zn/kg diet) or Zn-deficient (<1 mg Zn/kg diet) diet for 2 weeks before heart isolation. Perfused hearts were subjected to a 30 min ischaemia/2 h reperfusion (I/R) protocol, during which time ventricular arrhythmias were recorded and after which infarct size was measured, along with markers of anti-oxidant status. In separate experiments, hearts were challenged with the Zn chelator TPEN (10 µm) before ischaemia onset. Both dietary and TPEN-induced Zn depletion significantly extended infarct size; dietary Zn depletion was associated with reduced total cardiac glutathione (GSH) levels, while TPEN decreased cardiac superoxide dismutase 1 levels. TPEN, but not dietary Zn depletion, also suppressed ventricular arrhythmias and depressed vascular responses to nitric oxide. These findings demonstrate that both modes of Zn depletion worsen the outcome from I/R but through different mechanisms. Dietary Zn deficiency, resulting in reduced cardiac GSH, is the most appropriate model for determining the role of endogenous Zn in I/R injury.

Several studies analysed the associations between dietary carbohydrate intake, glycaemic index (GI) and glycaemic load (GL) and digestive system cancers; however, the results remain controversial. This study was to perform a meta-analysis evaluating the quantitative and dose–response associations between carbohydrate intake, GI and GL, and risk of digestive system cancers. We searched medical and biological databases up to June 2018 and identified twenty-six cohort studies and eighteen case–control studies. Meta-analytic fixed or random effects models were applied to process data. We also performed dose–response analysis, meta-regression and subgroup analyses. We found that high levels of GI were significantly associated with the risk of digestive system cancers at the highest compared with the lowest categories from cohort studies (summary relative risk (RR)=1·10, 95 % CI 1·05, 1·15). Similar effects were observed from case–control studies of the comparison between the extreme categories, but the difference did not reach statistical significance (summary OR=1·28, 95 % CI 0·97, 1·69). We also observed significant dose–response association between GI and digestive system cancers, with every 10-unit increase in GI (summary RR=1·003; 95 % CI 1·000, 1·012 for cohort studies; summary OR=1·09; 95 % CI 1·06, 1·11 for case–control studies). In addition, both cohort studies and case–control studies indicated that neither dietary carbohydrate intake nor GL bore any statistical relationship to digestive system cancers from the results of the highest compared with the lowest categories analyses and dose–response analyses. The results suggest a moderate association between high-GI diets and the risk of digestive system cancers.

Gluten is only partially digested by intestinal enzymes and can generate peptides that can alter intestinal permeability, facilitating bacterial translocation, thus affecting the immune system. Few studies addressed the role of diet with gluten in the development of colitis. Therefore, we investigate the effects of wheat gluten-containing diet on the evolution of sodium dextran sulphate (DSS)-induced colitis. Mice were fed a standard diet without (colitis group) or with 4·5 % wheat gluten (colitis + gluten) for 15 d and received DSS solution (1·5 %, w/v) instead of water during the last 7 d. Compared with the colitis group, colitis + gluten mice presented a worse clinical score, a larger extension of colonic injury area, and increased mucosal inflammation. Both intestinal permeability and bacterial translocation were increased, propitiating bacteria migration for peripheral organs. The mechanism by which diet with gluten exacerbates colitis appears to be related to changes in protein production and organisation in adhesion junctions and desmosomes. The protein α-E-catenin was especially reduced in mice fed gluten, which compromised the localisation of E-cadherin and β-catenin proteins, weakening the structure of desmosomes. The epithelial damage caused by gluten included shortening of microvilli, a high number of digestive vacuoles, and changes in the endosome/lysosome system. In conclusion, our results show that wheat gluten-containing diet exacerbates the mucosal damage caused by colitis, reducing intestinal barrier function and increasing bacterial translocation. These effects are related to the induction of weakness and disorganisation of adhesion junctions and desmosomes as well as shortening of microvilli and modification of the endocytic vesicle route.

We conducted a systematic review of randomised controlled trials (RCT) of increased intake of arachidonic acid (ARA) on fatty acid status and health outcomes in humans. We identified twenty-two articles from fourteen RCT. Most studies were conducted in adults. These used between 80 and 2000 mg ARA per d and were of 1–12 weeks duration. Supplementation with ARA doses as low as 80 mg/d increased the content of ARA in different blood fractions. Overall there seem to be few marked benefits for adults of increasing ARA intake from the typical usual intake of 100–200 mg/d to as much as 1000 mg/d; the few studies using higher doses (1500 or 2000 mg/d) also report little benefit. However, there may be an impact of ARA on cognitive and muscle function which could be particularly relevant in the ageing population. The studies reviewed here suggest no adverse effects in adults of increased ARA intake up to at least 1000–1500 mg/d on blood lipids, platelet aggregation and blood clotting, immune function, inflammation or urinary excretion of ARA metabolites. However, in many areas there are insufficient studies to make firm conclusions, and higher intakes of ARA are deserving of further study. Based on the RCT reviewed, there are not enough data to make any recommendations for specific health effects of ARA intake.

Fe therapy can be effective in heart failure patients both with and without anaemia. However, the role of Fe therapy in such patients is still uncertain. In this review, the aim was to evaluate the efficacy and safety of Fe therapy in adult patients with heart failure who have reduced ejection fraction (HFrEF). Multiple databases (PubMed, Medline, EMBASE, the Cochrane Library and Clinical Trials) were searched up to December 2017 and the reference lists of relevant articles obtained from the search were reviewed. Data extracted from randomised control trials (RCT) selected for the review were pooled using a fixed effects model or a random effects model, according to heterogeneity between trials. Nine RCT were included in this meta-analysis which included a total of 789 patients who received Fe therapy and who in turn were compared with 585 controls. There was significant improvement in the 6-min walk test (19·05 m, 95 % CI 10·48, 27·62) and peak VO2/kg (0·93 ml/kg per min, 95 % CI 0·16, 1·69) in the Fe supplementation arm. With Fe therapy, fewer patients were hospitalised for heart failure (OR: 0·42, 95 % CI 0·27, 0·65), but no relationship was found for total re-hospitalisation (OR: 0·70, 95 % CI 0·32, 1·51) or mortality (OR: 0·70, 95 % CI 0·38, 1·28). Fe therapy has the potential to improve exercise tolerance, reduce re-hospitalisations for patients with HFrEF having Fe deficiency. In addition, Fe supplementation was found to be safe, with no increased rate of adverse events.

The relationship between alcohol consumption and body weight is complex and inconclusive being potentially mediated by alcohol type, habitual consumption levels and sex differences. Heavy and regular alcohol consumption has been positively correlated with increasing body weight, although it is unclear whether this is due to alcohol consumption per se or to additional energy intake from food. This review explores the effects of alcohol consumption on food energy intake in healthy adults. CINAHL Plus, EMBASE, Medline and PsycINFO were searched through February 2018 for crossover and randomised controlled trials where an alcohol dose was compared with a non-alcohol condition. Study quality was assessed using the Effective Public Health Practice Project tool. A total of twenty-two studies involving 701 participants were included from the 18 427 papers retrieved. Studies consistently demonstrated no compensation for alcoholic beverage energy intake, with dietary energy intake not decreasing due to alcoholic beverage ingestion. Meta-analyses using the random-effects model were conducted on twelve studies and demonstrated that alcoholic beverage consumption significantly increased food energy intake and total energy intake compared with a non-alcoholic comparator by weighted mean differences of 343 (95 % CI 161, 525) and 1072 (95 % CI 820, 1323) kJ, respectively. Generalisability is limited to younger adults (18–37 years), and meta-analyses for some outcomes had substantial statistical heterogeneity or evidence of small-study effects. This review suggests that adults do not compensate appropriately for alcohol energy by eating less, and a relatively modest alcohol dose may lead to an increase in food consumption.

Muscle fibre types can transform from slow-twitch (slow myosin heavy chain (MyHC)) to fast-twitch (fast MyHC) or vice versa. Leucine plays a vital effect in the development of skeletal muscle. However, the role of leucine in porcine myofibre type transformation and its mechanism are still unclear. In this study, effects of leucine and microRNA-27a (miR-27a) on the transformation of porcine myofibre type were investigated in vitro. We found that leucine increased slow MyHC protein level and decreased fast MyHC protein level, increased the levels of phospho-protein kinase B (Akt)/Akt and phospho-forkhead box 1 (FoxO1)/FoxO1 and decreased the FoxO1 protein level. However, blocking the Akt/FoxO1 signalling pathway by wortmannin attenuated the role of leucine in porcine myofibre type transformation. Over-expression of miR-27a decreased slow MyHC protein level and increased fast MyHC protein level, whereas inhibition of miR-27a had an opposite effect. We also found that expression of miR-27a was down-regulated following leucine treatment. Moreover, over-expression of miR-27a repressed transformation from fast MyHC to slow MyHC caused by leucine, suggesting that miR-27a is interdicted by leucine and then contributes to porcine muscle fibre type transformation. Our finding provided the first evidence that leucine promotes porcine myofibre type transformation from fast MyHC to slow MyHC via the Akt/FoxO1 signalling pathway and miR-27a.

Fe deficiency is relatively common in pregnancy and has both short- and long-term consequences. However, little is known about the effect on the metabolism of other micronutrients. A total of fifty-four female rats were fed control (50 mg Fe/kg) or Fe-deficient diets (7·5 mg/kg) before and during pregnancy. Maternal liver, placenta and fetal liver were collected at day 21 of pregnancy for Cu and Zn analysis and to measure expression of the major genes of Cu and Zn metabolism. Cu levels increased in the maternal liver (P=0·002) and placenta (P=0·018) of Fe-deficient rats. Zn increased (P<0·0001) and Cu decreased (P=0·006) in the fetal liver. Hepatic expression of the Cu chaperones antioxidant 1 Cu chaperone (P=0·042) and cytochrome c oxidase Cu chaperone (COX17, P=0·020) decreased in the Fe-deficient dams, while the expression of the genes of Zn metabolism was unaltered. In the placenta, Fe deficiency reduced the expression of the chaperone for superoxide dismutase 1, Cu chaperone for superoxide dismutase (P=0·030), ceruloplasmin (P=0·042) and Zn transport genes, ZRT/IRT-like protein 4 (ZIP4, P=0·047) and Zn transporter 1 (ZnT1, P=0·012). In fetal liver, Fe deficiency increased COX17 (P=0·020), ZRT/IRT-like protein 14 (P=0·036) and ZnT1 (P=0·0003) and decreased ZIP4 (P=0·004). The results demonstrate that Fe deficiency during pregnancy has opposite effects on Cu and Zn levels in the fetal liver. This may, in turn, alter metabolism of these nutrients, with consequences for development in the fetus and the neonate.

Normal odd-chain SFA (OCSFA), particularly tridecanoic acid (n-13 : 0), pentadecanoic acid (n-15 : 0) and heptadecanoic acid (n-17 : 0), are normal components of dairy products, beef and seafood. The ratio of n-15 : 0:n-17 : 0 in ruminant foods (dairy products and beef) is 2:1, while in seafood and human tissues it is 1:2, and their appearance in plasma is often used as a marker for ruminant fat intake. Human elongases encoded by elongation of very long-chain fatty acid (ELOVL)1, ELOVL3, ELOVL6 and ELOVL7 catalyse biosynthesis of the dominant even-chain SFA; however, there are no reports of elongase function on OCSFA. ELOVL transfected MCF7 cells were treated with n-13 : 0, n-15 : 0 or n-17 : 0 (80 µm) and products analysed. ELOVL6 catalysed elongation of n-13 : 0→n-15 : 0 and n-15 : 0→n-17 : 0; and ELOVL7 had modest activity toward n-15 : 0 (n-15 : 0→n-17 : 0). No elongation activity was detected for n-17 : 0→n-19 : 0. Our data expand ELOVL specificity to OCSFA, providing the first molecular evidence demonstrating ELOVL6 as the major elongase acting on OCSFA n-13 : 0 and n-15 : 0 fatty acids. Studies of food intake relying on OCSFA as a biomarker should consider endogenous human metabolism when relying on OCSFA ratios to indicate specific food intake.

This study investigated the effects of a maternal dyslipidaemic (DLP) diet on lipid metabolism, microbial counts in faeces and hepatic and intestinal morphology in rat offspring with respect to sex during different phases of life. Wistar rats (dams) were fed a control (CTL) or DLP during gestation and lactation. After weaning, CTL and DLP offspring were fed a standard diet. The effects of a maternal DLP on body composition, biochemical parameters, faecal microbiota and intestinal and hepatic histomorphometric characteristics in rat offspring were evaluated at 30 and 90 d of age. The DLP diet during gestation and lactation caused lower birth weight and a greater weight gain percentage at the end of the 90-d period in both male and female offspring. Female pups from DLP dams had higher liver fat levels compared with CTL (P≤0·001) at 90 d of age. Males from DLP dams had greater visceral fat weight and lower Lactobacillus spp. faecal counts at 90 d of age (P≤0·001) as well as lower faecal fat excretion (P≤0·05) and Bacteroides spp. faecal counts (P≤0·001) at 30 d of age when compared with pups from CTL dams. However, both dams and DLP pups showed damage to intestinal villi. A maternal DLP alters intestinal function and lipid metabolism in a sex-specific manner and is a potential predisposing factor for health complications in offspring from the juvenile period to the adult period.

The effect of kiwi fruit at two dietary levels on the adaptation of intestinal fermentation over time in the growing pig was studied. A semi-synthetic fibre-free diet and two semi-synthetic diets containing kiwi fruit as a model fibre source (133 or 266 g/kg (DM basis); 28 or 48 g fibre/kg) were formulated and the diets contained titanium dioxide as an indigestible marker. A total of fourteen ileal cannulated pigs (41 kg body weight) were fed the fibre-free diet for 7 d followed by either the low or high kiwi fruit-containing diets (n 7/diet) for a further 44 d. Ileal digesta and faeces were collected at five times throughout the study. Ileal digesta were fermented (in vitro) with a standard pooled human faecal inoculum, while fresh pig faeces were used as inocula to ferment in vitro a standard purified fibre. Observations were normalised for diet DM intake using the marker. The 16S ribosomal RNA gene copy number of ileal and total faecal bacteria were high for the high-kiwi fruit level diet (P<0·05). The ileal bacteria tended to decrease over time (P<0·1), while the faecal bacteria increased (P<0·05), at the same rate for both diets. The amounts of crude protein and insoluble dietary fibre entering the hindgut changed over time similarly for both diets, whereas for starch it changed only for the low kiwi fruit-containing diet (P<0·05). Changes over time were also observed for the predicted hindgut valeric acid production and butyric acid absorption (P<0·05). In conclusion, adaptational changes over time of some characteristics of intestinal fermentation depended on the dietary level of kiwi fruit.

Non-communicable diseases are projected to become the most common causes of death in Africa by 2030. The impact on health of epidemiological and nutritional transitions in sub-Saharan Africa remains unclear. To assess the trends of dietary fatty acids over time in Uganda, we examined fatty acids in serum collected from individuals in rural south-west Uganda, at three time points over two decades. Independent cross-sectional samples of 915 adults and children were selected from the general population cohort in 1990 (n 281), 2000 (n 283) and 2008 (n 351). Serum phospholipid fatty acids were measured by GC. Multivariate regression analyses were performed to compare the geometric means of fatty acids by time period. Serum fatty acid profiling showed high proportions of SFA, cis-MUFA and industrial trans-fatty acids (iTFA), likely to be biomarkers of high consumption of palm oil and hydrogenated fats. In contrast, proportions of n-6 and n-3 PUFA from vegetable oils and fish were low. From 1990 to 2008, serum phospholipids showed increases in absolute amounts of SFA (17·3 % increase in adults and 26·4 % in children), MUFA (16·7 % increase in adults and 16·8 % in children) and n-6:n-3 PUFA (40·1 % increase in adults and 39·8 % in children). The amount of elaidic acid, iTFA from hydrogenated fats, increased in children (60·1 % increase). In this rural Ugandan population, we show evidence of unfavourable trends over time of dietary fatty acids.

Nutrition therapy is considered an important treatment of burn patients. The aim of the study was to delineate the nutritional support in severe burn patients and to investigate association between nutritional practice and clinical outcomes. Severe burn patients were enrolled (n 100). In 90 % of the cases, the burn injury covered above 70 % of the total body surface area. Mean interval from injury to nutrition start was 2·4 (sd 1·1) d. Sixty-seven patients were initiated with enteral nutrition (EN) with a median time of 1 d from injury to first feed. Twenty-two patients began with parenteral nutrition (PN). During the study, thirty-two patients developed EN intolerance. Patients received an average of about 70 % of prescribed energy and protein. Patients with EN providing <30 % energy had significantly higher 28- d and in-hospital mortality than patients with EN providing more than 30 % of energy. Mortality at 28 d was 11 % and in-hospital mortality was 45 %. Multiple regression analysis demonstrated that EN providing <30 % energy and septic shock were independent risk factors for 28- d prognosis. EN could be initiated early in severe burn patients. Majority patients needed PN supplementation for energy requirement and EN feeding intolerance. Post-pyloric feeding is more efficient than gastric feeding in EN tolerance and energy supplement. It is difficult for severe burn patients to obtain enough feeding, especially in the early stage of the disease. More than 2 weeks of underfeeding is harmful to recovery.

The effects of subclinical Zn deficiency on depletion and redistribution of body Zn were studied in weaned piglets. Forty-eight weaned piglets (German-Large-White×Land-Race×Piétrain; 50 % female, 50 % male-castrated; body weight 8·5 (sd 0·27) kg) were fed restrictively (450 g/d) a basal maize–soyabean meal-based diet supplemented with varying amounts of ZnSO4.7H2O (analysed dietary Zn: 28·1, 33·6, 38·8, 42·7, 47·5, 58·2, 67·8, 88·0 mg/kg diet) for an experimental period of 8 d. Analyses comprised Zn concentrations in soft tissues. Statistical analyses included regression models and k-means cluster analysis. Jejunum and kidney Zn correlated positively with dietary Zn (P<0·05). Other Zn pools responded in a non-linear fashion by declining (colon, epidermis, spleen) or increasing (mesenteric lymph follicles, thymus, skeletal muscle) below 63·6, 48·0, 47·5, 68·0, 43·0 and 53·1 mg Zn/kg diet, respectively (P<0·01). Above these thresholds, Zn concentrations in epidermis, mesenteric lymph follicles and skeletal muscle plateaued (P<0·0001), whereas they exhibited a decrease in colon and thymus (P<0·01) as well as a numerical increase in spleen. Clustering by dietary Zn concentration indicated clusters of varying Zn supply status and pathophysiological status. Clustering by biological matrices revealed a discrimination between storage, transport and excretion media as well as soft tissues. Taken together, novel response patterns indicated compensation reactions in tissues that are essential for the acute survival of growing animals (heart, skeletal muscle, immune tissues). Furthermore, this is to our knowledge the first study that mapped the gross Zn requirement by clustering tissue Zn concentrations between treatment groups.

To compare the growth and biosynthetic ability of long-chain PUFA (LC-PUFA) of the genetically improved farmed tilapia (GIFT) (Oreochromis niloticus) in different water salinities, an 8-week feeding trial was conducted on the GIFT juveniles at 0, 12 and 24 ‰ (parts per thousand; ppt), respectively, with three isonitrogenous (32 %) and isolipidic (8 %) diets (D1–D3). Diet D1 with fish oils (rich in LC-PUFA) as lipid source was used as the control, while D2 and D3 with vegetable oil (free LC-PUFA) blends as lipid source contained different ratios of linoleic acid (LA, 18 : 2n-6) and α-linolenic acid (ALA, 18 : 3n-3) at 4·04 (D2) and 0·54 (D3), respectively. At the end of feeding trial, the growth performance of D2 and D3 groups under all salinity treatments was as good as that of D1 group, which indicates that the GIFT juveniles may convert dietary LA and ALA into LC-PUFA to meet the requirement of essential fatty acids for normal growth and physiology. When fed the same diets, GIFT at 12 ppt had a better growth performance coupled with a higher liver and muscle arachidonic acid content than those in freshwater. Furthermore, brackish water (24 ppt) significantly promoted the mRNA levels of elongase 5 of very long-chain fatty acids (elovl5) and peroxisome proliferator-activated receptor α (pparα) in liver, when compared with freshwater. These results suggest that the GIFT may display better growth performance together with a relatively higher endogenous LC-PUFA biosynthetic ability under brackish water (12 and 24 ppt), probably through improving the expression of elovl5 and pparα in liver.

Renal disease has a high incidence in cats, and some evidence implicates dietary P as well. To investigate this further, two studies in healthy adult cats were conducted. Study 1 (36 weeks) included forty-eight cats, stratified to control or test diets providing 1·2 or 4·8 g/1000 kcal (4184 kJ) P (0 or approximately 3·6 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·6). Study 2 (29 weeks) included fifty cats, stratified to control or test diets, providing 1·3 or 3·6 g/1000 kcal (4184 kJ) P (0 or approximately 1·5 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·9). Health markers, glomerular filtration rate (GFR) and mineral balance were measured regularly, with abdominal ultrasound. Study 1 was halted after 4 weeks as the test group GFR reduced by 0·4 (95 % CI 0·3, 0·5) ml/min per kg, and ultrasound revealed changes in renal echogenicity. In study 2, at week 28, no change in mean GFR was observed (P >0·05); however, altered renal echogenicity was detected in 36 % of test cats. In agreement with previous studies, feeding a diet with Ca:P <1·0, a high total and inorganic P inclusion resulted in loss of renal function and changes in echogenicity suggestive of renal pathology. Feeding a diet containing lower total and inorganic P with Ca:P close to 1·0 led to more subtle structural changes in a third of test cats; however, nephrolithiasis occurred in both diet groups, complicating data interpretation. We conclude that the no observed adverse effects level for total dietary P in adult cats is lower than 3·6 g/1000 kcal (4184 kJ), however the effect of inorganic P sources and Ca:P require further investigation.

While strong evidence from clinical studies suggests beneficial effects of carnitine supplementation on metabolic health, serious safety concerns associated with carnitine supplementation have been raised from studies in mice. Considering that the carnitine doses in these mice studies were up to 100 times higher than those used in clinical studies, the present study aimed to address possible safety concerns associated with long-term supplementation of a carnitine dose used in clinical trials. Two groups of NMRI mice were fed either a control or a carnitine-supplemented diet (1 g/kg diet) from weaning to 19 months of age, and parameters of hepatic lipid metabolism and stress signalling and skeletal muscle gene expression were analysed in the mice at 19 months of age. Concentrations of free carnitine and acetylcarnitine in plasma and tissues were higher in the carnitine than in the control group (P<0·05). Plasma concentrations of free carnitine and acetylcarnitine were higher in mice at adult age (10 and 15 months) than at advanced age (19 months) (P<0·05). Hepatic mRNA and protein levels of genes involved in lipid metabolism and stress signalling and hepatic and plasma lipid concentrations did not differ between the carnitine and the control group. Skeletal muscle transcriptome analysis in 19-month-old mice revealed only a moderate regulation between carnitine and control group. Lifelong carnitine supplementation prevents an age-dependent impairment of plasma carnitine status, but safety concerns associated with long-term supplementation of carnitine at doses used in clinical trials can be considered as unfounded.

Few studies have examined the association of various types of Fe with colorectal cancer risk. The aim of this study was to investigate different forms and sources of Fe in relation to colorectal cancer risk in a Chinese population. A total of 2138 patients with colorectal cancer and 2144 sex- and age-matched (5-year interval) controls were recruited from July 2010 to November 2017. Dietary information was assessed by face-to-face interviews using a validated FFQ. Multivariable logistic regression was used to estimate the OR and 95 % CI on models. Intake of Fe from plants and Fe from white meat were inversely associated with the risk of colorectal cancer, while haem Fe and Fe from red meat were positively associated with colorectal cancer risk. The multivariable OR for the highest quartile v. the lowest quartile were 0·72 (95 % CI 0·59, 0·87, Ptrend<0·001) for Fe from plants, 0·54 (95 % CI 0·45, 0·66, Ptrend<0·001) for Fe from white meat, 1·26 (95 % CI 1·04, 1·53, Ptrend=0·005) for haem Fe and 1·83 (95 % CI 1·49, 2·24, Ptrend<0·001) for Fe from red meat intake, respectively. However, no significant association was found between the consumption of total dietary Fe, non-haem Fe, Fe from meat and colorectal cancer risk. This study showed that lower intake of Fe from plants and white meat, as well as higher intake of haem Fe and Fe from red meat, were associated with colorectal cancer risk in a Chinese population.

Humans can obtain pre-formed long-chain PUFA from the diet and are also able to convert essential fatty acids (EFA) to longer-chain PUFA. The metabolic pathway responsible for EFA interconversion involves alternating desaturation and carbon chain elongation reactions, and carbon chain shortening by peroxisomal β-oxidation. Studies using stable isotope tracers or diets supplemented with EFA show that capacity for PUFA synthesis is limited in humans, such that DHA (22 : 6n-3) synthesis in men is negligible. PUFA synthesis is higher in women of reproductive age compared with men. However, the magnitude of the contribution of hepatic PUFA synthesis to whole-body PUFA status remains unclear. A number of extra-hepatic tissues have been shown to synthesise PUFA or to express genes for enzymes involved in this pathway. The precise function of extra-hepatic PUFA synthesis is largely unknown, although in T lymphocytes PUFA synthesis is involved in the regulation of cell activation and proliferation. Local PUFA synthesis may also be important for spermatogenesis and fertility. One possible role of extra-hepatic PUFA synthesis is that it may provide PUFA in a timely manner to facilitate specific cell functions. If so, this may suggest novel insights into the effect of dietary PUFA and/or polymorphisms in genes involved in PUFA synthesis on health and tissue function.