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.

Recently there has been a considerable rise in the frequency of metabolic diseases, such as obesity, due to changes in lifestyle and resultant imbalances between energy intake and expenditure. Whey proteins are considered as potentially important components of a dietary solution to the obesity problem. However, the roles of individual whey proteins in energy balance remain poorly understood. This study investigated the effects of a high-fat diet (HFD) containing α-lactalbumin (LAB), a specific whey protein, or the non-whey protein casein (CAS), on energy balance, nutrient transporters expression and enteric microbial populations. C57BL/6J mice (n 8) were given an HFD containing either 20 % CAS or LAB as protein sources or a low-fat diet containing CAS for 10 weeks. HFD-LAB-fed mice showed a significant increase in cumulative energy intake (P=0·043), without differences in body weight, energy expenditure, locomotor activity, RER or subcutaneous and epididymal white adipose tissue weight. HFD-LAB intake led to a decrease in the expression of glut2 in the ileum (P=0·05) and in the fatty acid transporter cd36 (P<0·001) in both ileum and jejunum. This suggests a reduction in absorption efficiency within the small intestine in the HFD-LAB group. DNA from faecal samples was used for 16S rRNA-based assessment of intestinal microbiota populations; the genera Lactobacillus, Parabacteroides and Bifidobacterium were present in significantly higher proportions in the HFD-LAB group. These data indicate a possible functional relationship between gut microbiota, intestinal nutrient transporters and energy balance, with no impact on weight gain.

A more efficient utilisation of marine-derived sources of dietary n-3 long-chain PUFA (n-3 LC PUFA) in cultured Atlantic salmon (Salmo salar L.) could be achieved by nutritional strategies that maximise endogenous n-3 LC PUFA synthesis. The objective of the present study was to quantify the extent of n-3 LC PUFA biosynthesis and the resultant effect on fillet nutritional quality in large fish. Four diets were manufactured, providing altered levels of dietary n-3 substrate, namely, 18 : 3n-3, and end products, namely, 20 : 5n-3 and 22 : 6n-3. After 283 d of feeding, fish grew in excess of 3000 g and no differences in growth performance or biometrical parameters were recorded. An analysis of fatty acid composition and in vivo metabolism revealed that endogenous production of n-3 LC PUFA in fish fed a diet containing no added fish oil resulted in fillet levels of n-3 LC PUFA comparable with fish fed a diet with added fish oil. However, this result was not consistent among all treatments. Another major finding of this study was the presence of abundant dietary n-3 substrate, with the addition of dietary n-3 end product (i.e. fish oil) served to increase final fillet levels of n-3 LC PUFA. Specifically, preferential β-oxidation of dietary C18n-3 PUFA resulted in conservation of n-3 LC PUFA from catabolism. Ultimately, this study highlights the potential for endogenous synthesis of n-3 LC PUFA to, partially, support a substantial reduction in the amount of dietary fish oil in diets for Atlantic salmon reared in seawater.

This study aimed to examine in vivo starch digestion kinetics and to unravel the mechanisms of starch hydrolysing enzymes. Ninety pigs (23 (sd 2·1) kg body weight) were assigned to one of nine treatments in a 3×3 factorial arrangement, with starch source (barley, maize, high-amylose (HA) maize) and form (isolated, within cereal matrix, extruded) as factors. We determined starch digestion coefficients (DC), starch breakdown products and digesta retention times in four small-intestinal segments (SI1–4). Starch digestion in SI2 of pigs fed barley and maize, exceeded starch digestion of pigs fed HA maize by 0·20–0·33 DC units (P<0·01). In SI3–4, barley starch were completely digested, whereas the cereal matrix of maize hampered digestion and generated 16 % resistant starch in the small intestine (P<0·001). Extrusion increased the DC of maize and HA maize starch throughout the small intestine but not that of barley (P<0·05). Up to 25 % of starch residuals in the proximal small intestine of pigs was present as glucose and soluble α(1–4) maltodextrins. The high abundance of glucose, maltose and maltotriose in the proximal small intestine indicates activity of brush-border enzymes in the intestinal lumen, which is exceeded by α-amylase activity. Furthermore, we found that in vivo starch digestion exceeded our in vitro predictions for rapidly digested starch, which indicates that the role of the stomach on starch digestion is currently underestimated. Consequently, in vivo glucose release of slowly digestible starch is less gradual than expected, which challenges the prediction quality of the in vitro assay.

The aim of this study was to characterise changes in lean soft tissue (LST) and examine the contributions of energy intake, physical activity and breast-feeding practices to LST changes at 3 and 9 months postpartum. We examined current weight, LST (via dual-energy X-ray absorptiometry), dietary intake (3-d food diary), physical activity (Baecke questionnaire) and breast-feeding practices (3-d breast-feeding diary) in forty-nine women aged 32·9 (sd 3·8) years. Changes in LST varied from −2·51 to +2·50 kg with twenty-nine women gaining LST (1·1 (sd 0·7) kg, P<0·001) and twenty women losing LST (−0·9 (sd 0·8) kg, P<0·001). Energy intake (133 (SD 42) v. 109 (SD 33) kJ/kg, P=0·019) and % kJ from fat at 3 months postpartum was higher in women who gained LST at 9 months postpartum (gained LST=34 (sd 5) % kJ; lost LST=29 (sd 4) % kJ, P=0·002). Women who gained LST reported breast-feeding their infants more frequently (gained LST=8 (sd 3) feeds/d; lost LST=5 (sd 1) feeds/d, P=0·014) and for more time per d (gained LST=115 (sd 78) min/d; lost LST=59 (sd 34) min/d, P=0·016) at 9 months postpartum. Energy intake and % kJ from fat at 3 months were significant predictors of LST gain (β=0·08 (se 0·04) and 0·24 (se 0·09), respectively). This suggests that gain in LST may be associated with more frequent and longer episodes of breast-feeding at 9 months postpartum as well as dietary intake early in the postpartum period.

The effect of 38 µg (1500 IU) daily vitamin D3 supplementation, consumed with an Fe-fortified breakfast cereal for 8 weeks, on haematological indicators in Fe-deficient female subjects was investigated. Fifty Fe-deficient subjects (plasma ferritin concentration <20 µg/l; mean age: 27·4 (sd 9·4) years) were randomised to consume an Fe-fortified breakfast cereal containing 9 mg of Fe daily, with either a vitamin D3 supplement or placebo. Blood samples were collected at baseline, interim (4 weeks) and post-intervention (8 weeks) for measurement of Fe and vitamin D status biomarkers. The effect of intervention was analysed using mixed-model repeated-measures ANOVA. Significant increases were observed in two main haematological indices: Hb concentration and haematocrit level from baseline to post-intervention in the vitamin D group but not in the placebo group. The increase from baseline to post-intervention in Hb concentration in the vitamin D group (135 (sd 11) to 138 (sd 10) g/l) was significantly higher compared with the placebo group (131 (sd 15) to 128 (sd 13) g/l) (P=0·037). The increase in haematocrit level from baseline to post-intervention was also significantly higher in the vitamin D group (42·0 (sd 3·0) to 43·8 (sd 3·4) %) compared with the placebo group (41·2 (sd 4·3) to 40·7 (sd 3·6) %) (P=0·032). Despite the non-significant changes in plasma ferritin concentration, this study demonstrates that 38 µg supplemental vitamin D, consumed daily, with Fe-fortified breakfast cereal led to improvement in Hb concentration and haematocrit levels in women with low Fe stores. These findings may have therapeutic implications in the recovery of Fe status in Fe-deficient populations at a healthcare level.

Paediatric non-alcoholic fatty liver disease has increased in parallel with childhood obesity. Dietary habits, particularly products rich in sugars, may influence both hepatic fat and insulin resistance (homeostatic model assessment for insulin resistance (HOMA-IR)). The aim of the study was to examine the association of the consumption of foods and food components, dairy desserts and substitutes (DDS), sugar-sweetened beverages (SSB), as well as total and added sugars, with hepatic fat and HOMA-IR. Dietary intake (two non-consecutive 24 h-recalls), hepatic fat (MRI) and HOMA-IR were assessed in 110 overweight/obese children (10·6 (sd 1·1) years old). Linear regression analyses were used to examine the association of dietary intake with hepatic fat and HOMA-IR adjusted for potential confounders (sex, age, energy intake, maternal educational level, total and abdominal adiposity and sugar intake). The results showed that there was a negative association between cereal intake and hepatic fat (β=–0·197, P<0·05). In contrast, both SSB consumption (β=0·217; P=0·028) and sugar in SSB (β=0·210, P=0·035), but not DDS or sugar in DDS or other dietary components, were positively associated with hepatic fat regardless of potential confounders including total sugar intake. In conclusion, cereal intake might decrease hepatic fat, whereas SSB consumption and its sugar content may increase the likelihood of having hepatic steatosis. Although these observations need to be confirmed using experimental evidence, these results suggest that healthy lifestyle intervention programs are needed to improve dietary habits as well as to increase the awareness of the detrimental effects of SSB consumption early in life.

In the current context of unsustainable food systems, we aimed to develop and validate an index, the sustainable diet index (SDI), assessing the sustainability of dietary patterns, including multidimensional individual indicators of sustainability. Based on the FAO’s definition of sustainable diets, the SDI includes seven indicators categorised into four standardised sub-indexes, respectively, environmental, nutritional, economic and sociocultural. The index (range: 4–20) was obtained by summing the sub-indexes. We computed the SDI for 29 388 participants in the NutriNet-Santé cohort study, estimated its validity and identified potential socio-demographic or lifestyle differences across the SDI quintile. In our sample, the SDI (mean=12·10/20; 95 % CI 12·07, 12·13) was highly correlated to all the sub-indexes that exerted substantial influence on the participants’ ranking. The environmental and economical sub-indexes were the most and less correlated with the SDI (Pearson R2 0·66 and 0·52, respectively). Dietary patterns of participants with a high SDI (considered as more sustainable) were concordant with the already published sustainable diets. Participants with high SDI scores were more often women (24 %), post-secondary graduates (22 %) and vegetarians or vegans (7 %), without obesity (16 %). Finally, the SDI could be a useful tool to easily assess the sustainability-related changes in dietary patterns, estimate the association with long-term health outcomes and help guide future public health policies.

The aim of the study was to investigate how maternal dietary patterns and maternal/fetal cytokines are associated with birth weight and whether cytokines mediate the association. A total of 469 pregnant women and their children were recruited for this prospective study. Dietary patterns in pregnancy were identified using factor analysis of data from three consecutive 24 h dietary recalls. Maternal and umbilical blood serum cytokines (adiponectin (APN), IL-6 and interferon-γ) were measured via ELISA. Path analysis was used to explore the relationships between maternal diet, cytokines and birth weight. Four dietary patterns were identified: a mainly fruit, dairy products and poultry diet (FDP); a mainly vegetables, beans and pork diet (VBP); a mainly fish, shrimp and soup diet (FS) and a mainly tuber and egg diet (TE). Path analysis showed the order of effects of dietary patterns on birth weight was FS>FDP>TE>VBP (β=0·130, 0·109, –0·094 and 0·046, respectively). Only the TE pattern’s effect was negative. Maternal and fetal APN were positively associated with birth weight (β=0·045 and 0·226, respectively), and they mediated the association between the TE pattern and birth weight (indirect effect was 5·3 %). Maternal IL-6 was negatively associated with birth weight (β=–0·067) and mediated the association between maternal FDP and VBP patterns and birth weight (indirect effects were 10·1 and 100·0 %, respectively). All variables in the path explained 33·6 % of variation. These results suggested that maternal dietary patterns in pregnancy are associated with birth weight and mediated directly and indirectly through some maternal/fetal serum cytokines.

Ca and dairy product intakes may be inversely associated with all-cause and cause-specific mortality, and non-Ca components of dairy products, such as insulin-like growth factor-1, may be independently associated with mortality. We investigated associations of Ca and dairy product intakes with all-cause, all-cancer, colorectal cancer (CRC) and CHD mortality among 35 221 55- to 69-year-old women in the prospective Iowa Women’s Health Study, who were cancer-free in 1986. We assessed diet using a Willett FFQ, and associations using multivariable Cox proportional hazards regression. We estimated residuals from linear regression models of dairy products with dietary Ca to investigate total and specific dairy products independent of their Ca content. Through 2012, 18 687 participants died, including 4665 from cancer (including 574 from CRC) and 3603 from CHD. For those in the highest relative to the lowest quintiles of intake, the multivariable-adjusted hazard ratios (HR) and 95 % CI for total Ca (dietary plus supplemental) were 0·88 (0·83, 0·93; P trend=0·001) for all-cause mortality, 0·91 (0·81, 1·02; P trend=0·34) for all-cancer mortality, 0·60 (0·43, 0·83; P trend=0·002) for CRC mortality and 0·73 (0·64, 0·83; P trend <0·0001) for CHD mortality. The corresponding HR for associations of whole milk, whole milk residuals, and low-/non-fat milk residuals with all-cause mortality were 1·20 (95 % CI 1·13, 1·27), 1·20 (95 % CI 1·13, 1·28) and 0·91 (95 % CI 0·86, 0·96), respectively. These results suggest that Ca may be associated with lower risk of all-cause, CRC and CHD mortality, and that non-Ca components of milk may be independently associated with mortality.