Several studies have reported a significant association between the metabolic syndrome (MetS) and mortality around the world. Caveolin-1 (CAV-1) has been widely studied in dyslipidaemia, and several studies have indicated that CAV-1 genetic variations may correlate with dietary intake of fatty acids. This study aimed to investigate the interaction of CAV-1 rs3807992 with types of dietary fatty acid in the MetS risk. This cross-sectional study was carried out on 404 overweight and obese females. Dietary intake was obtained from a 147-item FFQ. The CAV-1 genotype was measured using the PCR-restriction fragment length polymorphism method. Anthropometric values and serum levels (TC, LDL, HDL, TAG and FBS) were measured by standard methods. It was observed that the (AA + AG) group had significantly higher BMI, waist circumference and DBP (P = 0·02, P = 0·02, and P = 0·01, respectively) and lower serum LDL, HDL and TC (P < 0·05) than the GG group. It was found that A allele carriers were at higher odds of the MetS (P = 0·01), abdominal obesity (P = 0·06), increased TAG concentration (P = 0·01), elevated blood pressure (BP) (P = 0·01), increased glucose concentration (P = 0·45) and decreased HDL-cholesterol concentration (P = 0·03). Moreover, the interaction of CAV-1 and SFA intake was significant in terms of the MetS (P = 0·03), LDL (P = 0·03) and BP (P = 0·01). Additionally, the (AA + AG) group was significantly related to PUFA intake in terms of the MetS (P = 0·04), TAG (P = 0·02), glucose (P = 0·02) and homoeostasis model assessment insulin resistance (P = 0·01). Higher PUFA consumption might attenuate the CAV-1 rs3807992 associations with the MetS, and individuals with greater genetic predisposition appeared to have a higher risk of the MetS, associated with higher SFA consumption.

l-Citrulline (l-Cit) is a non-essential amino acid that stimulates nitric oxide (NO) production and improves exercise performance by reducing muscle damage indices; however, the direct benefits of l-Cit on antioxidant markers are unclear. The aim of this study was to examine antioxidant responses to high-intensity interval exercise following acute l-Cit supplementation. Nine young men (21 (sd 1) years) participated in a double-blind crossover study in which they received 12 g of l-Cit and placebo (PL) an hour prior to high-intensity interval exercise on two occasions, separated by a 7-d washout period. Blood samples were obtained before (PRE), immediately after (IP), 10 (10P) and 30 min after exercise (30P) from the cubital vein using standard procedures. Serum concentrations of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and NO metabolites (NOx) were measured. The exercise protocol significantly elevated SOD (P = 0·01) and GPx (P = 0·048) from PRE to 10P in the l-Cit group with greater changes than the PL group. CAT concentrations increased IP (P = 0·014) and remained elevated at 10P (P = 0·03) and 30P (P = 0·015) in both the l-Cit and PL conditions. NOx concentrations increased IP (P = 0·05) in the l-Cit group with greater changes than PL group in PRE to IP, PRE to 10P and PRE to 30P (P < 0·05). Our data indicate that l-Cit supplementation (single 12 g dose pre-exercise) induces improvements in antioxidant markers following a session of high-intensity interval exercise in young men.

To investigate the influences of cobalt (Co) and folic acid (FA) on growth performance and rumen fermentation, Holstein male calves (n 40) were randomly assigned to four groups according to their body weights. Cobalt sulphate at 0 or 0·11 mg Co/kg DM and FA at 0 or 7·2 mg/kg DM were used in a 2 × 2 factorial design. Average daily gain was elevated with FA or Co supplementation, but the elevation was greater for supplementing Co in diets without FA than with FA. Supplementing FA or Co increased DM intake and total-tract nutrient digestibility. Rumen pH was unaltered with FA but reduced with Co supplementation. Concentration of rumen total volatile fatty acids was elevated with FA or Co inclusion. Acetate percentage and acetate to propionate ratio were elevated with FA inclusion. Supplementing Co decreased acetate percentage and increased propionate percentage. Activities of xylanase and α-amylase and populations of total bacteria, fungi, protozoa, Ruminococcus albus, Fibrobacter succinogenes and Prevotella ruminicola increased with FA or Co inclusion. Activities of carboxymethyl-cellulase and pectinase increased with FA inclusion and population of methanogens decreased with Co addition. Blood folates increased and homocysteine decreased with FA inclusion. Blood glucose and vitamin B12 increased with Co addition. The data suggested that supplementing 0·11 mg Co/kg DM in diets containing 0·09 mg Co/kg DM increased growth performance and nutrient digestibility but had no improvement on the effects of FA addition in calves.

We investigated the impact of increased alpha-linolenic acid (ALA) dietary levels on its plasma bioavailability and its bioconversion in n-3 long chain poly unsaturated fatty acids during a 60-d kinetics and the oxidative stress potentially associated. Rats were submitted to a normolipidic diet providing 0, 3, 10 and 24% ALA of dietary lipids for 0, 15, 30 and 60 days. The lipid peroxidation and oxidative stress (nitric oxide (NO) contents and catalase (CAT), superoxide dismutase (SOD), gluthation peroxidase (GPx) activities) were studied in the liver and plasma. When the diet was deprived in n-3 PUFAs, ALA, (eicosanoic acid) EPA and docosahexaenoic acid (DHA) levels decreased in all lipid fractions of plasma and in red blood cell (RBC) lipids. The addition of ALA in the diet linearly improves its bioavailability and its bioconversion in EPA (R²=0.98). By providing 10 to 24% ALA in dietary lipids (LA/ALA, 1·6 and 5·5 respectively), ALA and EPA were more broadly packaged in all lipid fractions (triglyceride (TAG), cholesterol ester (CE) and free fatty acids (FFA)) of plasma from 15 to 30 days timeframe. Only 3% ALA was sufficient to promote the maximal bioconversion of ALA in DHA in phospholipid (PL) and TAG fractions. Additionally, the improvement of ALA bioconversion in EPA and DHA did not impact the oxidative stress markers and limiting lipid peroxidation. To conclude, this study demonstrated that in rat, 10% ALA in the lipid diet for 15–30 days promotes its bioavailability and its bioconversion and allowed the greatest levels in plasma and RBCs.

Due to the important roles of resistance training and protein consumption in the prevention and treatment of sarcopenia, we assessed the efficacy of post-exercise Icelandic yogurt consumption on lean mass, strength and skeletal muscle regulatory factors in healthy untrained older males. Thirty healthy untrained older males (age = 68 ± 4 years) were randomly assigned to Icelandic yogurt (IR; n 15, 18 g of protein) or an iso-energetic placebo (PR; n 15, 0 g protein) immediately following resistance training (3×/week) for 8 weeks. Before and after training, lean mass, strength and skeletal muscle regulatory factors (insulin-like growth factor-1 (IGF-1), transforming growth factor-beta 1 (TGF-β1), growth differentiation factor 15 (GDF15), Activin A, myostatin (MST) and follistatin (FST)) were assessed. There were group × time interactions (P < 0·05) for body mass (IR: Δ 1, PR: Δ 0·7 kg), BMI (IR: Δ 0·3, PR: Δ 0·2 kg/m2), lean mass (IR: Δ 1·3, PR: Δ 0·6 kg), bench press (IR: Δ 4, PR: 2·3 kg), leg press (IR: Δ 4·2, PR: Δ 2·5 kg), IGF-1 (IR: Δ 0·5, Δ PR: 0·1 ng/ml), TGF-β (IR: Δ − 0·2, PR: Δ − 0·1 ng/ml), GDF15 (IR: Δ − 10·3, PR: Δ − 4·8 pg/ml), Activin A (IR: Δ − 9·8, PR: Δ − 2·9 pg/ml), MST (IR: Δ − 0·1, PR: Δ − 0·04 ng/ml) and FST (IR: Δ 0·09, PR: Δ 0·03 ng/ml), with Icelandic yogurt consumption resulting in greater changes compared with placebo. The addition of Icelandic yogurt consumption to a resistance training programme improved lean mass, strength and altered skeletal muscle regulatory factors in healthy untrained older males compared with placebo. Therefore, Icelandic yogurt as a nutrient-dense source and cost-effective supplement enhances muscular gains mediated by resistance training and consequently may be used as a strategy for the prevention of sarcopenia.

Several investigations revealed the association between ApoA2 concentration and lipid profile, inflammation and oxidative stress markers. Dietary habits also play a major role in the health status of individuals with type 2 diabetes mellitus (T2DM). This study aimed to investigate the interaction of ApoA2–256T > C with dietary indexes on ghrelin and leptin hormones together with biochemical markers among individuals with T2DM. A cross-sectional study was conducted on 726 randomly selected individuals with T2DM. A validated FFQ was used to evaluate Healthy Eating Index, Dietary Quality Index-International (DQI-I) and Dietary Phytochemical Index (DPI). ApoA2–256T > C genotypes were detected by real-time-PCR. Ghrelin, leptin and biochemical markers were also assessed. ANCOVA was used for the interaction between the polymorphism and dietary indexes. A significant interaction was observed between ApoA2–256T > C and DQI-I on high-sensitivity C-reactive protein (hs-CRP) level and superoxide dismutase (SOD) activity. Besides, the interaction of the SNP and DPI significantly affected hs-CRP and 8-isoprostane F2α (PGF2α) levels. CC in the second tertile of DPI had the lowest hs-CRP level, and it was elevated due to adhering to DQI-I (Pinteraction = 0·01 and 0·04, respectively). Moreover, T-allele (protective allele) carriers with the highest level of PGF2α and SOD activity were those in the second tertile of DPI and DQI-I, respectively (Pinteraction = 0·03 and 0·007, respectively). SOD activity, hs-CRP and PGF2α concentration may be modified in T-allele carriers and CC by the adherence to DPI and DQI-I, though additional studies are required to confirm these findings.

In May 2021, the Scientific Advisory Committee on Nutrition (SACN) published a risk assessment on lower carbohydrate diets for adults with type 2 diabetes (T2D)(1). The purpose of the report was to review the evidence on ‘low’-carbohydrate diets compared with the current UK government advice on carbohydrate intake for adults with T2D. However, since there is no agreed and widely utilised definition of a ‘low’-carbohydrate diet, comparisons in the report were between lower and higher carbohydrate diets. SACN’s remit is to assess the risks and benefits of nutrients, dietary patterns, food or food components for health by evaluating scientific evidence and to make dietary recommendations for the UK based on its assessment(2). SACN has a public health focus and only considers evidence in healthy populations unless specifically requested to do otherwise. Since the Committee does not usually make recommendations relating to clinical conditions, a joint working group (WG) was established in 2017 to consider this issue. The WG comprised members of SACN and members nominated by Diabetes UK, the British Dietetic Association, Royal College of Physicians and Royal College of General Practitioners. Representatives from NHS England and NHS Health Improvement, the National Institute for Health and Care Excellence and devolved health departments were also invited to observe the WG. The WG was jointly chaired by SACN and Diabetes UK.

The policy of Universal Salt Iodisation (USI) could reduce population’s thyroid volume (TVOL) in iodine deficiency areas. Conversely, the improved growth and developmental status of children might increase the TVOL accordingly. Whether the decreased TVOL by USI conceals the increase effect of height and weight on TVOL is unclear. The aim of this study was to analyse the association between height, weight, iodine supplementation and TVOL. Five national Iodine Deficiency Disorder surveys were matched into four pairs according to the purpose of analysis. County-level data of both detected by paired surveys were incorporated; 1:1 random pairing method was used to match counties or individuals. The difference of TVOL between different height, weight, different iodine supplementation measures groups and the association between TVOL and them were studied. The mean height and weight of children aged 8–10 years increased from 129·9 cm and 26·9 kg in 2002 to 136·2 cm and 32·1 kg in 2019, while the median TVOL decreased from 3·10 ml to 2·61 ml. Iodine supplementation measures can affect TVOL; after excluding iodine effects, the median TVOL was increased with the height and weight. On the other side, after excluding the influence of height and weight, the median TVOL remained decreased. Only age, weight and salt iodine were significantly associated with TVOL in multiple linear models. Development of height and weight in children is the evidence of improved nutrition. The decreased TVOL caused by iodised salt measures conceals the increase effect of height and weight on TVOL. Age, weight and salt iodine affect TVOL significantly.

An adequate intake of PUFA plays a vital role in human health. Therefore, it is important to assess PUFA intakes in different populations and validate them with biomarkers, but only a few small studies are in paediatric populations. We calculated the dietary intake of PUFA and their main food sources in children and assessed associations between PUFA intakes and plasma proportions. Dietary intakes of 7-year-old children (n 8242) enrolled in the Avon Longitudinal Study of Parents and Children were calculated from the parental-completed FFQ. Plasma PUFA were measured in 5571 children 8 months later, and 4380 children had complete dietary and plasma data. The association between dietary and plasma PUFA proportions was estimated using Spearman’s correlation coefficients, quintile cross-classification and Cohen’s κ coefficients. Mean total PUFA intake was 13·2 g/d (sd 4·2), contributing 6·5 % of total energy intake; n-6 PUFA contributed 5·2 % and n-3 PUFA 0·7 %. The n-6:n-3 ratio was 7·9:1. Mean intakes of EPA and DHA were 35·7 mg/d and 49·7 mg/d, respectively. Most n-3 and n-6 PUFA intakes were weakly correlated with their respective plasma lipids (0·07 ≤ r ≤ 0·16, P < 0·001). The correlation between dietary and plasma DHA was stronger though (r = 0·34, P < 0·001), supported by a modest level of agreement between quintiles (k = 0·32). The results indicate that the FFQ was able to reasonably rank the long-chain (LC) PUFA, DHA, in this paediatric population. Public health initiatives need to address the suboptimal ratio of n-6:n-3 PUFA and very low n-3 LC-PUFA intakes in school-age children in the UK.

Numerous epidemiological studies have suggested that nut intake is associated with a reduced risk of mortality. Although diets and lifestyles differ by regions or races/ethnicities, few studies have investigated the associations among non-white, non-Western populations. We evaluated the associations of total nut and peanut intakes with all-cause and cause-specific mortality in a population-based prospective cohort in Japan. Participants (age: ≥35 years at baseline in 1992; n 31 552) were followed up until death or the end of follow-up in 2008. Those with cancer, CHD or stroke at baseline were excluded. Dietary intake was assessed only at baseline by using a validated FFQ. In total, 2901 men died during 183 299 person-years and 2438 women died during 227 054 person-years. The mean intakes of total nuts were 1·8 and 1·4 g/d in men and women, respectively. Although peanut intake accounted for approximately 80 % of the total nut intake, total nut and peanut intakes were inversely associated with all-cause mortality in men after adjusting for all potential confounders. For example, compared with the lowest quartile category, the adjusted hazard ratio (95 % CI) of total nut intake for all-cause mortality in men of the highest quartile category was 0·85 (95 % CI 0·75, 0·96) (Pfor trend = 0·034). Peanut intake was inversely associated with digestive disease mortality in men and CVD mortality in women. Total nut and peanut intakes, even in low amounts, were associated with a reduced risk of mortality particularly in men.

Dyslipidaemia, a significant risk factor of CVD, is threatening human health worldwide. PUFA are crucial long-chain fatty acids for TAG synthesis and removal, potentially decreasing dyslipidaemia risk. We examined dyslipidaemia prevalence among 15 244 adults aged ≥ 20 years from National Health and Nutrition Examination Survey 2009–2016. Dyslipidaemia was defined as total cholesterol ≥ 240 mg/dl, or HDL-cholesterol < 40 mg/dl/50 mg/dl for males/females, respectively, or LDL-cholesterol ≥ 160 mg/dl, or TAG ≥ 200 mg/dl, or taking lipid-modifying medications. We measured the daily PUFA intake using a 24-h dietary recall. Demographics, social economics, and lifestyle factors were collected using questionnaires/interviews. Additionally, we measured Se and Hg levels in the whole blood. Logistic regression models were used to examine the association between PUFA and dyslipidaemia. The unweighted and weighted dyslipidaemia prevalences were 72·4% and 71·0 %, respectively. When grouped into tertiles, PUFA intake above 19·524 g/d was associated with an independent 19 % decrease in dyslipidaemia risk (OR = 0·81 (95 % CI 0·71, 0·94)) compared with the lowest tertile (PUFA intake ≤ 12·349 g/d). A threshold inverse association was further determined by the restricted cubic spline analysis. When PUFA intake was increased to its turning point, that is, 19 g/d, the lower nadir risk for dyslipidaemia was obtained (OR = 0·72 (95 % CI 0·56, 0·89)). When the exposure was the sum of α-linolenic acid and octadecatetraenoic acid, the inverse linear association remained. Dietary PUFA intake is a beneficial factor for dyslipidaemia among American adults, independent of many potential confounders, including Hg and Se.

Polycystic ovary syndrome (PCOS) is associated with a higher prevalence of sleep disturbances and obesity. Treatment of PCOS includes modifying lifestyle behaviours associated with weight management. However, poor sleep in the non-PCOS population has been associated with poorer lifestyle behaviours. The aim was to investigate whether sleep disturbance confounds or modifies the association between lifestyle factors and PCOS. This was a cross-sectional analysis from the Australian Longitudinal Study on Women’s Health cohort aged 31–36 years in 2009 were analysed (n 6067, 464 PCOS, 5603 non-PCOS). Self-reported data were collected on PCOS, anthropometry, validated modified version of the Active Australia Physical Activity survey, validated FFQ and sleep disturbances through latent class analysis. Women with PCOS had greater adverse sleep symptoms including severe tiredness (P = 0·001), difficulty sleeping (P < 0·001) and restless sleep (P < 0·001), compared with women without PCOS. Women with PCOS also had higher energy consumption (6911 (sd 2453) v. 6654 (sd 2215) kJ, P = 0·017), fibre intake (19·8 (sd 7·8) v. 18·9 (sd 6·9) g, P = 0·012) and diet quality (dietary guidelines index (DGI)) (88·1 (sd 11·6) v. 86·7 (sd 11·1), P = 0·008), lower glycaemic index (50·2 (sd 4·0) v. 50·7 (sd 3·9), P = 0·021) and increased sedentary behaviour (6·3 (sd 2·8) v. 5·9 (sd 2·8) h, P = 0·009). There was a significant interaction between PCOS and sleep disturbances for DGI (P = 0·035), therefore only for women who had adequate sleep was PCOS associated with a higher DGI. For women with poorer sleep, there was no association between PCOS and DGI. The association between PCOS and improved diet quality may only be maintained if women can obtain enough good quality sleep.

The aim of this study was to assess the association between alcohol intake and premature mortality (younger than 65 years) and to explore the effect of potential alcohol underreporting by heavy drinkers. We followed-up 20 272 university graduates. Four categories of alcohol intake were considered (abstainer, light, moderate and heavy consumption). Repeated measurements of alcohol intake and updated information on confounders were used in time-dependent Cox models. Potential underreporting of alcohol intake by some heavy drinkers (likely misclassified as light or moderate drinkers) was explicitly addressed in an attempt to correct potential underreporting by using indirect information. During 12·3 years of median follow-up (interquartile range: 6·8–15·0), 226 participants died before their 65th birthday. A higher risk of early mortality was found for the highest category of alcohol intake (≥50 g/d) in comparison with abstention (multivariable-adjusted hazard ratio (HR) = 2·82, 95 % CI 1·38, 5·79). In analyses of alcohol as a continuous variable, the multivariable-adjusted HR was 1·17 (95 % CI 1·08, 1·26), for each 10 g/d of alcohol. This harmful linear association was present both in uncorrected models and in models corrected for potential underreporting. No significant inverse association between light or moderate alcohol intake and premature mortality was observed, even after correcting for potential misclassification. Alcohol intake exhibited a harmful linear dose–response association with premature mortality (<65 years) in this young and highly educated Mediterranean cohort. Our attempts to correct for potential misclassification did not substantially change these results.

This work investigated the effects of repeated sweet taste exposure at breakfast on perceptions and intakes of other sweet foods, while also examining the effects due to duration of exposure (1/3 weeks), test context (breakfast/lunch) and associations between taste perceptions and intakes. Using a randomised controlled parallel-group design, participants (n 54, 18 male, mean age: 23·9 (sd 5·8) years, mean BMI: 23·6 (sd 3·5) kg/m2) were randomised to consume either a sweet breakfast (cereal with sucralose) (n 27) or an equienergetic non-sweet breakfast (plain cereal) (n 27) for 3 weeks. On days 0 (baseline), 7 and 21, pleasantness, desire to eat and sweetness were rated for other sweet and non-sweet foods and sweet food consumption was assessed in an ad libitum meal at breakfast and lunch. Using intention-to-treat analyses, no statistically significant effects of exposure were found at breakfast (largest F2,104 = 1·84, P = 0·17, ηp2 = 0·03) or lunch (largest F1,52 = 1·22, P = 0·27, ηp2 = 0·02), and using Bayesian analyses, the evidence for an absence of effect in all rating measures was strong to very strong (smallest BF01 = 297·97 (BF01error = 2·68 %)). Associations between ratings of pleasantness, desire to eat and intake were found (smallest r = 0·137, P < 0·01). Effects over time regardless of exposure were also found: sugars and percentage energy consumed from sweet foods increased throughout the study (smallest (F2,104 = 4·54, P = 0·01, ηp2 = 0·08). These findings demonstrate no effects of sweet taste exposure at breakfast for 1 or 3 weeks on pleasantness, desire for, sweetness or intakes of other sweet foods in either the same (breakfast) or in a different (lunch) meal context.