Improving the health and well-being of mothers and children is a priority worldwide. The present study aimed to examine the coexistence and correlates of malnutrition among mothers and under-five child pairs using Tanzania Demographic Health Survey 2015–16 data. Height-for-age, height-for-weight and weight-for-age Z-scores were used to assess the nutritional status of children, while body mass index was used to assess the nutritional status of mothers. Correlates of forms of malnutrition were assessed using multinomial logistic regression. Among 8083 pairs, 40⋅9 % were normal, 30⋅3 % were underweight, 17⋅5 % overweight and 11⋅3 % had double burden of malnutrition. The risk of being underweight is highest among the pairs with; children aged 13–59 months (relative risk ratio (RRR) = 2⋅33) and children with small birth weight (RRR = 2⋅67). Overweight is highest among pairs with; mothers aged 35–49 (RRR = 3⋅36), mothers with secondary education and above (RRR = 1⋅85), fathers aged 35+ (RRR = 1⋅38), professional fathers (RRR = 4⋅10) and richer households (RRR = 2⋅06). The double burden of malnutrition is highest among pairs with; children with small birth weight (RRR = 2⋅76), from rural households (RRR = 1⋅24) and from richer households (RRR = 1⋅41). There is a coexistence of forms of malnutrition among mothers and under-five child pairs in Tanzania. The study recommends using multidimensional approaches such as double-duty action for nutrition to eradicate all forms of malnutrition.

Obese mothers’ offspring develop obesity and metabolic alterations in adulthood. Poor postnatal dietary patterns also contribute to obesity and its comorbidities. We aimed to determine whether in obese mothers’ offspring an adverse postnatal environment, such as high-fat diet (HFD) consumption (second hit) exacerbates body fat accumulation, metabolic alterations and adipocyte size distribution. Female Wistar rats ate chow (C-5 %-fat) or HFD (maternal obesity (MO)-25 %-fat) from weaning until the end of lactation. Male offspring were weaned on either control (C/C and MO/C, maternal diet/offspring diet) or HFD (C/HF and MO/HF) diet. At 110 postnatal days, offspring were killed. Fat depots were excised to estimate adiposity index (AI). Serum glucose, triglyceride, leptin, insulin, insulin resistance index (HOMA-IR), corticosterone and dehydroepiandrosterone (DHEA) were determined. Adipocyte size distribution was evaluated in retroperitoneal fat. Body weight was similar in C/C and MO/C but higher in C/HF and MO/HF. AI, leptin, insulin and HOMA-IR were higher in MO/C and C/HF v. C/C but lower than MO/HF. Glucose increased in MO/HF v. MO/C. C/HF and MO/C had higher triglyceride and corticosterone than C/C, but lower corticosterone than MO/HF. DHEA and the DHEA/corticosterone ratio were lower in C/HF and MO/C v. C/C, but higher than MO/HF. Small adipocyte proportion decreased while large adipocyte proportions increased in MO/C and C/HF v. C/C and exacerbated in MO/HF v. C/HF. Postnatal consumption of a HFD by the offspring of obese mothers exacerbates body fat accumulation as well as the decrease of small and the increase of large adipocytes, which leads to larger metabolic abnormalities.

Zinc (Zn) is an essential mineral and its deficiency manifests in non-specific clinical signs that require long time to develop. The response of swine intestine to Zn restriction was evaluated to identify early changes that can be indicative of Zn deficiency. Twenty-seven pigs (body weight = 77⋅5 ± 2⋅5 kg) were assigned to one of three diets: diet without added Zn (Zn-restricted diet, ZnR), and ZnR-supplemented with either 50 (Zn50) or 100 mg of Zn/kg of diet (Zn100) of Zn supplied by ZnCl2. After 32 d consuming the diets, serum Zn concentration in ZnR pigs was below the range of 0⋅59–1⋅37 μg/ml considered sufficient, thereby confirming subclinical Zn deficiency. Pigs showed no obvious health or growth changes. RNA-seq analysis followed by qPCR showed decreased expression of metallothionein-1 (MT1) (P < 0⋅05) and increased expression of Zn transporter ZIP4 (P < 0⋅05) in jejunum and ileum of ZnR pigs compared with Zn-supplemented pigs. Ingenuity pathway analysis revealed that Zn50 and Zn100 induced changes in genes related to nucleotide excision repair and integrin signalling pathways. The top gene network in the ZnR group compared with Zn100 was related to lipid and drug metabolism; and compared with Zn50, was related to cellular proliferation, assembly and organisation. Dietary Zn concentrations resulted in differences in genes related to immune pathways. Our analysis showed that small intestine presents changes associated with Zn deficiency after 32 d of Zn restriction, suggesting that the intestine could be a sentinel organ for Zn deficiency.

The purpose of this investigation was to expand upon the limited existing research examining the test–retest reliability, cross-sectional validity and longitudinal validity of a sample of bioelectrical impedance analysis (BIA) devices as compared with a laboratory four-compartment (4C) model. Seventy-three healthy participants aged 19–50 years were assessed by each of fifteen BIA devices, with resulting body fat percentage estimates compared with a 4C model utilising air displacement plethysmography, dual-energy X-ray absorptiometry and bioimpedance spectroscopy. A subset of thirty-seven participants returned for a second visit 12–16 weeks later and were included in an analysis of longitudinal validity. The sample of devices included fourteen consumer-grade and one research-grade model in a variety of configurations: hand-to-hand, foot-to-foot and bilateral hand-to-foot (octapolar). BIA devices demonstrated high reliability, with precision error ranging from 0·0 to 0·49 %. Cross-sectional validity varied, with constant error relative to the 4C model ranging from −3·5 (sd 4·1) % to 11·7 (sd 4·7) %, standard error of the estimate values of 3·1–7·5 % and Lin’s concordance correlation coefficients (CCC) of 0·48–0·94. For longitudinal validity, constant error ranged from −0·4 (sd 2·1) % to 1·3 (sd 2·7) %, with standard error of the estimate values of 1·7–2·6 % and Lin’s CCC of 0·37–0·78. While performance varied widely across the sample investigated, select models of BIA devices (particularly octapolar and select foot-to-foot devices) may hold potential utility for the tracking of body composition over time, particularly in contexts in which the purchase or use of a research-grade device is infeasible.

We performed a systematic review and dose–response meta-analysis of randomised trials on the effects of olive oil consumption on blood lipids in adults. A systematic search was performed in PubMed, Scopus and Web of Science databases until May 2021. Randomised controlled trials (RCT) evaluating the effect of olive oil intake on serum total cholesterol (TC), TAG, LDL-cholesterol and HDL-cholesterol in adults were included. The mean difference (MD) and 95 % CI were calculated for each 10 g/d increment in olive oil intake using a random-effects model. A total of thirty-four RCT with 1730 participants were included. Each 10 g/d increase in olive oil consumption had minimal effects on blood lipids including TC (MD: 0·79 mg/dl; 95 % CI (−0·08, 1·66); I2 = 57 %; n 31, GRADE = low certainty), LDL-cholesterol (MD: 0·04 mg/dl, 95 % CI (−1·01, 0·94); I2 = 80 %; n 31, GRADE = very low certainty), HDL-cholesterol (MD: 0·22 mg/dl; 95 % CI (−0·01, 0·45); I2 = 38 %; n 33, GRADE = low certainty) and TAG (MD: 0·39 mg/dl; 95 % CI (−0·33, 1·11); I2 = 7 %; n 32, GRADE = low certainty). Levels of TC increased slightly with the increase in olive oil consumption up to 30 g/d (MD30 g/d: 2·76 mg/dl, 95 % CI (0·01, 5·51)) and then appeared to plateau with a slight downward curve. A trivial non-linear dose-dependent increment was seen for HDL-cholesterol, with the greatest increment at 20 g/d (MD20 g/d: 1·03 mg/dl, 95 % CI (−1·23, 3·29)). Based on existing evidence, olive oil consumption had trivial effects on levels of serum lipids in adults. More large-scale randomized trials are needed to present more reliable results.

Selenium (Se) is essential for selenoprotein synthesis, being thus important for immune and thyroid function, and for antioxidant defence. Some studies have shown that low levels of Se may associate with hypertensive disorders of pregnancy (HDP). Nevertheless, evidence supporting Se supplementation in pregnant or childbearing-age women is still lacking. In this context, this work aimed to systematically review the most recent scientific evidence to understand the relationship between Se levels and HDP. We performed a systematic review (protocol number: CRD42022310424) with literature of the last decade. PubMed, Scopus, Web of Science, registers and grey literature were searched to identify studies reporting measurement of Se levels in normotensive and hypertensive pregnant women (supplemented or not with Se). Study quality was assessed using the National Heart, Lung, and Blood Institute Study Quality Assessment Tools. Among the thirty included studies, a majority, 61 % (n 19) of the ‘good’ or ‘fair’ studies, reported a negative association between Se and HDP, and some studies, 39 % (n 11) of the ‘good’ or ‘fair’ studies, reported a lack of association. This review provides an important amount of quality evidence suggesting that low Se levels associate with the occurrence of HDP. Nevertheless, the gathered information is not enough to underlie a recommendation for Se supplementation in pregnancy to protect against HDP. Thus, this review emphasises the need for further well-designed randomised controlled trials that may provide blunt evidence regarding the benefits of Se supplementation during pregnancy.

Hormone-sensitive lipase (HSL) is one of the rate-determining enzymes in the hydrolysis of TAG, playing a crucial role in lipid metabolism. However, the role of HSL-mediated lipolysis in systemic nutrient homoeostasis has not been intensively understood. Therefore, we used CRISPR/Cas9 technique and Hsl inhibitor (HSL-IN-1) to establish hsla-deficient (hsla-/-) and Hsl-inhibited zebrafish models, respectively. As a result, the hsla-/- zebrafish showed retarded growth and reduced oxygen consumption rate, accompanied with higher mRNA expression of the genes related to inflammation and apoptosis in liver and muscle. Furthermore, hsla-/- and HSL-IN-1-treated zebrafish both exhibited severe fat deposition, whereas their expressions of the genes related to lipolysis and fatty acid oxidation were markedly reduced. The TLC results also showed that the dysfunction of Hsl changed the whole-body lipid profile, including increasing the content of TG and decreasing the proportion of phospholipids. In addition, the systemic metabolic pattern was remodelled in hsla-/- and HSL-IN-1-treated zebrafish. The dysfunction of Hsl lowered the glycogen content in liver and muscle and enhanced the utilisation of glucose plus the expressions of glucose transporter and glycolysis genes. Besides, the whole-body protein content had significantly decreased in the hsla-/- and HSL-IN-1-treated zebrafish, accompanied with the lower activation of the mTOR pathway and enhanced protein and amino acid catabolism. Taken together, Hsl plays an essential role in energy homoeostasis, and its dysfunction would cause the disturbance of lipid catabolism but enhanced breakdown of glycogen and protein for energy compensation.

Recent findings suggest that the distribution of protein intake throughout the day has an impact on various health outcomes in older adults, independently of the amount consumed. We evaluated the association between the distribution of dietary protein intake across meals and all-cause mortality in community-dwelling older adults. Data from 3225 older adults aged ≥ 60 years from the Seniors-ENRICA-1 cohort were examined. Habitual dietary protein consumption was collected in 2008–2010 and in 2012 through a validated diet history. Protein distribution across meals was calculated for each participant as the coefficient of variation (CV) of protein intake per meal, in sex-specific tertiles. Vital status was obtained from the National Death Index up to 30 January 2020. Cox proportional hazards regression was performed to determine the hazard ratios (HR) and their 95 % CI for the association between the distribution of daily protein intake across meals and all-cause mortality. Over a median follow-up of 10·6 years, 591 deaths occurred. After adjustment for potential confounders, the CV of total protein intake was not associated with all-cause mortality (HR and 95 % CI in the second and third tertile v. the lowest tertile: 0·94 (0·77, 1·15) and 0·88 (0·72, 1·08); Ptrend = 0·22). Similarly, the HR of all-cause mortality when comparing extreme tertiles of CV for types of protein were 0·89 (0·73, 1·10) for animal-protein intake and 1·02 (0·82, 1·25) for plant-protein intake. Dietary protein distribution across meals was not associated with all-cause mortality, regardless of protein source and amount, among older adults. Further studies should investigate whether this picture holds for specific causes of death.

Many epidemiological studies have emphasised the relation between carotenoid dietary intake and their circulating concentrations and beneficial health effects, such as lower risk of cardiometabolic diseases and cancer. However, there is dispute as to whether the attributed health benefits are due to native carotenoids or whether they are instead induced by their metabolites. Several categories of metabolites have been reported, most notably involving (a) modifications at the cyclohexenyl ring or the polyene chain, such as epoxides and geometric isomers, (b) excentric cleavage metabolites with alcohol-, aldehyde- or carboxylic acid-functional groups or (c) centric cleaved metabolites with additional hydroxyl, aldehyde or carboxyl functionalities, not counting their potential phase-II glucuronidated / sulphated derivatives. Of special interest are the apo-carotenoids, which originate in the intestine and other tissues from carotenoid cleavage by β-carotene oxygenases 1/2 in a symmetrical / non-symmetrical fashion. These are more water soluble and more electrophilic and, therefore, putative candidates for interactions with transcription factors such as NF-kB and Nrf2, as well as ligands for RAR–RXR nuclear receptor interactions. In this review, we discuss in vivo detected apo-carotenoids, their reported tissue concentrations, and potential associated health effects, focusing exclusively on the human situation and based on quantified / semi-quantified carotenoid metabolites proven to be present in humans.

In Bangladesh, only 34 % of the children aged 18–23 months old are given minimum acceptable diets of complementary foods. Objective of the study was to find the effects of complementary feeding counselling on nutritional status among 6–23 months old children of poor families. This was a community-based randomised control trial. A total of 192 children in two groups were randomly selected. Nutrition education was given for a period of 4 months with post-intervention follow-up for 2 months. After 4 months of intervention, the difference in height for age Z score, weight for height Z score and weight for age Z score were significantly higher in the intervention group than in the control group (1·01 ± 0·31 v. 0·19 ± 0·01, P =< 0·001; 1·34 ± 0·15 v 0·72 ± 0·11, P =< 0·001; 1·5 ± 0·24 v. 0·62 ± 0·04, P =< 0·001). Mid-upper arm circumference Z score also improved in the intervention group than in the control group (0·95 ± 0·03 v. 0·57 ± 0·12, P =< 0·001). Morbidity of the children in the intervention group significantly reduced than in the control group (49 % v 80·20 %, P =< 0·001). Higher feeding frequency (3–4 times) (71·9 % v. 45·8 %) and energy intake increased in the intervention group than in the control group. Promotion of complementary feeding from the family foods can improve the nutritional status of 6–23 months old children of poor families within a short period.

Olive oil (OO) polyphenols have been shown to improve HDL anti-atherogenic function, thus demonstrating beneficial effects against cardiovascular risk factors. The aim of the present study was to investigate the effect of extra virgin high polyphenol olive oil (HPOO) v. low polyphenol olive oil (LPOO) on the capacity of HDL to promote cholesterol efflux in healthy adults. In a double-blind, randomised cross-over trial, fifty participants (aged 38·5 (sd 13·9) years, 66 % females) were supplemented with a daily dose (60 ml) of HPOO (320 mg/kg polyphenols) or LPOO (86 mg/kg polyphenols) for 3 weeks. Following a 2-week washout period, participants crossed over to the alternate treatment. Serum HDL-cholesterol efflux capacity, circulating lipids (i.e. total cholesterol, TAG, HDL, LDL) and anthropometrics were measured at baseline and follow-up. No significant between-group differences were observed. Furthermore, no significant changes in HDL-cholesterol efflux were found within either the LPOO and HPOO treatment arms; mean changes were 0·54 % (95 % CI (0·29, 1·37)) and 0·10 % (95 % CI (0·74, 0·94)), respectively. Serum HDL increased significantly after LPOO and HPOO intake by 0·13 mmol/l (95 % CI (0·04, 0·22)) and 0·10 mmol/l (95 % CI (0·02, 0·19)), respectively. A small but significant increase in LDL of 0·14 mmol/l (95 % CI (0·001, 0·28)) was observed following the HPOO intervention. Our results suggest that additional research is warranted to further understand the effect of OO with different phenolic content on mechanisms of cholesterol efflux via different pathways in multi-ethnic populations with diverse diets.

Exercise and dietary interventions have been described to positively affect metabolic syndrome (MetS) via molecular-induced changes. The purpose of this study was to investigate the effects of dietary carbohydrate restriction and aerobic exercise (AE) on retinol binding protein 4 (RBP4) and fatty acid binding protein 5 (FABP5) in middle-aged men with MetS. The study had a randomised, double-blinded, parallel-controlled design. Forty middle-aged men with MetS (age: 53·97 ± 2·85 years, BMI = 31·09 ± 1·04 kg/m2) were randomly assigned to four groups, AE (n 10), ketogenic diet (KD; n 10), AE combined with KD (AE + KD; n 10) or control (C; n 10). RBP4, FABP5, body composition (body mass, BMI and body fat), insulin resistance, insulin sensitivity and MetS factors were evaluated prior to and after the 12-week intervention. AE + KD significantly decreased the body fat percentage (P = 0·006), BMI (P = 0·001), Zmets (P = 0·017), RBP4 (P = 0·017) and the homeostasis model of insulin resistance (HOMA-IR) (P = 0·001) as compared with control group and marginally significantly decreased the Zmets as compared with exercise group (P = 0·086). KD significantly decreased RBP4 levels as compared with control group (P = 0·041). Only the AE intervention (P = 0·045) significantly decreased FABP5 levels. Combining intervention of carbohydrate restriction with AE compared with carbohydrate restriction and AE alone improved RBP4, HOMA-IR as well as different body composition and MetS factors in middle-aged men with MetS.

As an internal time-keeping mechanism, circadian rhythm plays crucial role in maintaining homoeostasis when in response to nutrition change; meanwhile, branched-chain amino acids (BCAA) in skeletal muscle play an important role in preserving energy homoeostasis during fasting. Previous results from our laboratory suggested that fasting can influence peripheral circadian rhythm and BCAA metabolism in fish, but the relationship between circadian rhythm and BCAA metabolism, and whether circadian rhythm regulates BCAA metabolism to maintain physiological homoeostasis during fasting remains unclear. This study shows that the expression of fifteen core clock genes as well as KLF15 and Bcat2 is highly responsive to short-term fasting in fast muscle of Siniperca chuatsi, and the correlation coefficient between Clock and KLF15 expression is enhanced after fasting treatment. Furthermore, we demonstrate that the transcriptional expression of KLF15 is regulated by Clock, and the transcriptional expression of Bcat2 is regulated by KLF15 by using dual-luciferase reporter gene assay and Vivo-morpholinos-mediated gene knockdown technique. Therefore, fasting imposes a dynamic coordination of transcription between the circadian rhythm and BCAA metabolic pathways. The findings highlight the interaction between circadian rhythm and BCAA metabolism and suggest that fasting induces a switch in KLF15 expression through affecting the rhythmic expression of Clock, and then KLF15 promotes the transcription of Bcat2 to enhance the metabolism of BCAA, thus maintaining energy homoeostasis and providing energy for skeletal muscle as well as other tissues.

This review summarises evidence relating to a potential role for vitamin D supplementation in the prevention or treatment of coronavirus disease 2019 (COVID-19). Laboratory studies show that the active vitamin D metabolite 1,25-dihydroxyvitamin D induces innate antiviral responses and regulates immunopathological inflammation with potentially favourable implications for the host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Meta-analyses of cross-sectional, case-control and longitudinal studies report consistent protective associations between higher circulating 25-hydroxyvitamin D [25(OH)D] concentrations or vitamin D supplement use and reduced risk and severity of COVID-19. However, Mendelian randomisation studies testing for associations between genetically predicted circulating 25(OH)D concentrations and COVID-19 outcomes have yielded consistently null results. Positive findings from observational epidemiological studies may therefore have arisen as a result of residual or unmeasured confounding or reverse causality. Randomised controlled trials of prophylactic or therapeutic vitamin D supplementation to reduce risk or severity of COVID-19 reporting to date have yielded inconsistent findings. Results of further intervention studies are pending, but current evidence is insufficient to support routine use of vitamin D supplements as a therapeutic or prophylactic agent for COVID-19, or as an adjunct to augment immunogenicity of SARS-CoV-2 vaccination. Accordingly, national and international bodies have not made any recommendations regarding a role for vitamin D in the prevention or treatment of COVID-19.

The human health benefits of cardiometabolic disease prevention can be accompanied by planetary co-benefits. Focusing efforts towards young people, including children and adolescents, is conducive to disease prevention. In the context of cardiometabolic disease prevention, this review paper critically summarises the available literature on the acute cardiometabolic responses to physical activity and breakfast manipulations among young people. Given the seriousness of global climate change, which will disproportionally affect our younger generations, this review paper offers new insights into the inherent interactions between child–adolescent behaviour and cardiometabolic health from an environmental sustainability perspective to aid climate change mitigation efforts, including exploring future research avenues. A growing evidence base suggests acute moderate- to high-intensity exercise bouts can attenuate postprandial plasma glucose, insulin and triacylglycerol concentrations for up to 24–48 h in young people. Whether accumulating physical activity throughout the day with short, frequent bouts promotes cardiometabolic risk marker attenuations is unclear. Breakfast consumption may enhance free-living physical activity and reduce glycaemic responses to subsequent meals for a possible additive impact. If repeated habitually, attenuations in these cardiometabolic risk factors would be conducive to disease prevention, reducing the greenhouse gas emissions associated with disease diagnosis and treatment. To progress current understanding with high public health and planetary relevance, research among samples of ‘at risk’ young people that span cellular-level responses to ecologically valid settings and address human and planetary health co-benefits is needed. Indeed, certain physical activity opportunities, such as active travel to school, offer important direct co-benefits to humans and planetary health.