Malnutrition is a common feature of chronic and acute diseases, often associated with a poor prognosis, including worsening of clinical outcome, owing, among other factors, to dysfunction of the most internal organs and systems affecting the absorption, metabolism and elimination of drugs and nutrients. Taurine is involved in numerous biological processes and is required in increased amounts in response to pathological conditions. The aim of this study was to describe the behaviour of taurine in well-nourished (WN) rats and to analyse the influence of protein–energy undernutrition on the pharmacokinetic (PK) parameters of taurine, using a PK model. Wistar rats were randomly distributed into two groups, WN and undernourished (UN), and taurine was administered intravenously or orally at different doses: 1, 10 and 100 mg. Population pharmacokinetic modelling of plasma levels was performed using the NONMEM 7.2 program. Several distribution and absorption models were explored in combination with dose and/or time covariate effects. Covariates such as nutritional status, serum albumin, body weight and score of undernutrition were used. A two-compartment population pharmacokinetic model with zero-order endogenous formation, passive absorption, first-order kinetics distribution and non-linear elimination with parallel Michaelis–Menten excretion and reabsorption processes best described taurine pharmacokinetics. Undernutrition acted as a covariate reducing the Vmax of the active elimination process. Data analysis showed linear absorption and distribution, and non-linear elimination processes for taurine. Elimination of taurine was reduced in UN animals, suggesting that the reabsorption process via the secretion transporter was modified in that group.

Given the dynamic characteristic of an individual’s drinking behaviours, comprehensive consideration of alcohol consumption variation using repeated measures may improve insight into the nature of its association with blood pressure (BP) change. We examined the association between longitudinal alcohol consumption (trajectory and quantity) and changes in BP and pulse pressure (PP) among Korean aged ≥ 40 years living in rural areas. Totally, 1682 hypertension-free participants who completed all three health examinations (median, 5·3 years) were included. All three visits were used to determine the cumulative trajectory of and quantity of alcohol consumption and the latest two visits and the last visit were used for the recent trajectory and the most recent quantity of alcohol consumption, respectively. Changes in BP and PP from the baseline to the third visit were used as outcome. In men, ≥30 ml/d cumulative average alcohol consumption was associated with the greatest increase in systolic BP (SBP) in both baseline outcome-unadjusted (2·9 mmHg, P = 0·032) and -adjusted models (3·6 mmHg, P = 0·001), and the given association for the most recent alcohol consumption was observed in the baseline outcome-adjusted model (3·9 mmHg, P = 0·003). For PP, similar associations were observed only in the baseline outcome-adjusted model. No meaningful associations in diastolic BP in men and any BP or PP in women existed. The quantity of alcohol consumption rather than the trajectory may be significantly related to raised SBP, and a possible short-term influence of the most recent alcohol consumption may exist when baseline SBP is adjusted in men.

The effect and the role played by dietary α-lactalbumin (α-LAC) on hepatic fat metabolism are yet to be fully elucidated. We reported previously that α-LAC intake induced atherogenic dyslipidaemia in Balb/c mice. The aim of the present study was to investigate if this atherogenic effect could be due to a possible α-LAC-induced hepatic steatosis. We examine the ability of dietary α-LAC to induce liver steatosis, identifying the molecular mechanisms underlying hepatic lipid metabolism in association with the lipid profile, peripheral insulin resistance (IR) and changes in the hepatic oxidative environment. Male Balb/c mice (n 6) were fed with diets containing either chow or 14 % α-LAC for 4 weeks. The α-LAC-fed mice developed abdominal adiposity and IR. Moderate liver steatosis with increased TAG and NEFA contents was correlated with atherogenic dyslipidaemia. There was increased nuclear expression of liver X receptor αβ (LXRαβ), sterol regulatory element-binding protein-1c (SREBP-1c) and PPARγ transcription factors and of the cytosolic enzymes acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase involved in the hepatic de novo lipogenesis. The opposite was found for the nuclear receptor PPARα and the mitochondrial enzyme carnitine palmitoyltransferase-1 (CPT-1), leading to reduced fatty acid β-oxidation (FAO). These changes were associated with a significant decrease in both p-Thr172-AMP-activated protein kinase α (AMPKα) (inactivation) and p-Ser79-ACC1 (activation) and with a more oxidative liver environment increasing lipid peroxidation and protein oxidation and reducing GSH:GSSG ratio in the α-LAC-fed mice. In conclusion, 4 weeks of 14 % α-LAC feeding induced liver steatosis associated with atherogenic dyslipidaemia, IR and oxidative stress by enhancing nuclear LXRαβ/SREBP-1c/PPARγ expression and diminishing PPARα/CPT-1 expression and AMPKα phosphorylation shifting the hepatic FAO toward fatty acid synthesis in Balb/c mice.

The present study determined the ability of the Mini Nutritional Assessment (MNA) to predict care need in older people. We analysed the datasets of the Taiwan Longitudinal Study on Aging. The 1999 survey containing the MNA items served as the baseline and the 2003 survey served as the endpoint. Of the 4440 participants, 2890 were aged  ≥ 65 years and served as subjects in the present study. After excluding 150 subjects having incomplete data, 2740 were rated for nutritional status with the normalised long-form (LF) and short-form (SF) MNA-Taiwan version 1 (T1) and version 2 (T2) and evaluated with logistic regression analysis for cross-sectional associations of the rated nutritional status with care need, controlled for age, sex, education level, living arrangement and physical activity. Receiver operating characteristic curves were generated for evaluating the ability of the MNA to predict care need. After further excluding 250 subjects who had care need at baseline and seventy-six who were lost to follow-up, 2414 were evaluated for the ability of the MNA to predict subsequent care need with logistic regression analysis. The results demonstrated that all the MNA predicted concurrent and subsequent care need well. The OR for needing subsequent care in the ‘at-risk’ and ‘malnourished’ groups were, respectively, 2·04 and 3·33 for the MNA-T1-LF, 2·10 and 5·35 for the MNA-T2-LF, 1·49 and 2·48 MNA-T1-SF, and 1·80 and 3·44 for the MNA-T2-SF (all P< 0·05), and the respective Nagelkerke R2 values were 0·190, 0·191, 0·184 and 0·192. In conclusion, all the four MNA have the ability to predict future care need, including the MNA-T2-SF, which appears to have great potential for practical applicability.

The objective was to verify the association between body dissatisfaction (BD) – constituted by the desire to lose weight – with family and personal aspects related to the shape of the body and weight control practices in female adolescents. A cross-sectional, observational epidemiological study with adolescents aged 12–19 years, enrolled in classes of the 8th and 9th years of public schools belonging to the urban area of the city of Caxias do Sul/Rio Grande do Sul, Brazil, was conducted. A self-applicable questionnaire was used. BD was assessed using a silhouette scale. Multivariate regression was performed using Poisson regression with robust variation, hierarchically using a pre-established conceptual model, using the prevalence ratio (PR) adjusted with 95 % CI as a measure of effect. A significance level of 5 % (P ≤ 0·05) was considered. Among the 685 female students, 77·2 % had BD. The father’s incentive to diet sometimes (PR 1·19; 95 % CI 1·07, 1·32; P ≤ 0·001) and always (PR 1·15; 95 % CI 1·03, 1·28; P ≤ 0·001), trying to lose weight (PR 1·63; 95 % CI 1·33, 1·99; P ≤ 0·001), dieting five times or more (PR 1·22; 95 % CI 1·09, 1·36; P ≤ 0·001) and skipping meals less than once a week (PR 1·16; 95 % CI 1·04, 1·29; P = 0·026) increased the chances of having BD. In conclusion, among the investigated parents’ behaviours, only the father’s incentive to go on a diet was associated with BD. Adolescent weight control practices increased the chances of having BD. Thus, it facilitates the identification of this condition at an early stage, enabling adequate treatment and prevention of health complications.

Tea contains polyphenols such as flavonoids, anthocyanidins, flavanols and phenolic acids which in laboratory studies have reported to promote antioxidant enzyme formation, reduces excess inflammation, slow cancer cell proliferation and promote apoptosis. Evidence from epidemiological studies on the effect of tea consumption on prostate cancer (CaP) incidence has been conflicting. We analysed data from 25 097 men within the intervention arm of the 155 000 participant Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Histologically confirmed cases of prostate cancer were reported in 3088 men (12·3 %) during the median 11·5 year follow-up. Tea consumption was assessed with a FFQ. Baseline characteristics were compared between groups using χ2 and Kruskal–Wallis tests. Cox regression models were used to assess associations between tea intake and CaP incidence. There was no statistical difference between the risk of CaP between men who never drank tea to those who drank tea at any quantity. Amongst tea drinkers, those in the highest third of consumption group had a small but significantly lower risk compared with those in the lowest third (11·2 % v. 13·2 % hazard ratio 1·16; (95 % CI 1·05, 1·29), P = 0·004). This pattern persisted with adjustments for demographics and lifestyle. In conclusion, among tea drinkers, there was a small positive association between drinking tea and a reduced risk of prostate cancer. It does not support starting to drink tea, if men previously did not, to reduce the risk. Further research is needed to establish whether tea is justified for future prospective nutritional intervention studies investigating CaP prevention.

Frequent ultra-processed food (UPF) consumption is consistently associated with poor health outcomes. Little is known about UPF intake during early childhood and its effects on growth. We assessed UPF in relation to child anthropometry, bone maturation, and their nutrition profiles in a rural Ecuadorian community. Covariate-adjusted regression models estimated relationships between UPF intake from a 24-hour Food Frequency Questionnaire and three outcomes: linear growth, weight status and bone maturation. Nutrient Profiling Models (NPM) evaluated a convenience sample of UPF (n 28) consumed by children in the community. In this cohort (n 125; mean age = 33·92 (sd 1·75) months), 92·8 % consumed some form of UPF the previous day. On average, children consuming UPF four to twelve times per day (highest tertile) had lower height-for-age z-scores than those with none or a single instance of UPF intake (lowest tertile) (β = –0·43 [se 0·18]; P = 0·02). Adjusted stunting odds were significantly higher in the highest tertile relative to the lowest tertile (OR: 3·07, 95 % CI 1·11, 9·09). Children in the highest tertile had significantly higher bone age z-scores (BAZ) on average compared with the lowest tertile (β = 0·58 [se 0·25]; P = 0·03). Intake of savoury UPF was negatively associated with weight-for-height z-scores (β = –0·30 [se 0·14]; P = 0·04) but positively associated with BAZ (β = 0·77 [se 0·23]; P < 0·001). NPM indicated the availability of unhealthy UPF to children, with excessive amounts of saturated fats, free sugars and sodium. Findings suggest that frequent UPF intake during early childhood may be linked to stunted growth (after controlling for bone age and additional covariates), despite paradoxical associations with bone maturation.

Changes between diet quality and health-related quality of life (HR-QoL) over 12 years were examined in men and women, in 2844 adults (46 % males; mean age 47·3 (sd 9·7) years) from the Australian Diabetes, Obesity and Lifestyle study with data at baseline, 5 and 12 years. Dietary intake was assessed with a seventy-four-item FFQ. Diet quality was estimated with the Dietary Guideline Index, Mediterranean-Dietary Approaches to Stop Hypertension Diet Intervention for Neurological Delay Index (MIND) and Dietary Inflammatory Index. HR-QoL in terms of global, physical component summary (PCS) and mental component summary (MCS) was assessed with the Short-Form Health Survey-36. Fixed effects regression models adjusted for confounders were performed. Mean MCS increased from baseline (49·0, sd 9·3) to year 12 (50·7, sd 9·1), whereas mean PCS decreased from baseline (51·7, sd 7·4) to year 12 (49·5, sd 8·6). For the total sample, an improvement in MIND was associated with an improvement in global QoL (β = 0·28, 95 % CI (0·007, 0·55)). In men, an improvement in MIND was associated with an improvement in global QoL (β = 0·28, 95 % CI (0·0004, 0·55)). In women, improvement in MIND was associated with improvements in global QoL (β = 0·62 95 % CI (0·38, 0·85)), MCS (β = 0·75, 95 % CI (0·29, 1·22)) and PCS (β = 0·75, 95 % CI (0·29, 1·22)). Positive changes in diet quality were associated with broad improvements in HR-QoL, and most benefits were observed in women when compared to men. These findings support the need for strategies to assist the population in consuming healthy dietary patterns to lead to improvements in HR-QoL.

Rapid prenatal and postnatal weight gain seem to alter appetite regulation and hypothalamic functions through different pathways; however, little is known on how early life growth trajectories may influence appetitive traits in school-age. We aimed to explore the associations between weight trajectories from birth to 5 years and appetitive traits at 7. Participants were from the Generation XXI birth cohort (n 3855). Four weight trajectories were investigated: ‘normal weight gain’ (closely overlaps the 50th percentile in the weight-for-age curve), ‘weight gain during infancy’ (low birth weight and weight gain mainly during infancy), ‘weight gain during childhood’ (continuous weight gain since birth) and ‘persistent weight gain’ (always showing higher weight than the average). Appetitive traits were assessed through the Children’s Eating Behaviour Questionnaire. Associations were tested using generalised linear models, adjusted for maternal and child characteristics. Compared with ‘normal weight gain’, those in the other growth trajectories showed greater enjoyment of food and eating in response to food stimuli (i.e. Food Responsiveness) but were less able to compensate for prior food intake and ate faster at 7 (i.e. less Satiety Responsiveness and Slowness in Eating). Also, those with ‘weight gain during infancy’ showed to have greater Emotional Overeating and less Emotional Undereating and were fussier. Associations were stronger if greater weight gain occurred during infancy. Early infancy seems to be a sensitive period in the development of later appetitive traits. The control of rapid growth during infancy, besides strategies focused on the overall environment where children are living, is necessary.

The associations of different lipid measures and related indices with incident hypertension during a median follow-up of 12·89 years were examined. Fasting levels of total cholesterol (TC), TAG, HDL-cholesterol and LDL-cholesterol, and related indices (TC/HDL-cholesterol and TAG/HDL-cholesterol) were determined in 7335 Iranian adults (men = 3270) free of hypertension, aged 39·0 (sd 13·2) years. Multivariate Cox proportional hazard regression was applied and lipid parameters were considered either as categorical or continuous variables. During follow-up, 2413 (men = 1126) participants experienced hypertension. Using the first quartile as reference, significant trends were found between quartiles of TAG, HDL-cholesterol, TC/HDL-cholesterol and TAG/HDL-cholesterol in multivariate models; moreover considering these measures as continuous variables, a 1 sd increase in each of these parameters was significantly associated with the risk of incident hypertension; the corresponding hazard ratios and CI were 1·06 (95 % CI 1·02, 1·10), 0·94 (95 % CI 0·89, 0·98), 1·04 (95 % CI 1·01, 1·09) and 1·04 (95 % CI 1·01, 1·07), respectively. The associations between lipid measures and incident hypertension did not change after excluding lipid lowering drug users and those with type 2 diabetes mellitus and these associations were independent of the categories of baseline blood pressure (P for interaction > 0·08). These findings indicate that TAG, TAG/HDL-cholesterol and TC/HDL-cholesterol were independently associated with higher risk, while HDL-cholesterol was associated with lower risk of incident hypertension.

Type 2 diabetes mellitus (T2DM) is characterised by chronic hyperglycaemia. Despite the efficacy of conventional pharmacotherapy, some individuals do not reach glycaemic goals and require adjuvant therapies. Taurine, a semi-essential amino acid, decreases blood glucose and cholesterol levels in rodents and humans. However, glycated hemoglobin (HbA1c) has not been evaluated in randomised controlled trials after taurine treatment for more than 12 weeks. This study aims to evaluate the effect of taurine administration on glycaemic, lipid, inflammatory, anthropometric and dietary parameters in individuals with T2DM. A randomised, double-blind, placebo-controlled clinical trial will be conducted at the Clinical Research Center of a tertiary public hospital. Participants with T2DM (n 94) will be recruited and randomised to receive 3 g of taurine or placebo, twice/day, orally, for 12 weeks. Blood samples will be collected before and after 12 weeks of treatment, when HbA1c, fasting glucose, insulin, albuminuria, creatinine, total cholesterol and fractions, triglycerides, C-reactive protein, TNF-α, IL 1, 4, 5, 6, 10 and 13 will be evaluated. Anthropometric parameters and 24-hour food recall will also be evaluated. The study will evaluate the effect of taurine treatment on biochemical and anthropometric parameters in individuals with T2DM. These results will guide the decision-making to indicate taurine treatment as an adjunct in individuals with T2DM who have not reached their glycaemic goal.

Nuts are an important component of a healthy diet, but little has been known about their effects on muscle health. Therefore, this study examined the association between nut consumption and low muscle strength among Korean adults. This cross-sectional analysis was conducted using single 24-h recall and handgrip strength data from 3962 younger adults 19–39 years, 6921 middle-aged adults 40–64 years and 3961 older adults ≥65 years participated in the seventh cycle (2016–2018) of the Korea National Health and Nutrition Examination Survey. Low muscle strength was defined as handgrip strength <28 kg for men and <18 kg for women. Sex-specific OR were obtained for younger, middle-aged and older adults using multivariable logistic regression analyses. About one in four Korean adults were consuming nuts (using a culinary definition) with peanut being the most frequently consumed type. After adjustment for age, BMI, total energy intake, household income, alcohol consumption, smoking, resistance exercise, medical history and dietary protein intake, nut consumption was associated with the lower risk of low muscle strength among older adults ≥65 years (men: OR 0·55, 95 % CI (0·38, 0·79); women: OR 0·69, 95 % CI (0·51, 0·93)); however, this association was not observed among younger adults 19–39 years or middle-aged adults 40–64 years. Our results suggest that consuming nuts might be beneficial in lowering the risk of low muscle strength among Korean older adults.

The present study aimed to compare the effects of drinking different types of coffee before a high-glycaemic index (GI) meal on postprandial glucose metabolism and to assess the effects of adding milk and sugar into coffee. In this randomised, crossover, acute feeding study, apparently healthy adults (n 21) consumed the test drink followed by a high-GI meal in each session. Different types of coffee (espresso, instant, boiled and decaffeinated, all with milk and sugar) and plain water were tested in separate sessions, while a subset of the participants (n 10) completed extra sessions using black coffees. Postprandial levels of glucose, insulin, active glucagon-like peptide 1 (GLP-1) and nitrotyrosine between different test drinks were compared using linear mixed models. Results showed that only preloading decaffeinated coffee with milk and sugar led to significantly lower glucose incremental AUC (iAUC; 14 % lower, P = 0·001) than water. Preloading black coffees led to greater postprandial glucose iAUC than preloading coffees with milk and sugar added (12–35 % smaller, P < 0·05 for all coffee types). Active GLP-1 and nitrotyrosine levels were not significantly different between test drinks. To conclude, preloading decaffeinated coffee with milk and sugar led to a blunted postprandial glycaemic response after a subsequent high-GI meal, while adding milk and sugar into coffee could mitigate the impairment effect of black coffee towards postprandial glucose responses. These findings may partly explain the positive effects of coffee consumption on glucose metabolism.

The purpose of this study was to determine whether n-3 PUFA result in an effect on endothelial function that is in addition to that of acute exercise. For 4 weeks, male Sprague–Dawley rats were subjected to a diet based on n-3 PUFA or a standard diet. In each diet group, ten rats were submitted to an acute treadmill exercise while the remaining ten acted as sedentary controls. The running speed was progressively increased until the animals were exhausted. Endothelial function was then assessed by measuring isometric tension in rings of the thoracic aorta. In vessels precontracted with 0·1 μm-phenylephrine, responses to acetylcholine (ACh) were significantly improved following acute exercise in all diet groups. When PUFA supplementation was compared to the standard diet no significant difference was found in response to ACh, either at rest or after an acute exercise. Pretreatment of rings with Nω-nitro-l-arginine methyl esther (50 μm) inhibited the ACh-mediated vasorelaxation in all groups. Response to 10 μm-nifedipine, an L-type Ca2+ channel antagonist, was similarly enhanced after acute exercise in both standard and PUFA diets. Furthermore, response to 0·01 μm-nifedipine was significantly higher after acute exercise only in the PUFA diet. In conclusion, in our ‘healthy’ rat model with ‘normal’ baseline endothelial function, acute exercise improves response to ACh while PUFA supplementation alone or in combination with acute exercise has no effect on endothelium-dependent vasorelaxation. However, PUFA may potentiate the acute exercise effect on smooth muscle cell relaxation via L-type Ca2+ channel modifications.