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Sleep habits are directly related to risk of obesity, and this relationship may be partly mediated through food choices and eating behaviour. Short sleep duration, impaired sleep quality and suboptimal sleep timing are all implicated in weight gain and adverse cardiometabolic health, at least partly mediated through their associations with diet quality. Short-term sleep restriction leads to increased energy intake, and habitually short sleepers report dietary intakes that indicate a less healthy diet compared with adequate sleepers. Evidence is emerging that sleep extension interventions in short sleepers may reduce intake of sugars and overall energy intake. Poor sleep quality, night shift work patterns and social jetlag are also associated with lower diet quality and consumption of energy-dense foods. Incorporating sleep advice into weight management interventions may be more effective than energy-restricted diets and exercise advice alone. However, there are a lack of intervention studies that aim to lengthen sleep, improve sleep quality or adjust irregular sleep timing to investigate the impact on dietary intakes and eating behaviour in participants aiming to lose weight or maintain weight loss. Finally, future research should take account of individual characteristics such as age, sex, life stage and changing working practices when designing combined lifestyle interventions including sleep behaviour change for health and well-being.
The Winter Conference 2021 focused on the theme of obesity and the brain, with symposia on the consequences of obesity on brain function, developments in behavioural change interventions, neurobiology of appetite regulation and obesity treatment, and personalised medicine for obesity prevention and treatment. The first plenary lecture discussed sweetness perceptions and how non-nutritive sweeteners may lead to a mismatch between metabolic signals and reward systems in the brain, and the second plenary lecture presented novel approaches to the treatment of binge-eating disorders. This short report summarises the content of these scientific sessions.
To investigate associations and interactions between sleep duration and social jetlag status with nutrient intake, nutrient status, body composition and cardio-metabolic risk factors in a nationally representative UK adult population.
A cross-sectional study using 4-d food diary and self-reported sleep data from the UK National Diet and Nutrition Survey Rolling Programme 2008–2017.
UK free-living population.
Totally, 5015 adults aged 19–64 years.
Thirty-four per cent were short sleepers (< 7 h); 7 % slept ≥ 9 h; 14 % had > 2 h difference in average sleep duration between weeknights and weekend nights (social jetlag). Compared to those reporting optimal sleep duration (≥ 7–< 9 h), short sleep was associated with higher intakes of non-milk extrinsic sugars (NMES) (0·9 % energy, 95 % CI: 0·4, 1·4), total carbohydrate (0·8 % energy, 95 % CI: 0·2, 1·4) and a lower non-starch polysaccharides fibre intake (–0·5 g/d, 95 % CI –0·8, –0·2). There was a significant interaction between short sleep and social jetlag for fibre intakes, where adequate sleepers with social jetlag as well as all short sleepers (regardless of social jetlag) had lower fibre intakes than adequate sleepers with no social jetlag. Short sleep, but not social jetlag, was associated with greater adiposity, but there were no differences in other markers of cardiometabolic disease risk.
The present study reports that both short sleep and social jetlag are associated with higher intakes of NMES, but only sleep duration is associated with markers of adiposity. Social jetlag was associated with lower fibre intakes even in individuals with adequate weekly sleep duration, suggesting catch-up sleep does not prevent the adverse impact of irregular sleep habits on food choices.
New occurrences of flask-shaped and envelope-bearing microfossils, including the predominantly Cambrian taxon Granomarginata, are reported from new localities, as well as from earlier in time (Ediacaran) than previously known. The stratigraphic range of Granomarginata extends into the Cambrian System, where it had a cosmopolitan distribution. This newly reported Ediacaran record includes areas from Norway (Baltica), Newfoundland (Avalonia) and Namibia (adjacent to the Kalahari Craton), and puts the oldest global occurrence of Granomarginata in the Indreelva Member (< 563 Ma) of the Stáhpogieddi Formation on the Digermulen Peninsula, Arctic Norway. Although Granomarginata is rare within the assemblage, these new occurrences together with previously reported occurrences from India and Poland, suggest a potentially widespread palaeogeographic distribution of Granomarginata through the middle–late Ediacaran interval. A new flask-shaped microfossil Lagoenaforma collaris gen. et sp. nov. is also reported in horizons containing Granomarginata from the Stáhpogieddi Formation in Norway and the Dabis Formation in Namibia, and flask-shaped fossils are also found in the Gibbett Hill Formation in Newfoundland. The Granomarginata–Lagoenaforma association, in addition to a low-diversity organic-walled microfossil assemblage, occurs in the strata postdating the Shuram carbon isotope excursion, and may eventually be of use in terminal Ediacaran biostratigraphy. These older occurrences of Granomarginata add to a growing record of body fossil taxa spanning the Ediacaran–Cambrian boundary.
To examine associations of tree nut snack (TNS) consumption with diet quality and cardiovascular disease (CVD) risk in UK adults from National Diet and Nutrition Survey (NDNS) 2008–2014.
Cross-sectional analysis using data from 4-d food diaries, blood samples and physical measurements for CVD risk markers. To estimate diet quality, modified Mediterranean Diet Score (MDS) and modified Healthy Diet Score (HDS) were applied. Associations of TNS consumption with diet quality and markers of CVD risk were investigated using survey-adjusted multivariable linear regression adjusted for sex, age, ethnicity, socio-economic and smoking status, region of residency and total energy and alcohol intake.
UK free-living population.
4738 adults (≥19 years).
TNS consumers had higher modified MDS and HDS relative to non-consumers. TNS consumers also had lower BMI, WC, SBP and DBP and higher HDL compared to non-consumers, although a dose-related fully adjusted significant association between increasing nut intake (g per 4184 kJ/1000 kcal energy intake) and lower marker of CVD risk was only observed for SBP. TNS consumption was also associated with higher intake of total fat, mono-, n-3 and n-6 polyunsaturated fatty acids, fibre, vitamin A, thiamin, folate, vitamin C, vitamin E, potassium, magnesium, phosphorus, selenium and iron; and lower intake of saturated fatty acids, trans fatty acids, total carbohydrate, starch, free sugar, sodium and chloride.
TNS consumers report better dietary quality and consumption was associated with lower CVD risk factors. Encouraging replacement of less healthy snacks with TNS should be encouraged as part of general dietary guidelines.
Adherence to dietary guidelines (DG) may result in higher intake of polyphenols via increased consumption of fruits, vegetables and whole grains. We compared polyphenol dietary intake and urinary excretion between two intervention groups in the Cardiovascular risk REduction Study: Supported by an Integrated Dietary Approach study: a 12-week parallel-arm, randomised controlled trial (n 161; sixty-four males, ninety-seven females; aged 40–70 years). One group adhered to UK DG, whereas the other group consumed a representative UK diet (control). We estimated polyphenol dietary intake, using a 4-d food diary (4-DFD) and FFQ, and analysed 24-h polyphenol urinary excretion by liquid chromatography-tandem MS on a subset of participants (n 46 control; n 45 DG). A polyphenol food composition database for 4-DFD analysis was generated using Phenol-Explorer and USDA databases. Total polyphenol intake by 4-DFD at endpoint (geometric means with 95 % CI, adjusted for baseline and sex) was significantly higher in the DG group (1279 mg/d per 10 MJ; 1158, 1412) compared with the control group (1084 mg/d per 10 MJ; 980, 1197). The greater total polyphenol intake in the DG group was attributed to higher intake of anthocyanins, proanthocyanidins and hydroxycinnamic acids, with the primary food sources being fruits, cereal products, nuts and seeds. FFQ estimates of flavonoid intake also detected greater intake in DG compared with the control group. 24-h urinary excretion showed consistency with 4-DFD in their ability to discriminate between dietary intervention groups for six out of ten selected, individual polyphenols. In conclusion, following UK DG increased total polyphenol intake by approximately 20 %, but not all polyphenol subclasses corresponded with this finding.
Low heart rate variability (HRV) predicts sudden cardiac death. Long-chain (LC) n-3 PUFA (C20–C22) status is positively associated with HRV. This cross-sectional study investigated whether vegans aged 40–70 years (n 23), whose diets are naturally free from EPA (20 : 5n-3) and DHA (22 : 6n-3), have lower HRV compared with omnivores (n 24). Proportions of LC n-3 PUFA in erythrocyte membranes, plasma fatty acids and concentrations of plasma LC n-3 PUFA-derived lipid mediators were significantly lower in vegans. Day-time interbeat intervals (IBI), adjusted for physical activity, age, BMI and sex, were significantly shorter in vegans compared with omnivores (mean difference −67 ms; 95 % CI −130, −3·4, P<0·05), but there were no significant differences over 24 h or during sleep. Vegans had higher overall HRV, measured as 24 h standard deviation of normal-to-normal intervals (SDNN) (mean adjusted difference 27 ms; 95 % CI 1, 52, P=0·039). Conversely, vegans presented with decreased 8 h day-time HRV: mean adjusted difference in SDNN −20 ms; 95 % CI −37, −3, P=0·021, with no differences during nocturnal sleep. Day-time parameters of beat-to-beat HRV (root of the mean of the sum of the squares of differences between adjacent normal-to-normal intervals, percentage of adjacent normal-to-normal intervals that differ by >50 % and high-frequency power) were similarly lower in vegans, with no differences during sleep. In conclusion, vegans have higher 24 h SDNN, but lower day-time HRV and shorter day-time IBI relative to comparable omnivores. Vegans may have reduced availability of precursor markers for pro-resolving lipid mediators; it remains to be determined whether there is a direct link with impaired cardiac function in populations with low-n-3 status.
The prevalence of type 2 diabetes (T2D) is predicted to reach unprecedented levels in the next few decades. In addition to excess body weight, there may be other overlapping dietary drivers of impaired glucose homeostasis that are associated with an obesogenic diet, such as regular exposure to postprandial spikes in blood glucose arising from diets dominated by highly refined starches and added sugars. Strategies to reduce postprandial hyperglycaemia by optimising the functionality of foods would strengthen efforts to reduce the risk of T2D. Berry bioactives, including anthocyanins, are recognised for their inhibitory effects on carbohydrate digestion and glucose absorption. Regular consumption of berries has been associated with a reduction in the risk of T2D. This review aims to examine the evidence from in vitro, animal and human studies, showing that berries and berry anthocyanins may act in the gut to modulate postprandial glycaemia. Specifically, berry extracts and anthocyanins inhibit the activities of pancreatic α-amylase and α-glucosidase in the gut lumen, and interact with intestinal sugar transporters, sodium-dependent glucose transporter 1 and GLUT2, to reduce the rate of glucose uptake into the circulation. Growing evidence from randomised controlled trials suggests that berry extracts, purées and nectars acutely inhibit postprandial glycaemia and insulinaemia following oral carbohydrate loads. Evidence to date presents a sound basis for exploring the potential for using berries/berry extracts as an additional stratagem to weight loss, adherence to dietary guidelines and increasing physical exercise, for the prevention of T2D.
Studies of the relationship between obesity and chronic kidney disease (CKD) in nationally representative population samples are limited. Our study aimed to determine if overweight and obesity were independently associated with the risk for CKD in the 2010 Health Survey for England (HSE).
The HSE is an annually conducted cross-sectional study. In 2010 serum creatinine was included to determine the incidence of CKD in the population. CKD was defined as estimated glomerular filtration rate (eGFR) <60 ml/min per 1·73 m2 using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula. Multivariable logistic regression models were developed to calculate odds ratios and 95 % confidence intervals for CKD risk by BMI (reference category: BMI=18·5–24·9 kg/m2) and adjusted for age, gender, ethnicity, smoking, diabetes and hypertension.
A random sample of nationally representative households in England.
Adults (n 3463) with calculable eGFR and BMI were included.
The prevalence of CKD was 5·9 %. The risk of CKD was over 2·5 times higher in obese participants compared with normal-weight participants in the fully adjusted model (BMI=30·0–39·9 kg/m2: adjusted OR=2·78 (95 % CI 1·75, 4·43); BMI ≥ 40·0 kg/m2: adjusted OR=2·68 (95 % CI 1·05, 6·85)).
Obesity is associated with an increased risk of CKD in a national sample of the UK population, even after adjustment for known CKD risk factors, which may have implications for CKD screening and future national health service planning and delivery.
Long-chain n-3 PUFA can lower blood pressure (BP) but their acute effects on cardiac output, BP and systemic vascular resistance (SVR) in response to dynamic exercise are uncertain. We compared the effects of high-fat meals rich in EPA (20 : 5n-3), DHA (22 : 6n-3) or oleic acid (control) on cardiac output, BP and SVR in response to exercise stress testing. High-fat meals (50 g fat) containing high-oleic sunflower oil enriched with 4·7 g of either EPA or DHA v. control (high-oleic sunflower oil only) were fed to twenty-two healthy males using a randomised cross-over design. Resting measurements of cardiac output, heart rate and BP were made before and hourly over 5 h following the meal. A standardised 12 min exercise test was then conducted with further measurements made during and post-exercise. Blood samples were collected at fasting, 5 h postprandially and immediately post-exercise for the analysis of lipid, glucose and 8-isoprostane-F2α (8-iso-PGF2α). Plasma concentrations of EPA and DHA increased by 0·22 mmol/l 5 h following the EPA and DHA meals, respectively, compared with the control (P < 0·001). Resting cardiac output and 8-iso-PGF2α increased similarly following all meals and there were no significant differences in cardiac output during exercise between the meals. SVR was lower at 5 h and during exercise following the DHA but not EPA meal, compared with the control meal, by 4·9 % (95 % CI 1·3, 8·4; P < 0·01). Meals containing DHA appear to differ from EPA with regard to their effects on cardiovascular haemodynamics during exercise.
The amount and type of dietary fat have long been associated with the risk of CVD. Arterial stiffness and endothelial dysfunction are important risk factors in the aetiology of CHD. A range of methods exists to assess vascular function that may be used in nutritional science, including clinic and ambulatory blood pressure monitoring, pulse wave analysis, pulse wave velocity, flow-mediated dilatation and venous occlusion plethysmography. The present review focuses on the quantity and type of dietary fat and effects on blood pressure, arterial compliance and endothelial function. Concerning fat quantity, the amount of dietary fat consumed habitually appears to have little influence on vascular function independent of fatty acid composition, although single high-fat meals postprandially impair endothelial function compared with low-fat meals. The mechanism is related to increased circulating lipoproteins and NEFA which may induce pro-inflammatory pathways and increase oxidative stress. Regarding the type of fat, cross-sectional data suggest that saturated fat adversely affects vascular function whereas polyunsaturated fat (mainly linoleic acid (18 : 2n-6) and n-3 PUFA) are beneficial. EPA (20 : 5n-3) and DHA (22 : 6n-3) can reduce blood pressure, improve arterial compliance in type 2 diabetics and dyslipidaemics, and augment endothelium-dependent vasodilation. The mechanisms for this vascular protection, and the nature of the separate physiological effects induced by EPA and DHA, are priorities for future research. Since good-quality observational or interventional data on dietary fatty acid composition and vascular function are scarce, no further recommendations can be suggested in addition to current guidelines at the present time.
Dietary isoflavones are thought to be cardioprotective due to their structural similarity to oestrogen. Oestrogen is believed to have beneficial effects on endothelial function and may be one of the mechanisms by which premenopausal women are protected against CVD. Decreased NO production and endothelial NO synthase activity, and increased endothelin-1 concentrations, impaired lipoprotein metabolism and increased circulating inflammatory factors result from oestrogen deficiency. Oestrogen acts by binding to oestrogen receptors α and β. Isoflavones have been shown to bind with greater affinity to the latter. Oestrogen replacement therapy is no longer thought to be a safe treatment for prevention of CVD; isoflavones are a possible alternative. Limited evidence from human intervention studies suggests that isoflavones may improve endothelial function, but the available data are not conclusive. Animal studies provide stronger support for a role of isoflavones in the vasculature, with increased vasodilation and endothelial NO synthase activity demonstrated. Cellular mechanisms underlying the effects of isoflavones on endothelial cell function are not yet clear. Possible oestrogen receptor-mediated pathways include modulation of gene transcription, and also non-genomic oestrogen receptor-mediated signalling pathways. Putative non-oestrogenic pathways include inhibition of reactive oxygen species production and up regulation of the protein kinase A pathway (increasing NO bioavailability). Further research is needed to unravel effects of isoflavones on intracellular regulation of the endothelial function. Moreover, there is an urgent need for adequately powered, robustly designed human intervention studies in order to clarify the present equivocal findings.
The increase in CVD incidence following the menopause is associated with oestrogen loss. Dietary isoflavones are thought to be cardioprotective via their oestrogenic and oestrogen receptor-independent effects, but evidence to support this role is scarce. Individual variation in response to diet may be considerable and can obscure potential beneficial effects in a sample population; in particular, the response to isoflavone treatment may vary according to genotype and equol-production status. The effects of isoflavone supplementation (50 mg/d) on a range of established and novel biomarkers of CVD, including markers of lipid and glucose metabolism and inflammatory biomarkers, have been investigated in a placebo-controlled 2×8-week randomised cross-over study in 117 healthy post-menopausal women. Responsiveness to isoflavone supplementation according to (1) single nucleotide polymorphisms in a range of key CVD genes, including oestrogen receptor (ER) α and β and (2) equol-production status has been examined. Isoflavones supplementation was found to have no effect on markers of lipids and glucose metabolism. Isoflavones improve C-reactive protein concentrations but do not affect other plasma inflammatory markers. There are no differences in response to isoflavones according to equol-production status. However, differences in HDL-cholesterol and vascular cell adhesion molecule 1 response to isoflavones v. placebo are evident with specific ERβ genotypes. In conclusion, isoflavones have beneficial effects on C-reactive protein, but not other cardiovascular risk markers. However, specific ERβ gene polymorphic subgroups may benefit from isoflavone supplementation.
The biokinetics of newly absorbed vitamin E in blood components was investigated in normolipidaemic males. Subjects (n 12) ingested encapsulated 150 mg 2H-labelled RRR-α-tocopheryl acetate with a standard meal. Blood was collected at 3, 6, 9, 12, 24 and 48 h post-ingestion. 2H-Labelled and pre-existing unlabelled α-tocopherol (α-T) was determined in plasma, lipoproteins, erythrocytes, platelets and lymphocytes by LC–MS. In all blood components, labelled α-T concentration significantly increased while unlabelled decreased following ingestion (P<0·0001). Significant differences in labelled α-T biokinetic parameters were found between lipoproteins. Time of maximum concentration was significantly lower in chylomicrons, while VLDL had a significantly greater maximum α-T concentration and area under the curve (AUC) (P<0·05). The largest variability occurred in chylomicron α-T transport. Erythrocyte labelled α-T concentrations increased gradually up to 24 h while α-T enrichment of platelets and lymphocytes was slower, plateauing at 48 h. Platelet enrichment with labelled α-T was biphasic, the initial peak coinciding with the labelled α-T peak in chylomicrons. Erythrocyte and HDL AUC were significantly correlated (P<0·005), as was platelet and HDL AUC (P<0·05). There was a lower turnover of pre-existing α-T in platelets and lymphocytes (maximum 25 % labelled α-T) compared to plasma and erythrocytes (maximum 45 % labelled α-T). These data indicate that different processes exist in the uptake and turnover of α-T by blood components and that chylomicron α-T transport is a major determinant of inter-individual variation in vitamin E response. This is important for the understanding of α-T transport and uptake into tissues.
Vitamin E absorption requires the presence of fat; however, limited information exists on the influence of fat quantity on optimal absorption. In the present study we compared the absorption of stable-isotope-labelled vitamin E following meals of varying fat content and source. In a randomised four-way cross-over study, eight healthy individuals consumed a capsule containing 150 mg 2H-labelled RRR-α-tocopheryl acetate with a test meal of toast with butter (17·5 g fat), cereal with full-fat milk (17·5 g fat), cereal with semi-skimmed milk (2·7 g fat) and water (0 g fat). Blood was taken at 0, 0·5, 1, 1·5, 2, 3, 6 and 9 h following ingestion, chylomicrons were isolated, and 2H-labelled α-tocopherol was analysed in the chylomicron and plasma samples. There was a significant time (P<0·001) and treatment effect (P<0·001) in 2H-labelled α-tocopherol concentration in both chylomicrons and plasma between the test meals. 2H-labelled α-tocopherol concentration was significantly greater with the higher-fat toast and butter meal compared with the low-fat cereal meal or water (P<0·001), and a trend towards greater concentration compared with the high-fat cereal meal (P=0·065). There was significantly greater 2H-labelled α-tocopherol concentration with the high-fat cereal meal compared with the low-fat cereal meal (P<0·05). The 2H-labelled α-tocopherol concentration following either the low-fat cereal meal or water was low. These results demonstrate that both the amount of fat and the food matrix influence vitamin E absorption. These factors should be considered by consumers and for future vitamin E intervention studies.
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