The role of the sarcopenic obesity (SO) phenotype for disease risk prediction has been tested in several observational studies, but results have been contrasting due to the application of different diagnostic models(1–3). This study applies the newly proposed the European Society for Clinical Nutrition and Metabolism (ESPEN)-European Association for the Study of Obesity (EASO) definition of SO(4) to a representative population of adults aged 50 years and older to evaluate its performance in the identification of prevalent cases of SO and its association with measures of cognitive function.

Data from individuals aged 50-85 years was collected from the National Health and Nutrition Examination Survey 1999-2002 waves. At the screening phase of the SO definition following the definition of the European Society for Clinical Nutrition and Metabolism and the European

Association for the Study of Obesity (ESPEN-EASO), body mass index and waist circumference were used to evaluate obesity, while sarcopenia cases were identified using the SARC-F questionnaire (a self-report questionnaire to screen sarcopenia). Sarcopenia was diagnosed based on knee extensor isometric strength per weight (KES/W) and a percentage of appendicular lean mass per weight, while fat mass percent measured by Dual-energy X-ray absorptiometry was used to determine obesity. Cognitive function in older participants was assessed using the Digit Symbol Substitution Test (DSST), while memory-related question was used for middle-aged individuals or older participants without DSST scores.

Participants aged 50–85 years were men (44.7%) with a mean age of 66.7 years, and most participants aged 60 years and over (87.4%). The prevalence of SO was 32.5%, 20.9% and 15.3% at screening, diagnosis phase I, and diagnosis phase II of the ESPEN-EASO definition, respectively. The prevalence of cognitive impairment was 14.8% in participants aged 50-59 years and 29.5% in participants aged 60-85 years. There were associations between SO and cognitive impairment at diagnosis phase I (Odds ratio (OR): 1.6, 95%CI (confidence interval) 1.1-2.4) and phase II (OR: 1.9, 95%CI 1.1-3.3). These associations were significant among participants aged 60-85 years (phase I, OR: 2.2, 95%CI 1.4-3.4; phase II, OR: 2.8, 95%CI 1.6-4.8), but not among those aged 50-59 years.

The new ESPEN-EASO definition of SO identified a high prevalence of SO cases. A significant association between SO and poor cognitive function in older individuals was observed.

It is estimated that more than one-tenth of adults aged ≥60 years are now classified as having sarcopenic obesity (SO), a clinical condition characterised by the concurrent presence of sarcopenia (low muscle mass and weakness) and obesity (excessive fat mass). Independently, sarcopenia and obesity are associated with a high risk of numerous adverse health outcomes including CVD and neurological conditions (e.g. dementia), but SO may confer a greater risk, exceeding either condition alone. This imposes a substantial burden on individuals, healthcare systems and society. In recent years, an increasing number of observational studies have explored the association between SO and the risk of CVD; however, results are mixed. Moreover, the pathophysiology of SO is governed by a complex interplay of multiple mechanisms including insulin resistance, inflammation, oxidative stress, hormonal shifts and alteration of energy balance, which may also play a role in the occurrence of various CVD. Yet, the exact mechanisms underlying the pathological connection between these two complex conditions remain largely unexplored. The aim of this review is to examine the association between SO and CVD. Specifically, we seek to: (1) discuss the definition, epidemiology and diagnosis of SO; (2) reconcile previously inconsistent findings by synthesising evidence from longitudinal studies on the epidemiological link between SO and CVD and (3) discuss critical mechanisms that may elucidate the complex and potentially bidirectional relationships between SO and CVD.

Dementia is a significant public health priority with approximately 55 million cases worldwide, and this number is predicted to quadruple by 2050. Adherence to a healthy diet and achieving optimal nutritional status are vital strategies to improve brain health. The importance of this area of research has been consolidated into the new term ‘nutritional psychiatry’. Dietary nitrate, closely associated with the intake of fruits and vegetables, is a compound that is increased in dietary patterns such as the Mediterranean and MIND diets and has protective effects on cognition and brain health. Nitrate is characterised by a complex metabolism and is the precursor of the nitrate–nitrite–nitric oxide (NO) pathway contributing to systemic NO generation. A higher intake of dietary nitrate has been linked to protective effects on vascular outcomes including blood pressure and endothelial function. However, the current evidence supporting the protective effects of dietary nitrate on brain health is less convincing. This article aims to provide a critical appraisal of the current evidence for dietary nitrate supplementation for improving brain health and provide suggestions for future research.

Beetroot (BR) is a rich source of nitrate (NO3-) that has been shown to reduce blood pressure (BP). Yet, no studies have examined the vascular benefits of BR in whole-food form and whether the effects are modified by age. This study was a four-arm, randomised, open-label, cross-over design in twenty-four healthy adults (young n 12, age 27 ± 4 years, old n 12, age 64 ± 5 years). Participants consumed whole-cooked BR at portions of (NO3- content in brackets) 100 g (272 mg), 200 g (544 mg) and 300 g (816 mg) and a 200-ml solution containing 1000 mg of potassium nitrate (KNO3) on four separate occasions over a 4-week period (≥7-d washout period). BP, plasma NO3- and nitrite (NO2-) concentrations, and post-occlusion reactive hyperaemia via laser Doppler, were measured pre- and up to 5-h post-intervention. Data were analysed by repeated-measures ANOVA. Plasma NO2- concentrations were higher in the young v. old at baseline and post-intervention (P < 0·05). All NO3- interventions decreased systolic and diastolic BP in young participants (P < 0·05), whereas only KNO3 (at 240–300 min post-intake) significantly decreased systolic (–4·8 mmHg, −3·5 %, P = 0·024) and diastolic (–5·4 mmHg, −6·5 %, P = 0·007) BP in older participants. In conclusion, incremental doses of dietary NO3- reduced systolic and diastolic BP in healthy young adults whereas in the older group a significant decrease was only observed with the highest dose. The lower plasma NO2- concentrations in older participants suggest that there may be mechanistic differences in the production of NO from dietary NO3- in young and older populations.

We used an established mediation analysis to investigate the role of adiposity in the relation between serum 25(OH)D with markers of inflammation and glucose and insulin metabolism. We used data from National Health and Nutrition Examination Survey (2005–2010), to evaluate the associations between serum 25(OH)D and markers of insulin resistance (IR) or inflammation, and whether these associations are mediated by adiposity factors. Analysis of co-variance and conceptual causal mediation analysis were conducted taking into consideration the survey design and sample weights. BMI was found to have significant mediation effects (to varied extent) on the associations between serum 25(OH)D and CRP, apo-B, fasting glucose, insulin, HOMA-IR, HOMA-B and HbA1c (all P < 0·05). Both WC and apVAT were also found to partly mediate the associations between serum 25 25(OH)D with CRP, FBG, HbA1c, TAG and HDL-cholesterol (all P < 0·05). These findings support the importance of optimising 25(OH)D status in conditions with abnormal adiposity (i.e. obesity) and treatments for the prevention of cardiometabolic diseases affecting adipose tissue metabolism (i.e. weight loss).

We explored the role of lipid accumulation products and visceral adiposity on the association between red meat consumption (RMC) and markers of insulin resistance (IR) and inflammation in USA adults. Data on RMC and health outcome measurements were extracted from the 2005–2010 US National Health and Nutrition Examination Surveys. Overall 16 621 participants were included in the analysis (mean age = 47·1 years, 48·3 % men). ANCOVA and ‘conceptus causal mediation’ models were applied while accounting for survey design. In adjusted models, a lower RMC was significantly associated with a cardio-protective profile of IR and inflammation. BMI had significant mediation effects on the association between RMC and C-reactive protein (CRP), apo B, fasting blood glucose (FBG), insulin, homoeostatic model assessment of IR and β-cell function, glycated Hb (HbA1c), TAG:HDL ratio and TAG glucose (TyG) index (all Ps < 0·05). Both waist circumference and anthropometrically predicted visceral adipose tissue mediated the association between RMC and CRP, FBG, HbA1c, TAG:HDL ratio and TyG index (all Ps < 0·05). Our findings suggest that adiposity, particularly the accumulation of abdominal fat, accounts for a significant proportion of the associations between red meat consumption, IR and inflammation.

CVD are characterised by a multi-factorial pathogenesis. Key pathogenetic steps in the development of CVD are the occurrence of endothelial dysfunction and formation of atherosclerotic lesions. Reduced nitric oxide (NO) bioavailability is a primary event in the initiation of the atherosclerotic cascade. NO is a free radical with multiple physiological functions including the regulation of vascular resistance, coagulation, immunity and oxidative metabolism. The synthesis of NO proceeds via two distinct pathways identified as enzymatic and non-enzymatic. The former involves the conversion of arginine into NO by the NO synthases, whilst the latter comprises a two-step reducing process converting inorganic nitrate $({\rm NO}_3^ - )$ into nitrite and subsequently NO.

Inorganic ${\rm NO}_3^ - $ is present in water and food, particularly beetroot and green leafy vegetables. Several investigations have therefore used the non-enzymatic NO pathway as a target for nutritional supplementation (${\rm NO}_3^ - $ salts) or dietary interventions (high-${\rm NO}_3^ - $ foods) to increase NO bioavailability and impact on cardiovascular outcomes. Some studies have reported positive effects of dietary ${\rm NO}_3^ - $ on systolic blood pressure and endothelial function in patients with hypertension and chronic heart failure. Nevertheless, results have been inconsistent and the size of the effect appears to be declining in older individuals. Additionally, there is a paucity of studies for disorders such as diabetes, CHD and chronic kidney failure. Thus, whilst dietary ${\rm NO}_3^ - $ supplementation could represent an effective and viable strategy for the primary and secondary prevention of age-related cardiovascular and metabolic diseases, more large-scale, robust studies are awaited to confirm or refute this notion.

A number of socio-economic, biological and lifestyle characteristics change with advancing age and place very old adults at increased risk of micronutrient deficiencies. The aim of this study was to assess vitamin and mineral intakes and respective food sources in 793 75-year-olds (302 men and 491 women) in the North-East of England, participating in the Newcastle 85+ Study. Micronutrient intakes were estimated using a multiple-pass recall tool (2×24 h recalls). Determinants of micronutrient intake were assessed with multinomial logistic regression. Median vitamin D, Ca and Mg intakes were 2·0 (interquartile range (IQR) 1·2–6·5) µg/d, 731 (IQR 554–916) mg/d and 215 (IQR 166–266) mg/d, respectively. Fe intake was 8·7 (IQR 6·7–11·6) mg/d, and Se intake was 39·0 (IQR 27·3–55·5) µg/d. Cereals and cereal products were the top contributors to intakes of folate (31·5 %), Fe (49·2 %) and Se (46·7 %) and the second highest contributors to intakes of vitamin D (23·8 %), Ca (27·5 %) and K (15·8 %). More than 95 % (n 756) of the participants had vitamin D intakes below the UK’s Reference Nutrient Intake (10 µg/d). In all, >20 % of the participants were below the Lower Reference Nutrient Intake for Mg (n 175), K (n 238) and Se (n 418) (comparisons with dietary reference values (DRV) do not include supplements). As most DRV are not age specific and have been extrapolated from younger populations, results should be interpreted with caution. Participants with higher education, from higher social class and who were more physically active had more nutrient-dense diets. More studies are needed to inform the development of age-specific DRV for micronutrients for the very old.

Very old people (referred to as those aged 85 years and over) are the fastest growing age segment of many Western societies owing to the steady rise of life expectancy and decrease in later life mortality. In the UK, there are now more than 1·5 million very old people (2·5 % of total population) and the number is projected to rise to 3·3 million or 5 % over the next 20 years. Reduced mobility and independence, financial constraints, higher rates of hospitalisation, chronic diseases and disabilities, changes in body composition, taste perception, digestion and absorption of food all potentially influence either nutrient intake or needs at this stage of life. The nutritional needs of the very old have been identified as a research priority by the British Nutrition Foundation's Task Force report, Healthy Ageing: The Role of Nutrition and Lifestyle. However, very little is known about the dietary habits and nutritional status of the very old. The Newcastle 85+ study, a cohort of more than 1000 85-year olds from the North East of England and the Life and Living in Advanced Age study (New Zealand), a bicultural cohort study of advanced ageing of more than 900 participants from the Bay of Plenty and Rotorua regions of New Zealand are two unique cohort studies of ageing, which aim to assess the spectrum of health in the very old as well as examine the associations of health trajectories and outcomes with biological, clinical and social factors as each cohort ages. The nutrition domain included in both studies will help to fill the evidence gap by identifying eating patterns, and measures of nutritional status associated with better, or worse, health and wellbeing. This review will explore some of this ongoing work.

Food and nutrient intake data are scarce in very old adults (85 years and older) – one of the fastest growing age segments of Western societies, including the UK. Our primary objective was to assess energy and macronutrient intakes and respective food sources in 793 85-year-olds (302 men and 491 women) living in North-East England and participating in the Newcastle 85+ cohort Study. Dietary information was collected using a repeated multiple-pass recall (2×24 h recalls). Energy, macronutrient and NSP intakes were estimated, and the contribution (%) of food groups to nutrient intake was calculated. The median energy intake was 6·65 (interquartile ranges (IQR) 5·49–8·16) MJ/d – 46·8 % was from carbohydrates, 36·8 % from fats and 15·7 % from proteins. NSP intake was 10·2 g/d (IQR 7·3–13·7). NSP intake was higher in non-institutionalised, more educated, from higher social class and more physically active 85-year-olds. Cereals and cereal products were the top contributors to intakes of energy and most macronutrients (carbohydrates, non-milk extrinsic sugars, NSP and fat), followed by meat and meat products. The median intakes of energy and NSP were much lower than the estimated average requirement for energy (9·6 MJ/d for men and 7·7 MJ/d for women) and the dietary reference value (DRV) for NSP (≥18 g/d). The median SFA intake was higher than the DRV (≤11 % of dietary energy). This study highlights the paucity of data on dietary intake and the uncertainties about DRV for this age group.

Randomised controlled trials (RCT) testing the effects of antioxidant supplements on endothelial function (EF) have reported conflicting results. We aimed to investigate the effects of supplementation with antioxidant vitamins C and E on EF and to explore factors that may provide explanations for the inconsistent results. We searched four databases (MEDLINE, Embase, Cochrane Library and Scopus) from inception until May 2014 for RCT involving adult participants aged ≥ 18 years who were supplemented with vitamins C and E alone or in combination for more than 2 weeks and reporting changes in EF measured using flow mediated dilation or forearm blood flow. Data were pooled as standardised mean difference (SMD) and analysed using a random-effects model. Significant improvements in EF were observed in trials supplementing with vitamin C alone (500–2000 mg/d) (SMD: 0·25, 95 % CI 0·02, 0·49, P= 0·043) and vitamin E alone (300–1800 IU/d; 1 IU vitamin E = 0·67 mg natural vitamin E) (SMD: 0·48, 95 % CI 0·23, 0·72, P= 0·0001), whereas co-administration of both vitamins was ineffective (vitamin C: 500–2000 mg/d; vitamin E: 400–1200 IU/d) (SMD: 0·12, 95 % CI − 0·18, 0·42, P= 0·428). The effect of vitamin C supplementation on EF increased significantly with age (β 0·023, 95 % CI 0·001, 0·05, P= 0·042). There was a significant negative correlation between baseline plasma vitamin E concentration and the effect of vitamin E supplementation on EF (β − 0·03, 95 % CI − 0·06, − 0·001, P= 0·029). Supplementation with either vitamin C or vitamin E alone improves EF. However, subgroup analysis emphasises the importance of careful characterisation and selection of a population group which may benefit from such supplementation.

The Dietary Approach to Stop Hypertension (DASH) is recommended to lower blood pressure (BP), but its effects on cardiometabolic biomarkers are unclear. A systematic review and meta-analysis of randomised controlled trials (RCT) was conducted to determine the effects of the DASH diet on cardiovascular risk factors. Medline, Embase and Scopus databases were searched from inception to December 2013. Inclusion criteria were as follows: (1) DASH diet; (2) RCT; (3) risk factors including systolic and diastolic BP and glucose, HDL, LDL, TAG and total cholesterol concentrations; (4) control group. Random-effects models were used to determine the pooled effect sizes. Meta-regression analyses were carried out to examine the association between effect sizes, baseline values of the risk factors, BMI, age, quality of trials, salt intake and study duration. A total of twenty articles reporting data for 1917 participants were included in the meta-analysis. The duration of interventions ranged from 2 to 24 weeks. The DASH diet was found to result in significant decreases in systolic BP ( − 5·2 mmHg, 95 % CI − 7·0, − 3·4; P< 0·001) and diastolic BP ( − 2·6 mmHg, 95 % CI − 3·5, − 1·7; P< 0·001) and in the concentrations of total cholesterol ( − 0·20 mmol/l, 95 % CI − 0·31, − 0·10; P< 0·001) and LDL ( − 0·10 mmol/l, 95 % CI − 0·20, − 0·01; P= 0·03). Changes in both systolic and diastolic BP were greater in participants with higher baseline BP or BMI. These changes predicted a reduction of approximately 13 % in the 10-year Framingham risk score for CVD. The DASH diet improved cardiovascular risk factors and appeared to have greater beneficial effects in subjects with an increased cardiometabolic risk. The DASH diet is an effective nutritional strategy to prevent CVD.