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There is a dearth of data on Se status in very old adults. The aims of this study were to assess Se status and its determinants in 85-year-olds living in the Northeast of England by measuring serum Se and selenoprotein P (SELENOP) concentrations and glutathione peroxidase 3 (GPx3) activity. A secondary aim was to examine the interrelationships between each of the biomarkers. In total, 757 participants (463 women, 293 men) from the Newcastle 85+ Study were included. Biomarker concentrations were compared with selected cut-offs (serum Se: suboptimal 70 µg/l and deficient 45 µg/l; SELENOP: suboptimal 4·5 mg/l and deficient 2·6 mg/l). Determinants were assessed using linear regressions, and interrelationships were assessed using restricted cubic splines. Median (inter-quartile range) concentrations of serum Se, SELENOP and of GPx3 activity were 53·6 (23·6) µg/l, 2·9 (1·9) mg/l and 142·1 (50·7) U/l, respectively. Eighty-two percentage and 83 % of participants had suboptimal serum Se (< 70 µg/l) and SELENOP (< 4·5 mg/l), and 31 % and 40 % of participants had deficient serum Se (< 45 µg/l) and SELENOP (< 2·6 mg/l), respectively. Protein intake was a significant determinant of Se status. Additional determinants of serum Se were sex, waist:hip ratio, self-rated health and disease, while sex, BMI and physical activity were determinants of GPx3 activity. There was a linear association between serum Se and SELENOP, and nonlinear associations between serum Se and GPx3 activity and between SELENOP and GPx3 activity. These findings indicate that most participants had suboptimal Se status to saturate circulating SELENOP.
Indigenous peoples and ethnic minority groups often experience poor diet quality and poor health outcomes. Such inequities may be partially due to nutrition interventions not meeting the unique cultural and linguistic needs of these population groups, which could be achieved using co-creation and/or personalised approaches. Cultural adaptation or tailoring of nutrition interventions has shown promise in improving some aspects of dietary intake, but this requires careful consideration to ensure it does not inadvertently exacerbate dietary inequities. The aim of this narrative review was to examine examples of cultural adaptations and/or tailoring of public health nutrition interventions that improved the dietary intake and to consider implications for the optimal design and implementation of personalised and precision nutrition interventions. This review identified six examples of cultural adaptation and/or tailoring of public health nutrition intervention in Indigenous peoples and ethnic minority groups across Australia, Canada and the US. All studies used deep socio-cultural adaptations, such as the use of Indigenous storytelling, and many included surface-level adaptations, such as the use of culturally appropriate imagery in intervention materials. However, it was not possible to attribute any improvements in dietary intake to cultural adaptation and/or tailoring per se, and the minimal reporting on the nature of adaptations limited our ability to determine whether the interventions used true co-creation to design content or were adapted from existing interventions. Findings from this review outline opportunities for personalised nutrition interventions to use co-creation practices to design, deliver and implement interventions in collaboration with Indigenous and ethnic minority groups.
The present paper reviews progress in research on dietary fibre and human health over the past five decades. There is now convincing evidence from prospective cohort studies that diets low in dietary fibre are associated with increased risk of common non-communicable diseases including CVD, type 2 diabetes and colorectal cancer. These findings provide strong support for hypotheses proposed by Denis Burkitt 50 years ago, based on very limited evidence but with considerable imagination and insight. For the first two to three decades of this period, research on dietary fibre was hampered by the lack of consensus about the definition, and measurement, of this complex and diverse dietary component and by the lack of appropriate tools for investigating the gut microbiome that is central to understanding mechanisms of action. Recent technical and scientific advances in microbiome research (based on fast, low-cost, DNA sequencing) are facilitating investigation of the associations between dietary fibre, the gut microbiome and human health. Current challenges include the need for agreement about the characteristics of a healthy gut microbiome. Although the health benefits attributed to higher dietary fibre intake are likely to be shared with most types of dietary fibre, one should anticipate that different sources of dietary fibre and the other components (resistant starch and non-digestible oligosaccharides) that make up dietary fibre will have characteristically different effects on human physiology and disease risk. In conclusion, population-level intakes of dietary fibre are low and there is a public health priority to develop and implement more effective interventions to increase intake.
Optimum nutrition plays a major role in the achievement and maintenance of good health. The Nutrition Society of the UK and Ireland and the Sabri Ülker Foundation, a charity based in Türkiye and focused on improving public health, combined forces to highlight this important subject. A hybrid conference was held in Istanbul, with over 4000 delegates from sixty-two countries joining the proceedings live online in addition to those attending in person. The primary purpose was to inspire healthcare professionals and nutrition policy makers to better consider the role of nutrition in their interactions with patients and the public at large to reduce the prevalence of non-communicable diseases such as obesity and type 2 diabetes. The event provided an opportunity to share and learn from different approaches in the UK, Türkiye and Finland, highlighting initiatives to strengthen research in the nutritional sciences and translation of that research into nutrition policy. The presenters provided evidence of the links between nutrition and disease risk and emphasised the importance of minimising risk and implementing early treatment of diet-related disease. Suggestions were made including improving health literacy and strengthening policies to improve the quality of food production and dietary behaviour. A multidisciplinary approach is needed whereby Governments, the food industry, non-governmental groups and consumer groups collaborate to develop evidence-based recommendations and appropriate joined-up policies that do not widen inequalities. This summary of the proceedings will serve as a gateway for those seeking to access additional information on nutrition and health across the globe.
A multi-disciplinary expert group met to discuss vitamin D deficiency in the UK and strategies for improving population intakes and status. Changes to UK Government advice since the 1st Rank Forum on Vitamin D (2009) were discussed, including rationale for setting a reference nutrient intake (10 µg/d; 400 IU/d) for adults and children (4+ years). Current UK data show inadequate intakes among all age groups and high prevalence of low vitamin D status among specific groups (e.g. pregnant women and adolescent males/females). Evidence of widespread deficiency within some minority ethnic groups, resulting in nutritional rickets (particularly among Black and South Asian infants), raised particular concern. Latest data indicate that UK population vitamin D intakes and status reamain relatively unchanged since Government recommendations changed in 2016. Vitamin D food fortification was discussed as a potential strategy to increase population intakes. Data from dose–response and dietary modelling studies indicate dairy products, bread, hens’ eggs and some meats as potential fortification vehicles. Vitamin D3 appears more effective than vitamin D2 for raising serum 25-hydroxyvitamin D concentration, which has implications for choice of fortificant. Other considerations for successful fortification strategies include: (i) need for ‘real-world’ cost information for use in modelling work; (ii) supportive food legislation; (iii) improved consumer and health professional understanding of vitamin D’s importance; (iv) clinical consequences of inadequate vitamin D status and (v) consistent communication of Government advice across health/social care professions, and via the food industry. These areas urgently require further research to enable universal improvement in vitamin D intakes and status in the UK population.
Professor John Mather, you’ve been a key player at NASA for a long time, winning the Nobel Prize in Physics in 2006 and being one of the 100 most influential people in the world according to Time magazine’s list in 2007.
Across the globe, there has been a marked increase in longevity, but significant inequalities remain. These are exacerbated by inadequate access to proper nutrition and health care services and to reliable information to make the decisions related to nutrition and health care. Many in economically developing as well as developed societies are plagued with the double-burden of energy excess and undernutrition. This has resulted in mental and physical deterioration, increased non-communicable disease rates, lost productivity, increased medical costs and reduced quality of life. While adequate nutrition is fundamental to good health at all stages of the life course, the impact of diet on prolonging good quality of life during ageing remains unclear. For progress to continue, there is need for new and/or innovative approaches to promoting health as individuals age, as well as qualitative and quantitative biomarkers and other accepted tools that can measure improvements in physiological integrity throughout life. A framework for progress has been proposed by the World Health Organization in their Global Strategy and Action Plan on Ageing and Health. Here, we focused on the impact of nutrition within this framework, which takes a broad, person-centred emphasis on healthy ageing, stressing the need to better understand each individual's intrinsic capacity, their functional abilities at various life stages, and the impact of their mental, and physical health, as well as the environments they inhabit.
Obtaining objective, dietary exposure information from individuals is challenging because of the complexity of food consumption patterns and the limitations of self-reporting tools (e.g., FFQ and diet diaries). This hinders research efforts to associate intakes of specific foods or eating patterns with population health outcomes.
Dietary exposure can be assessed by the measurement of food-derived chemicals in urine samples. We aimed to develop methodologies for urine collection that minimised impact on the day-to-day activities of participants but also yielded samples that were data-rich in terms of targeted biomarker measurements.
Urine collection methodologies were developed within home settings.
Different cohorts of free-living volunteers.
Home collection of urine samples using vacuum transfer technology was deemed highly acceptable by volunteers. Statistical analysis of both metabolome and selected dietary exposure biomarkers in spot urine collected and stored using this method showed that they were compositionally similar to urine collected using a standard method with immediate sample freezing. Even without chemical preservatives, samples can be stored under different temperature regimes without any significant impact on the overall urine composition or concentration of forty-six exemplar dietary exposure biomarkers. Importantly, the samples could be posted directly to analytical facilities, without the need for refrigerated transport and involvement of clinical professionals.
This urine sampling methodology appears to be suitable for routine use and may provide a scalable, cost-effective means to collect urine samples and to assess diet in epidemiological studies.
Colorectal cancer (CRC) is the 3rd most common cancer worldwide. Obesity, and its lifestyle determinants, physical inactivity and poor diet, increase CRC risk. However, the effects of weight loss by bariatric surgery on CRC risk are unclear. Epigenetic mechanisms involving microRNAs that lead to dysregulated gene expression may mediate the effects of obesity and weight loss on CRC risk. We hypothesised that microRNAs are i) aberrantly expressed in obese individuals compared with healthy non-obese individuals and ii) modulated by significant weight loss following bariatric surgery.
We used data and samples from the Biomarkers of Colorectal Cancer after Bariatric Surgery (BOCABS) Study. Obese patients listed for bariatric surgery and age- and sex-matched healthy non-obese adults (Controls) were recruited at North Tyneside General Hospital. Rectal mucosal biopsies were collected at baseline and six months post-surgery from obese participants and at baseline only from Controls. Using Next Generation Sequencing and bioinformatics analysis, a panel of 8 microRNAs was selected and validated by quantitative PCR in colorectal mucosal biopsies.
Results and discussion
Data were available for 20 control participants and for 22 obese participants with matched pre- and post-surgery samples. Next Generation Sequencing revealed that compared with non-obese individuals, obese individuals showed differential expression of 112 microRNAs (p < 0.05). Roux-en-Y gastric bypass, resulted in differential expression of 60 microRNAs, when compared with expression levels at baseline (p < 0.05). A total of 36 microRNAs differed significantly in both i) the obese with non-obese and ii) the pre- and post-surgery comparisons. Validation by quantitative PCR demonstrated that expression of miR-31, miR-215, miR-3196 and miR-4516 was significantly (P < 0.05) higher in obese than in non-obese individuals. Weight loss, (mean 28.5kg) following Roux-en-Y gastric bypass, reduced expression of miR-31, miR-215 and miR-3196 significantly (P < 0.05) to expression levels that were comparable with those in Controls. These differentially expressed microRNAs are implicated in pathways linked with inflammation, obesity and cancer.
The pattern of microRNA expression in macroscopically-normal human colorectal mucosa differed substantially between obese and non-obese individuals. However, six months after Roux-en-Y gastric bypass, the pattern of microRNA expression was similar to that in non-obese Controls. This suggests that surgically-induced weight loss may normalise microRNA expression in the human colorectal mucosa and so reduce CRC risk.
Adherence to the Mediterranean dietary pattern (MeDiet) and adiposity, respectively, decreases and increases the risk of multiple common age-related diseases through several mechanisms including inflammation, reactive oxygen species (ROS) production in the mitochondria, and DNA methylation. For example, adverse changes in platelets from obese and overweight adults include hyperaggregability and increased ROS. Since platelets are anuclear, their prothrombotic function is fully orchestrated by the mitochondria and the only DNA present is the mitochondrial DNA (mtDNA). In this study, we tested the hypothesis that MeDiet influences patterns of mtDNA methylation in platelets from older adults with greater adiposity.
Material and methods
We selected 134 participants with overweight or obesity (mean BMI = 35.5 ± 5.1 and age = 62 ± 10 years) from the “Susceptibility to particle health effects, miRNA and exosomes”(SPEHRE) Study. Dietary intake was assessed using a food frequency questionnaire and MeDiet adherence was calculated using the MeDiet Score described by Martínez-González et al.(2012). MtDNA was extracted from platelets, linearized, bisulfite converted and DNA methylation was quantified by pyrosequencing at 13 CpG in seven genes that encode for tRNAs (MT-TF and MT-TL1), regulatory regions (D-Loop and MT-OLR), and subunits of the electron-transport-chain (MT-CO1, MT-CO2, and MT-CO3).
In these participants, MeDiet score ranged from 3 to 12 (mean = 6.5), with higher scores reflecting greater MeDiet adherence. Regression analysis showed that higher MeDiet score was associated with lower D-loop (β = -0.031, P = 0.019) and higher MT-CO2 CpG1 (β = 0.040, P = 0.023) methylation. No associations were found between MeDiet Score and methylation level at MT-CO1(2 CpGs), MT-CO2(CpG2), MT-CO3(2 CpGs), MT-TL1(2 CpGs), MT-TF(CpG1), MT-OLR(3 CpGs).In addition, there was no association between mtDNA methylation and BMI.
The D-loop is critical for mitochondrial function since it initiates mtDNA replication and transcription. Increased D-loop methylation has been associated with reduced mitochondrial functionality, and insulin resistance. Our results suggest that higher adherence to MeDiet lowers D-loop methylation which may protect against obesity-related comorbidities (e.g. insulin resistance).
Higher MeDiet scores are associated with MT-CO2 CpG1 hypermethylation. MT-CO2 encodes for a subunit of the Cytochrome-C-oxidase, a highly regulated enzyme involved in the oxidative metabolism. MT-CO2 demethylation, induced by Valproic-Acid administration, has been reported to be associated with increased ROS production. Our results suggest a possible role of MeDiet in mitochondrial ROS regulation via methylation of MT-CO2.
For the first time, we observed associations between MeDiet adherence and mtDNA methylation. Validation of these findings in independent cohorts is required.
Selenium is an essential micronutrient with biochemical and cellular effects through activities of 25 selenocysteine-containing selenoproteins. Selenoproteins are anti-inflammatory and have antioxidant properties. Severe selenium deficiency causes muscle weakness and atrophy in humans however the effects of moderate selenium deficiency are unclear. The aims of this study are twofold: 1) to determine dietary selenium intakes and contributing food sources in very old adults and; 2) to determine whether dietary selenium intakes are associated with 5-year trajectories of muscle function: hand-grip strength (HGS) and Timed-Up-and-Go (TUG).
Cross-sectional (baseline) and prospective (1.5, 3 and 5-year follow-up) analyses of 845 participants aged 85 years from the Newcastle 85 + study were assessed for HGS and TUG performance using standardized protocols (Antoneta et al. 2016). Baseline dietary intakes were assessed using 24-hour multiple pass recall methods on two separate days (Mendonça et al. 2016). The top selenium food contributors (~90%) and the adequacy of intakes were determined i.e. those with intakes < LRNI, between the LRNI and RNI and > RNI. Linear mixed models explored the associations between selenium intake categories and time on the prospective, 5-year change in HGS and TUG in all participants, males and females.
Median intakes of selenium were 39, 48 and 35μg for all participants, males and females, respectively. Selenium intakes were below the LRNI in 51% of participants (median 27μg) whilst 15% had intakes ≥ the RNI (median 85μg). Only 13.3% of females and 16.9 % of males met the RNI. The top selenium contributors were cereals (46%), meat (22%), fish (10%), milk (6%), eggs (4%) and potatoes (3%) making up 91% of selenium intakes. Those with the lowest intakes had 2.72 kg lower HGS and 2.36s slower TUG compared to those with higher intakes (P < 0.005). There was no association between selenium intake in HGS or TUG, but time had a significant effect on the rate of change over 5-years in both parameters (P < 0.001).
Overall these results show that poor dietary selenium intakes are common in very old adults and that cereal and cereal products are major sources of selenium in this population. Whilst low selenium intakes are associated with worse HGS and TUG performance in the cross-sectional analysis, no significant associations were observed in the prospective analyses.
There is strong evidence that foods containing dietary fibre protect against colorectal cancer, resulting at least in part from its anti-proliferative properties. This study aimed to investigate the effects of supplementation with two non-digestible carbohydrates, resistant starch (RS) and polydextrose (PD), on crypt cell proliferative state (CCPS) in the macroscopically normal rectal mucosa of healthy individuals. We also investigated relationships between expression of regulators of apoptosis and of the cell cycle on markers of CCPS. Seventy-five healthy participants were supplemented with RS and/or PD or placebo for 50 d in a 2 × 2 factorial design in a randomised, double-blind, placebo-controlled trial (the Dietary Intervention, Stem cells and Colorectal Cancer (DISC) Study). CCPS was assessed, and the expression of regulators of the cell cycle and of apoptosis was measured by quantitative PCR in rectal mucosal biopsies. SCFA concentrations were quantified in faecal samples collected pre- and post-intervention. Supplementation with RS increased the total number of mitotic cells within the crypt by 60 % (P = 0·001) compared with placebo. This effect was limited to older participants (aged ≥50 years). No other differences were observed for the treatments with PD or RS as compared with their respective controls. PD did not influence any of the measured variables. RS, however, increased cell proliferation in the crypts of the macroscopically-normal rectum of older adults. Our findings suggest that the effects of RS on CCPS are not only dose, type of RS and health status-specific but are also influenced by age.
Little is known about who would benefit from Internet-based personalised nutrition (PN) interventions. This study aimed to evaluate the characteristics of participants who achieved greatest improvements (i.e. benefit) in diet, adiposity and biomarkers following an Internet-based PN intervention. Adults (n 1607) from seven European countries were recruited into a 6-month, randomised controlled trial (Food4Me) and randomised to receive conventional dietary advice (control) or PN advice. Information on dietary intake, adiposity, physical activity (PA), blood biomarkers and participant characteristics was collected at baseline and month 6. Benefit from the intervention was defined as ≥5 % change in the primary outcome (Healthy Eating Index) and secondary outcomes (waist circumference and BMI, PA, sedentary time and plasma concentrations of cholesterol, carotenoids and omega-3 index) at month 6. For our primary outcome, benefit from the intervention was greater in older participants, women and participants with lower HEI scores at baseline. Benefit was greater for individuals reporting greater self-efficacy for ‘sticking to healthful foods’ and who ‘felt weird if [they] didn’t eat healthily’. Participants benefited more if they reported wanting to improve their health and well-being. The characteristics of individuals benefiting did not differ by other demographic, health-related, anthropometric or genotypic characteristics. Findings were similar for secondary outcomes. These findings have implications for the design of more effective future PN intervention studies and for tailored nutritional advice in public health and clinical settings.
Early-life stress (ELS) has previously been identified as a risk factor for cognitive decline, but this work has predominantly focused on clinical groups and indexed traditional cognitive domains. It, therefore, remains unclear whether ELS is related to cognitive function in healthy community-dwelling older adults, as well as whether any effects of ELS also extend to social cognition. To test each of these questions, the Childhood Trauma Questionnaire (CTQ) was administered to 484 older adults along with a comprehensive neuropsychological test battery and a well-validated test of social cognitive function. The results revealed no differences in global cognition according to overall experiences of ELS. However, a closer examination into the different ELS subscales showed that global cognition was poorer in those who had experienced physical neglect (relative to those who had not). Social cognitive function did not differ according to experiences to ELS. These results indicate that the relationship between ELS and cognition in older age may be dependent on the nature of the trauma experienced.