The relationship of nutritional risk with diet quality and health outcomes in community-dwelling older adults.

OBJECTIVES: To identify early nutritional risk in older populations, simple screening approaches are needed. This study aimed to compare nutrition risk scores, calculated from a short checklist, with diet quality and health outcomes, both at baseline and prospectively over a 2.5-year follow-up period; the association between baseline scores and risk of mortality over the follow-up period was assessed. METHODS: The study included 86 community-dwelling older adults in Southampton, UK, recruited from outpatient clinics. At both assessments, hand grip strength was measured using a Jamar dynamometer. Diet was assessed using a short validated food frequency questionnaire; derived 'prudent' diet scores described diet quality. Body mass index (BMI) was calculated and weight loss was self-reported. Nutrition risk scores were calculated from a checklist adapted from the DETERMINE (range 0-17). RESULTS: The mean age of participants at baseline (n = 86) was 78 (SD 8) years; half (53%) scored 'moderate' or 'high' nutritional risk, using the checklist adapted from DETERMINE. In cross-sectional analyses, after adjusting for age, sex and education, higher nutrition risk scores were associated with lower grip strength [difference in grip strength: - 0.09, 95% CI (- 0.17, - 0.02) SD per unit increase in nutrition risk score, p = 0.017] and poorer diet quality [prudent diet score: - 0.12, 95% CI (- 0.21, - 0.02) SD, p = 0.013]. The association with diet quality was robust to further adjustment for number of comorbidities, whereas the association with grip strength was attenuated. Nutrition risk scores were not related to reported weight loss or BMI at baseline. In longitudinal analyses there was an association between baseline nutrition risk score and lower grip strength at follow-up [fully-adjusted model: - 0.12, 95% CI (- 0.23, - 0.02) SD, p = 0.024]. Baseline nutrition risk score was also associated with greater risk of mortality [unadjusted hazard ratio per unit increase in score: 1.29 (1.01, 1.63), p = 0.039]; however, this association was attenuated after adjustment for sex and age. CONCLUSIONS: Cross-sectional associations between higher nutrition risk scores, assessed from a short checklist, and poorer diet quality suggest that this approach may hold promise as a simple way of screening older populations. Further larger prospective studies are needed to explore the predictive ability of this screening approach and its potential to detect nutritional risk in older adults.

Noncanonical autophagy at ER exit sites regulates procollagen turnover.

Type I collagen is the main component of bone matrix and other connective tissues. Rerouting of its procollagen precursor to a degradative pathway is crucial for osteoblast survival in pathologies involving excessive intracellular buildup of procollagen that is improperly folded and/or trafficked. What cellular mechanisms underlie this rerouting remains unclear. To study these mechanisms, we employed live-cell imaging and correlative light and electron microscopy (CLEM) to examine procollagen trafficking both in wild-type mouse osteoblasts and osteoblasts expressing a bone pathology-causing mutant procollagen. We found that although most procollagen molecules successfully trafficked through the secretory pathway in these cells, a subpopulation did not. The latter molecules appeared in numerous dispersed puncta colocalizing with COPII subunits, autophagy markers and ubiquitin machinery, with more puncta seen in mutant procollagen-expressing cells. Blocking endoplasmic reticulum exit site (ERES) formation suppressed the number of these puncta, suggesting they formed after procollagen entry into ERESs. The punctate structures containing procollagen, COPII, and autophagic markers did not move toward the Golgi but instead were relatively immobile. They appeared to be quickly engulfed by nearby lysosomes through a bafilomycin-insensitive pathway. CLEM and fluorescence recovery after photobleaching experiments suggested engulfment occurred through a noncanonical form of autophagy resembling microautophagy of ERESs. Overall, our findings reveal that a subset of procollagen molecules is directed toward lysosomal degradation through an autophagic pathway originating at ERESs, providing a mechanism to remove excess procollagen from cells.

An overview of appetite decline in older people.

Poor appetite is a common problem in older people living at home and in care homes, as well as hospital inpatients. It can contribute to weight loss and nutritional deficiencies, and associated poor healthcare outcomes, including increased mortality. Understanding the causes of reduced appetite and knowing how to measure it will enable nurses and other clinical staff working in a range of community and hospital settings to identify patients with impaired appetite. A range of strategies can be used to promote better appetite and increase food intake.

The feasibility and acceptability of training volunteer mealtime assistants to help older acute hospital inpatients: the Southampton Mealtime Assistance Study.

AIMS AND OBJECTIVES: To determine the feasibility and acceptability of using trained volunteers as mealtime assistants for older hospital inpatients. BACKGROUND: Poor nutrition among hospitalised older patients is common in many countries and associated with poor outcomes. Competing time pressures on nursing staff may make it difficult to prioritise mealtime assistance especially on wards where many patients need help. DESIGN: Mixed methods evaluation of the introduction of trained volunteer mealtime assistants on an acute female medicine for older people ward in a teaching hospital in England. METHODS: A training programme was developed for volunteers who assisted female inpatients aged 70 years and over on weekday lunchtimes. The feasibility of using volunteers was determined by the proportion recruited, trained, and their activity and retention over one year. The acceptability of the training and of the volunteers' role was obtained through interviews and focus groups with 12 volunteers, nine patients and 17 nursing staff. RESULTS: Fifty-nine potential volunteers were identified: 38 attended a training session, of whom 29 delivered mealtime assistance, including feeding, to 3911 (76%) ward patients during the year (mean duration of assistance 5·5 months). The volunteers were positive about the practical aspects of training and ongoing support provided. They were highly valued by patients and ward staff and have continued to volunteer. CONCLUSIONS: Volunteers can be recruited and trained to help acutely unwell older female inpatients at mealtimes, including feeding. This assistance is sustainable and is valued. RELEVANCE TO CLINICAL PRACTICE: This paper describes a successful method for recruitment, training and retention of volunteer mealtime assistants. It includes a profile of those volunteers who provided the most assistance, details of the training programme and role of the volunteers and could be replicated by nursing staff in other healthcare units.

Southampton Mealtime Assistance Study: design and methods.

BACKGROUND: Malnutrition is common in older people in hospital and is associated with adverse clinical outcomes including increased mortality, morbidity and length of stay. This has raised concerns about the nutrition and diet of hospital in-patients. A number of factors may contribute to low dietary intakes in hospital, including acute illness and cognitive impairment among in-patients. The extent to which other factors influence intake such as a lack of help at mealtimes, for patients who require assistance with eating, is uncertain. This study aims to evaluate the effectiveness of using trained volunteer mealtime assistants to help patients on an acute medical ward for older people at mealtimes. METHODS/DESIGN: The study design is quasi-experimental with a before (year one) and after (year two) comparison of patients on the intervention ward and parallel comparison with patients on a control ward in the same department. The intervention in the second year was the provision of trained volunteer mealtime assistance to patients in the intervention ward. There were three components of data collection that were repeated in both years on both wards. The first (primary) outcome was patients' dietary intake, collected as individual patient records and as ward-level balance data over 24 hour periods. The second was clinical outcome data assessed on admission and discharge from both wards, and 6 and 12 months after discharge. Finally qualitative data on the views and experience of patients, carers, staff and volunteers was collected through interviews and focus groups in both years to allow a mixed-method evaluation of the intervention. DISCUSSION: The study will describe the effect of provision of trained volunteer mealtime assistants on the dietary intake of older medical in-patients. The association between dietary intake and clinical outcomes including malnutrition risk, body composition, grip strength, length of hospital stay and mortality will also be determined. An important component of the study is the use of qualitative approaches to determine the views of patients, relatives, staff and volunteers on nutrition in hospital and the impact of mealtime assistance. TRIAL REGISTRATION: Trial registered with ClinicalTrials.gov NCTO1647204.

Deficient degradation of homotrimeric type I collagen, α1(I)3 glomerulopathy in oim mice.

Col1a2-deficient (oim) mice synthesize homotrimeric type I collagen due to nonfunctional proα2(I) collagen chains. Our previous studies revealed a postnatal, progressive type I collagen glomerulopathy in this mouse model, but the mechanism of the sclerotic collagen accumulation within the renal mesangium remains unclear. The recent demonstration of the resistance of homotrimeric type I collagen to cleavage by matrix metalloproteinases (MMPs), led us to investigate the role of MMP-resistance in the glomerulosclerosis of Col1a2-deficient mice. We measured the pre- and post-translational expression of type I collagen and MMPs in glomeruli from heterozygous and homozygous animals. Both the heterotrimeric and homotrimeric isotypes of type I collagen were equally present in whole kidneys of heterozygous mice by immunohistochemistry and biochemical analysis, but the sclerotic glomerular collagen was at least 95-98% homotrimeric, suggesting homotrimeric type I collagen is the pathogenic isotype of type I collagen in glomerular disease. Although steady-state MMP and Col1a1 mRNA levels increased with the disease progression, we found these changes to be a secondary response to the deficient clearance of MMP-resistant homotrimers. Increased renal MMP expression was not sufficient to prevent homotrimeric type I collagen accumulation.

Transforming growth factor-ß1/Smad3-independent epithelial-mesenchymal transition in type I collagen glomerulopathy.

The glomerulofibrotic Col1a2-deficient mouse model demonstrates glomerular homotrimeric type I collagen deposition in mesangial and subendothelial spaces. In this report, we investigate the role of transforming growth factor ß1 (TGF-ß1) in myofibroblast activation and epithelial-mesenchymal transition (EMT) in this glomerulopathy. Immunohistochemical analyses of glomerular α-sma, desmin, vimentin, and proliferating cell nuclear antigen demonstrated parietal epithelial cell proliferation and EMT in late stages of the glomerulopathy in the Col1a2-deficient mice. Glomerular TGF-ß1 RNA and protein were not elevated in 1- and 3-month-old mice as determined by quantitative reverse transcriptase-polymerase chain reaction and protein immunoassay analyses. To investigate further whether TGF-ß1 plays a role in the glomerulopathy outside of the 1- and 3-month time periods, the Col1a2-deficient mice were bred with Smad3 knockout mice. If the glomerular fibrosis in the Col1a2-deficient mice is mediated by the TGF-ß1/Smad3 transcription pathway, it was hypothesized that the resultant Col1a2-deficient/Smad3-deficient mice would exhibit attenuated glomerular homotrimer deposition. However, the Col1a2-deficient/Smad3-deficient kidneys were similarly affected as compared to age-matched Col1a2-deficient kidneys, suggesting that homotrimeric type I collagen deposition in the Col1a2-deficient mouse is independent of TGF-ß1/Smad3 signaling. Deposition of homotrimeric type I collagen appears to be the initiating event in this glomerulopathy, providing evidence that EMT and myofibroblast activation occur following initiation, consistent with a secondary wound-healing response independent of TGF-ß1.

Osteoblast Malfunction Caused by Cell Stress Response to Procollagen Misfolding in α2(I)-G610C Mouse Model of Osteogenesis Imperfecta.

Glycine (Gly) substitutions in collagen Gly-X-Y repeats disrupt folding of type I procollagen triple helix and cause severe bone fragility and malformations (osteogenesis imperfecta [OI]). However, these mutations do not elicit the expected endoplasmic reticulum (ER) stress response, in contrast to other protein-folding diseases. Thus, it has remained unclear whether cell stress and osteoblast malfunction contribute to the bone pathology caused by Gly substitutions. Here we used a mouse with a Gly610 to cysteine (Cys) substitution in the procollagen α2(I) chain to show that misfolded procollagen accumulation in the ER leads to an unusual form of cell stress, which is neither a conventional unfolded protein response (UPR) nor ER overload. Despite pronounced ER dilation, there is no upregulation of binding immunoglobulin protein (BIP) expected in the UPR and no activation of NF-κB signaling expected in the ER overload. Altered expression of ER chaperones αB crystalline and HSP47, phosphorylation of EIF2α, activation of autophagy, upregulation of general stress response protein CHOP, and osteoblast malfunction reveal some other adaptive response to the ER disruption. We show how this response alters differentiation and function of osteoblasts in culture and in vivo. We demonstrate that bone matrix deposition by cultured osteoblasts is rescued by activation of misfolded procollagen autophagy, suggesting a new therapeutic strategy for OI. © 2016 American Society for Bone and Mineral Research.

Can trained volunteers make a difference at mealtimes for older people in hospital? A qualitative study of the views and experience of nurses, patients, relatives and volunteers in the Southampton Mealtime Assistance Study.

BACKGROUND: Malnutrition is common amongst hospitalised older patients and associated with increased morbidity and mortality. Poor dietary intake results from factors including acute illness and cognitive impairment but additionally patients may have difficulty managing at mealtimes. Use of volunteers to help at mealtimes is rarely evaluated. OBJECTIVES: To obtain multiple perspectives on nutritional care of older inpatients, acceptability of trained volunteers and identify important elements of their assistance. DESIGN: A qualitative study 1 year before and after introduction of volunteer mealtime assistants on one ward and parallel comparison with a control ward in a Medicine for Older People department at a UK university hospital. PARTICIPANTS AND METHODS: Semi-structured interviews and focus groups, in baseline and intervention years, with purposively sampled nursing staff at different levels of seniority; patients or close relatives; and volunteers. RESULTS: At baseline staff felt under pressure with insufficient people assisting at mealtimes. Introducing trained volunteers was perceived by staff and patients to improve quality of mealtime care by preparing patients for mealtimes, assisting patients who needed help, and releasing nursing time to assist dysphagic or drowsy patients. There was synergy with other initiatives, notably protected mealtimes. Interviews highlighted the perceived contribution of chronic poor appetite and changes in eating patterns to risk of malnutrition. CONCLUSIONS: Improved quality of mealtime care attributed to volunteers' input has potential to enhance staff morale and patients'/relatives' confidence. A volunteer mealtime assistance scheme may work best when introduced in context of other changes reflecting commitment to improving nutrition. IMPLICATIONS FOR PRACTICE: (i) A mealtime assistance scheme should incorporate training, supervision and support for volunteers; (ii) Good relationships and a sense of teamwork can develop between wards staff and volunteers; (iii) Impact may be maximised in the context of 'protected mealtimes'.

Does living in a food insecure household impact on the diets and body composition of young children? Findings from the Southampton Women's Survey.

BACKGROUND: Little is known about food insecurity in the UK. The aims of this study were to assess the prevalence and factors associated with food insecurity in a UK cohort and to examine whether the diets, reported health and anthropometry of young food insecure children differed from those of other children. METHODS: The Southampton Women's Survey is a prospective cohort study in which detailed information about the diets, lifestyle and body composition of 3000 women was collected before and during pregnancy. Between 2002 and 2006, 1618 families were followed up when the child was 3 years old. Food insecurity was determined using the Household Food Security Scale. The child's height and weight were measured; diet was assessed by food frequency questionnaire. RESULTS: 4.6% of the households were food insecure. Food insecurity was more common in families where the mothers were younger, smokers, of lower social class, in receipt of financial benefits and who had a higher deprivation score (all p<0.05). In comparison with other 3-year-old children, those living in food insecure households were likely to have worse parent-reported health and to have a diet of poorer quality, characterised by greater consumption of white bread, processed meat and chips, and by a lower consumption of vegetables (all p<0.05). They did not differ in height or body mass index. CONCLUSIONS: Our data suggest that there are significant numbers of food insecure families in the UK. The poorer reported health and diets of young food insecure children have important implications for their development and lifelong health.