- Email: [email protected]
Diet quality and telomere length in older Australian men and women
Abstracts / Journal of Nutrition & Intermediary Metabolism 8 (2017) 60e121
E-mail address: [email protected] (C.K. Yao). Background/Aims: Defective carbohydrate fermentation has previously been described in individuals with ulcerative colitis (UC). Additionally, low fibre but high protein intakes have been reported in UC patients and may contribute to its pathogenesis. We aimed to compare the (1) habitual dietary fibre and protein intake and (2) carbohydrate fermentation ability in UC patients and of healthy controls (HC). Methods: Patients with UC in remission and HC without recent fibre supplementation were included. Seven-day food records were used to compare mean (SEM) dietary intake for fibre, resistant starch, oligosaccharides and protein between cohorts and against Nutrient Reference Values using FoodWorks. 48-h faecal samples were assessed for daily faecal and starch output, pH and water content. Starch utilisation, a marker of carbohydrate fermentation, was also compared between groups. Data were analysed using unpaired t-tests, Fisher's exact or Mann-Whitney tests. Results: Eight UC patients and 9 HCs were studied. Mean ± SD consumption of protein (88 ± 10 vs. 99 ± 11 g/d; p ¼ 0.50), fibre (24 ± 2 vs. 28 ± 4 g/d; p ¼ 0.45) and its components was similar between UC vs HC respectively. Only 44% HC and 25% UC patients met fibre recommendations (p ¼ 0.62). None of the faecal indices differed except for faecal water content (25% higher in UC patients). Starch utilisation was similar in UC patients (median 96%, range: 85-99%) and HCs (95%, 86-100%; p ¼ 0.49). Conclusions: Habitual protein and fibre intake did not differ in this UC cohort compared to those of HCs. Fibre utilisation was similar not supporting a carbohydrate fermentative defect. Instead, UC patients had a greater faecal water content, indicating functional impairment of the colonic epithelium. Funding source(s): Ferring Pharmaceuticals PLASMA CYSTEINE PREDICTS WEIGHT REGAIN AFTER BARIATRIC SURGERY S.E. Hanvold 1, 2, A.M. Aas 2, K.J. Vinknes 1, N.E. Bastani 1, C. Turner 3, E.B. Løken 1, T. Mala 4, H. Refsum 1, 3. 1 Dept. of Nutrition, Uni. of Oslo, Norway; 2 Section of Nutrition & Dietetics, Oslo Uni. Hospital Aker, Norway; 3 Department of Pharmacology, University of Oxford, UK; 4 Department of Morbid Obesity & Bariatric surgery, Oslo Uni. Hospital Aker, Norway E-mail address: [email protected] (H. Refsum). Background/Aims: Plasma concentrations of amino acids, in particular total cysteine (tCys) and branched-chained and aromatic amino acids (BCAAs, AAAs) are associated with obesity. Recent data suggest a causal association between tCys and obesity. In this study, we examined the association of selected plasma amino acids with changes in BMI from 2 to 4 y (DBMI2-4y) after Roux-en-Y gastric bypass (RYGB). Methods: Patients (n ¼ 165, 74.5% women) were investigated 2 and 4 y after RYGB. The associations of plasma AAAs, BCAAs and tCys at 2 y with BMI2y and with DBMI2-4y were studied by linear and logistic regression, adjusted for age and sex. Results: AAAs, BCAAs and tCys at 2 y were positively associated with BMI2y (r ¼ 0.23-0.27, p 0.003 for all), but only plasma tCys2y was associated with DBMI2-4y (r ¼ 0.21, p ¼ 0.015). The risk of gaining 2 BMI units from 2 to 4 y was higher for those with tCys2y in quartile 4 vs. those in quartile 1 (OR: 2.96; 95%CI: 1.06-8.23). The mean (SE) DBMI2-4y was 2.3 (0.4) kg/m2 in quartile 4 compared to 1.0 (0.4) kg/m2 in quartile 1 (p ¼ 0.025). Conclusions: High plasma tCys at 2 y after RYGB is associated with later weight regain. If tCys is causally associated with obesity, it may provide a treatment strategy against weight regain after bariatric surgery. Funding source(s): The Norwegian Extra Foundation for Health and Rehabilitation THE IMPACT OF SODIUM ON INFLAMMATION RELATED TO MULTIPLE SCLEROSIS E. Mowbray, Y.C. Probst, K. Walton. Faculty of Science, Medicine and Health, School of Medicine, University of Wollongong, NSW, Australia E-mail address: [email protected] (E. Mowbray). Background/Aims: The aetiology of Multiple Sclerosis is still unknown;
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however certain environmental factors paired with a genetic predisposition have been implicated in the onset of the disease. Recent studies have suggested dietary sodium as a contributing factor to Multiple Sclerosis exacerbation, which includes increased rate of relapse, severity of symptoms and increased number of T2-MRI lesions, which are indicative of disease progression. This review aimed to determine the impact of sodium on inflammation and autoimmunity related to Multiple Sclerosis. Methods: A systematic literature review was conducted using the databases Scopus, Medline and PubMed to locate appropriate studies. Articles were restricted to those published in the past 15 years (2001 - 2016), and being an emerging area of research the search was open to all populations and study designs. Results: Nine peer-reviewed articles were located for inclusion. Results showed in vitro augmentation of the immune response when cells were exposed to high-salt media. Similarly, disease was exacerbated and associated inflammation was increased in vivo in mice that were fed a high-salt diet. Human subjects who consumed a high-salt diet also had an increased number of T2-MRI lesions and a higher relapse rate. Conclusions: High-salt conditions and intakes of high amounts of dietary salt contribute to a heightened autoimmune response and increased neuroinflammation in mice and in human subjects. Results are suggestive of a relationship between high dietary salt intake and Multiple Sclerosis pathophysiology and therefore higher-level evidence studies on this relationship are indicated. Funding source(s): N/A DIET QUALITY AND TELOMERE LENGTH IN OLDER AUSTRALIAN MEN AND WOMEN C.M. Milte, A.P. Russell, K. Ball, D. Crawford, J. Salmon, S.A. McNaughton. Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, VIC, Australia E-mail address: [email protected] (C.M. Milte). Background/Aims: Telomere length is a biomarker of cellular ageing, with longer telomeres associated with longevity and reduced risk of chronic disease in older age. Consumption of a healthy diet may contribute to longevity via its impact on cellular ageing but studies on diet and telomere length to date have been limited and their findings equivocal. The aim of this study is to examine associations between three indices of diet quality and telomere length in older men and women. Methods: Adults aged 57-68 years participating in the Wellbeing, Eating and Exercise for a Long Life (WELL) study in Victoria, Australia (n ¼ 679, 49% men) completed a postal survey including a 111-item food frequency questionnaire in 2012. Diet quality was assessed via three indices, the Dietary Guideline Index, the Recommended Food Score and the Mediterranean Diet Score. Relative telomere length was measured by quantitative polymerase chain reaction. Associations between diet quality and telomere length were assessed using linear regression adjusted for covariates. Results: After adjustment for age, sex, education, smoking, physical activity and body mass index (BMI), there were no significant associations between any measure of diet quality and relative telomere length. Conclusions: While diet quality was not associated with telomere length in the current study, future research should consider repeated measures of telomere length, to examine the impact of diet on rate of telomere shortening in longitudinal studies. Funding source(s): ARC; Diabetes Australia Research Trust; NHMRC ROLE OF THE HEPATOPORTAL SYSTEM IN THE REVERSAL OF INSULIN RESISTANCE IN RATS H.M. Johnson, E.L. Stanfield, K.S. Bell-Anderson. School of Life and Environmental Sciences and Charles Perkins Centre, The University of Sydney, Australia E-mail address: [email protected] (H.M. Johnson). Background/Aims: Insulin resistance is the primary characteristic underlying the development of T2DM. We have previously shown that highfat diet-induced insulin resistance in rats can be ameliorated by a single glucose meal, but the mechanism has yet to be elucidated. Our aim was to determine if this effect is mediated by gut or portal factors.
E-mail address: [email protected] (C.K. Yao). Background/Aims: Defective carbohydrate fermentation has previously been described in individuals with ulcerative colitis (UC). Additionally, low fibre but high protein intakes have been reported in UC patients and may contribute to its pathogenesis. We aimed to compare the (1) habitual dietary fibre and protein intake and (2) carbohydrate fermentation ability in UC patients and of healthy controls (HC). Methods: Patients with UC in remission and HC without recent fibre supplementation were included. Seven-day food records were used to compare mean (SEM) dietary intake for fibre, resistant starch, oligosaccharides and protein between cohorts and against Nutrient Reference Values using FoodWorks. 48-h faecal samples were assessed for daily faecal and starch output, pH and water content. Starch utilisation, a marker of carbohydrate fermentation, was also compared between groups. Data were analysed using unpaired t-tests, Fisher's exact or Mann-Whitney tests. Results: Eight UC patients and 9 HCs were studied. Mean ± SD consumption of protein (88 ± 10 vs. 99 ± 11 g/d; p ¼ 0.50), fibre (24 ± 2 vs. 28 ± 4 g/d; p ¼ 0.45) and its components was similar between UC vs HC respectively. Only 44% HC and 25% UC patients met fibre recommendations (p ¼ 0.62). None of the faecal indices differed except for faecal water content (25% higher in UC patients). Starch utilisation was similar in UC patients (median 96%, range: 85-99%) and HCs (95%, 86-100%; p ¼ 0.49). Conclusions: Habitual protein and fibre intake did not differ in this UC cohort compared to those of HCs. Fibre utilisation was similar not supporting a carbohydrate fermentative defect. Instead, UC patients had a greater faecal water content, indicating functional impairment of the colonic epithelium. Funding source(s): Ferring Pharmaceuticals PLASMA CYSTEINE PREDICTS WEIGHT REGAIN AFTER BARIATRIC SURGERY S.E. Hanvold 1, 2, A.M. Aas 2, K.J. Vinknes 1, N.E. Bastani 1, C. Turner 3, E.B. Løken 1, T. Mala 4, H. Refsum 1, 3. 1 Dept. of Nutrition, Uni. of Oslo, Norway; 2 Section of Nutrition & Dietetics, Oslo Uni. Hospital Aker, Norway; 3 Department of Pharmacology, University of Oxford, UK; 4 Department of Morbid Obesity & Bariatric surgery, Oslo Uni. Hospital Aker, Norway E-mail address: [email protected] (H. Refsum). Background/Aims: Plasma concentrations of amino acids, in particular total cysteine (tCys) and branched-chained and aromatic amino acids (BCAAs, AAAs) are associated with obesity. Recent data suggest a causal association between tCys and obesity. In this study, we examined the association of selected plasma amino acids with changes in BMI from 2 to 4 y (DBMI2-4y) after Roux-en-Y gastric bypass (RYGB). Methods: Patients (n ¼ 165, 74.5% women) were investigated 2 and 4 y after RYGB. The associations of plasma AAAs, BCAAs and tCys at 2 y with BMI2y and with DBMI2-4y were studied by linear and logistic regression, adjusted for age and sex. Results: AAAs, BCAAs and tCys at 2 y were positively associated with BMI2y (r ¼ 0.23-0.27, p 0.003 for all), but only plasma tCys2y was associated with DBMI2-4y (r ¼ 0.21, p ¼ 0.015). The risk of gaining 2 BMI units from 2 to 4 y was higher for those with tCys2y in quartile 4 vs. those in quartile 1 (OR: 2.96; 95%CI: 1.06-8.23). The mean (SE) DBMI2-4y was 2.3 (0.4) kg/m2 in quartile 4 compared to 1.0 (0.4) kg/m2 in quartile 1 (p ¼ 0.025). Conclusions: High plasma tCys at 2 y after RYGB is associated with later weight regain. If tCys is causally associated with obesity, it may provide a treatment strategy against weight regain after bariatric surgery. Funding source(s): The Norwegian Extra Foundation for Health and Rehabilitation THE IMPACT OF SODIUM ON INFLAMMATION RELATED TO MULTIPLE SCLEROSIS E. Mowbray, Y.C. Probst, K. Walton. Faculty of Science, Medicine and Health, School of Medicine, University of Wollongong, NSW, Australia E-mail address: [email protected] (E. Mowbray). Background/Aims: The aetiology of Multiple Sclerosis is still unknown;
85
however certain environmental factors paired with a genetic predisposition have been implicated in the onset of the disease. Recent studies have suggested dietary sodium as a contributing factor to Multiple Sclerosis exacerbation, which includes increased rate of relapse, severity of symptoms and increased number of T2-MRI lesions, which are indicative of disease progression. This review aimed to determine the impact of sodium on inflammation and autoimmunity related to Multiple Sclerosis. Methods: A systematic literature review was conducted using the databases Scopus, Medline and PubMed to locate appropriate studies. Articles were restricted to those published in the past 15 years (2001 - 2016), and being an emerging area of research the search was open to all populations and study designs. Results: Nine peer-reviewed articles were located for inclusion. Results showed in vitro augmentation of the immune response when cells were exposed to high-salt media. Similarly, disease was exacerbated and associated inflammation was increased in vivo in mice that were fed a high-salt diet. Human subjects who consumed a high-salt diet also had an increased number of T2-MRI lesions and a higher relapse rate. Conclusions: High-salt conditions and intakes of high amounts of dietary salt contribute to a heightened autoimmune response and increased neuroinflammation in mice and in human subjects. Results are suggestive of a relationship between high dietary salt intake and Multiple Sclerosis pathophysiology and therefore higher-level evidence studies on this relationship are indicated. Funding source(s): N/A DIET QUALITY AND TELOMERE LENGTH IN OLDER AUSTRALIAN MEN AND WOMEN C.M. Milte, A.P. Russell, K. Ball, D. Crawford, J. Salmon, S.A. McNaughton. Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, VIC, Australia E-mail address: [email protected] (C.M. Milte). Background/Aims: Telomere length is a biomarker of cellular ageing, with longer telomeres associated with longevity and reduced risk of chronic disease in older age. Consumption of a healthy diet may contribute to longevity via its impact on cellular ageing but studies on diet and telomere length to date have been limited and their findings equivocal. The aim of this study is to examine associations between three indices of diet quality and telomere length in older men and women. Methods: Adults aged 57-68 years participating in the Wellbeing, Eating and Exercise for a Long Life (WELL) study in Victoria, Australia (n ¼ 679, 49% men) completed a postal survey including a 111-item food frequency questionnaire in 2012. Diet quality was assessed via three indices, the Dietary Guideline Index, the Recommended Food Score and the Mediterranean Diet Score. Relative telomere length was measured by quantitative polymerase chain reaction. Associations between diet quality and telomere length were assessed using linear regression adjusted for covariates. Results: After adjustment for age, sex, education, smoking, physical activity and body mass index (BMI), there were no significant associations between any measure of diet quality and relative telomere length. Conclusions: While diet quality was not associated with telomere length in the current study, future research should consider repeated measures of telomere length, to examine the impact of diet on rate of telomere shortening in longitudinal studies. Funding source(s): ARC; Diabetes Australia Research Trust; NHMRC ROLE OF THE HEPATOPORTAL SYSTEM IN THE REVERSAL OF INSULIN RESISTANCE IN RATS H.M. Johnson, E.L. Stanfield, K.S. Bell-Anderson. School of Life and Environmental Sciences and Charles Perkins Centre, The University of Sydney, Australia E-mail address: [email protected] (H.M. Johnson). Background/Aims: Insulin resistance is the primary characteristic underlying the development of T2DM. We have previously shown that highfat diet-induced insulin resistance in rats can be ameliorated by a single glucose meal, but the mechanism has yet to be elucidated. Our aim was to determine if this effect is mediated by gut or portal factors.