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The effect of a low carbohydrate high fat diet on emerging biochemical markers of cardiometabolic risk
- Deaglan McCullough, Tanja Harrison, Katie Lane, Lynne Boddy, Farzad Amirabdollahian, Michael Schmidt, Kevin Enright, Claire Stewart, Ian Davies
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- Journal:
- Proceedings of the Nutrition Society / Volume 79 / Issue OCE2 / 2020
- Published online by Cambridge University Press:
- 10 June 2020, E530
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Worldwide, cardiovascular disease (CVD) is the number 1 cause of mortality and is associated with insulin resistance (IR). Emerging biomarkers such as FGF21 and adiponectin are associated with cardiometabolic risk. Low carbohydrate, high fat (LCHF) diets have been reported to reduce cardiometabolic risk markers; however, few studies have compared a LCHF diet vs. a high carbohydrate (HC), lower fat diet under ad libitum conditions on adiponectin and FGF21. The purpose of this study was to investigate the effects of an ad libitum LCHF vs. HC diet on IR, FGF21 and adiponectin in 16 healthy adults. Ethical approval: Liverpool John Moores University Research Ethics Committee (16/ELS/029); registered with ClinicalTrials.gov (Ref. NCT03257085). Participants were randomly assigned to a HC diet (n = 8, the UK Eatwell guidelines; ≥ 50% of energy from carbohydrates) or a LCHF diet (n = 8, consume < 50 g/day of carbohydrates). All provided plasma samples at 0, 4 and 8 weeks. FGF21 (R&D Systems) was analysed via ELISA and adiponectin, insulin and glucose were analysed via immunoassay technology (Randox Evidence Investigator™ Metabolic Syndrome Arrays I & II). Mann Whitney, Friedmans, Wilcoxon tests and 2×3 ANOVA (IBM SPSS 25®) were undertaken to investigate significant differences between and within groups. The homeostatic model assessment (HOMA) was used to calculate IR. FGF21 significantly (P = 0.04) decreased (Mdn, IQR:148.16, 78.51–282.02 to 99.4, 39.87–132.29 pg/ml) after 4 weeks and significantly (P = 0.02) increased (Mdn, IQR:167.38, 80.82–232.89 pg/ml) by 8 weeks vs. baseline with LCHF. No significant differences (P > 0.05) were observed between groups. Adiponectin was significantly (P = 0.03) different at week 4 only between groups. Adiponectin increased after 4 weeks (Mdn, IQR:13.44, 9.12–25.47 to 16.64, 11.96–21.51 ng/ml) but was only significantly (P = 0.03) different by 8 weeks vs. baseline in the HC group (Mdn, IQR:16, 10.8–27.43 ng/ml). Adiponectin remained unchanged (P = 0.96) in the LCHF group. HOMA significantly decreased with both diets after 8 weeks only (mean ± SD, LCHF: 2.9 ± 1.3 to 1.8 ± 0.8, HC: 2.5 ± 0.6 to 1.9 ± 0.6, P = 0.008) but was not significantly (P = 0.60) different between groups. These preliminary data reveal that while both diets improved insulin sensitivity, they may do so by different mechanisms. Future studies are warranted to investigate further, how a LCHF vs. HC diet affects FGF21 and adiponectin, and the subsequent regulation of IR. Furthermore, studies that extend these findings by determining the impact of LCHF vs. HC on peripheral metabolism to determine potential nutrition-mediated mechanisms of metabolic adaptation are warranted.
The effect of a low carbohydrate high fat diet on apolipoproteins and cardiovascular risk
- Deaglan McCullough, Tanja Harrison, Katie Lane, Lynne Boddy, Farzad Amirabdollahian, Michael Schmidt, Kevin Enright, Claire Stewart, Ian Davies
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- Journal:
- Proceedings of the Nutrition Society / Volume 79 / Issue OCE2 / 2020
- Published online by Cambridge University Press:
- 10 June 2020, E677
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Apolipoproteins (apo) regulate lipoprotein characteristics and lipid metabolism. ApoC-III is a regulator of triglyceride-rich lipoprotein (TRL) metabolism and apolipoproteins are important biomarkers for cardiovascular disease (CVD) risk prediction. A low carbohydrate high fat (LCHF) diet improves cardiometabolic risk, especially via reduction of TRL. However, few studies have compared a LCHF vs. a high carbohydrate (HC), lower fat diet under ad libitum conditions on apoC-III levels. The objectives of this investigation were to measure the effect of a LCHF vs. a HC diet on apoC-III, apoA1, apoB and apoB/apoA1 in 16 healthy Caucasian adults aged 19–64. Ethical approval: Liverpool John Moores University Research Ethics Committee (16/ELS/029); registered with ClinicalTrials.gov (Ref. NCT03257085). Participants randomly assigned to a HC diet (UK Eatwell guidelines; ≥ 50% of energy from carbohydrates) (n = 8), or a LCHF diet (consume < 50 g/day of carbohydrates) (n = 8) provided plasma samples at 0, 4 and 8 weeks. ApoA1 and apoB were analysed by an automated chemistry analyser (Daytona, Randox Laboratories Ltd, UK). ApoC-III was analysed via ELISA (Thermo Fisher Ltd, USA). Factorial 2×3 ANOVA and ANCOVA (IBM SPSS 25®) were undertaken to investigate significant differences and to control for variables influenced by baseline measures and visceral adipose tissue (VAT). Results show 0, 4, and 8 weeks respectively: ApoC-III (LCHF: 19.12 ± 9.14, 16.05 ± 7.95, 15.11 ± 3.17 mg/dl; HC: 22.13 ± 8.38, 28.22 ± 13.85, 22.22 ± 7.7 mg/dl) showed no significant (P = 0.319) change. No significant (P = 0.23) change was also observed in ApoB (LCHF: 107.25 ± 20.35, 111.38 ± 24.81, 111.43 ± 19.93 mg/dl; HC: 94.38 ± 20.79, 105.00 ± 20.13, 99.00 ± 29.09 mg/dl). Similarly apoA1 (LCHF: 158.71 ± 14.27, 166.50 ± 23.09, 173.00 ± 29.42 mg/dl; HC: 164.71 ± 30.25, 172.50 ± 29.44, 174.00 ± 32.83 mg/dl) showed no significant change (P = 0.76). This resulted in a relatively unchanged apoB/A1 throughout the study in both diets (P = 0.30). No significant (P > 0.05) differences were found after 4 weeks or between groups also. ANCOVA revealed a trend (P = 0.06) in apoC-III for a difference between groups (LCHF: Δ-6.6 mg/dl vs. HC: Δ1.2 mg/dl) after 8 weeks but no significant (P > 0.05) changes in other apolipoproteins were detected. These preliminary data reveal that a LCHF diet does not improve the apolipoprotein profile; however, when accounting for other metabolic risk factors (i.e. VAT) there was a trend towards lowering apoC-III levels (P = 0.06). Modulation of apoC-III may lead to improved lipid metabolism, but higher-powered studies are warranted before any improvement on CVD risk can be inferred.
Contributors
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- By Victoria M. Allen, Frederic Amant, Sarah Armstrong, Thomas F. Baskett, Michael A. Belfort, Meredith Birsner, Renee D. Boss, Leanne Bricker, Josaphat K. Byamugisha, Giorgio Capogna, Michael P. Casaer, Frank A. Chervenak, Vicki Clark, Filip Claus, Malachy O. Columb, Charles Cox, Jean T. Cox, Vegard Dahl, John Davison, Jan Deprest, Clifford S. Deutschman, Roland Devlieger, Karim Djekidel, Steven Dymarkowski, Roshan Fernando, Clare Fitzpatrick, Sreedhar Gaddipati, Thierry Girard, Emily Gordon, Ian A. Greer, David Grooms, Sina Haeri, Katy Harrison, Edward J. Hayes, Michelle Hladunewich, Andra H. James, Tracey Johnston, Bellal Joseph, Erin Keely, Ruth Landau, Stephen E. Lapinsky, Susanna I. Lee, Larry Leeman, Hennie Lombaard, Stephen Lu, Alison MacArthur, Laura A. Magee, Paul E. Marik, Laurence B. McCullough, Alexandre Mignon, Carlo Missant, Jack Moodley, Lisa E. Moore, Kate Morse, Warwick D. Ngan Kee, Catherine Nelson-Piercy, Clemens M. Ortner, Geraldine O’Sullivan, Luis D. Pacheco, Fathima Paruk, Melina Pectasides, Nigel Pereira, Patricia Peticca, Sharon T. Phelan, Felicity Plaat, Lauren A. Plante, Michael P. Plevyak, Dianne Plews, Wendy Pollock, Laura C. Price, Peter Rhee, Leiv Arne Rosseland, Kathryn M. Rowan, Helen Ryan, Helen Scholefield, Neil S. Seligman, Nadir Sharawi, Alex Sia, Bob Silver, Mieke Soens, Ulrich J. Spreng, Silvia Stirparo, Nova Szoka, Andrew Tang, Kha M. Tran, Els Troost, Lawrence C. Tsen, Derek Tuffnell, Kristel Van Calsteren, Marc Van de Velde, Marcel Vercauteren, Chris Verslype, Peter von Dadelszen, Carl Waldman, Michelle Walters, Linda Watkins, Paul Westhead, Cynthia A. Wong, Gerda G. Zeeman, Joost J. Zwart
- Edited by Marc van de Velde, Helen Scholefield, Lauren A. Plante
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- Book:
- Maternal Critical Care
- Published online:
- 05 July 2013
- Print publication:
- 04 July 2013, pp ix-xiv
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Flexible filamentous virus structures from fiber diffraction
- Gerald Stubbs, Amy Kendall, Michele McDonald, Wen Bian, Timothy Bowles, Sarah Baumgarten, Ian McCullough, Jian Shi, Phoebe Stewart, Esther Bullitt, David Gore, Said Ghabrial
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- Journal:
- Powder Diffraction / Volume 23 / Issue 2 / June 2008
- Published online by Cambridge University Press:
- 29 February 2012, pp. 113-117
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Fiber diffraction data have been obtained from Narcissus mosaic virus, a potexvirus from the family Flexiviridae, and soybean mosaic virus (SMV), a potyvirus from the family Potyviridae. Analysis of the data in conjunction with cryo-electron microscopy data allowed us to determine the symmetry of the viruses and to make reconstructions of SMV at 19 Å resolution and of another potexvirus, papaya mosaic virus, at 18 Å resolution. These data include the first well-ordered data ever obtained for the potyviruses and the best-ordered data from the potexviruses, and offer the promise of eventual high resolution structure determinations.
Eradication of a Large Outbreak of a Single Strain of vanB Vancomycin-Resistant Enterococcus faecium at a Major Australian Teaching Hospital
- Keryn J. Christiansen, Patricia A. Tibbett, William Beresford, John W. Pearman, Rosie C. Lee, Geoffrey W. Coombs, Ian D. Kay, Frances G. O'Brien, Silvano Palladino, Charles R. Douglas, Philip D. Montgomery, Terri Orrell, Allison M. Peterson, Frank P. Kosaras, James P. Flexman, Christopher H. Heath, Cheryll A. McCullough
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 25 / Issue 5 / May 2004
- Published online by Cambridge University Press:
- 02 January 2015, pp. 384-390
- Print publication:
- May 2004
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Objective:
To demonstrate that nosocomial transmission of vancomycin-resistant enterococci (VRE) can be terminated and endemicity prevented despite widespread dissemination of an epidemic strain in a large tertiary-care referral hospital.
Interventions:Two months after the index case was detected in the intensive care unit, 68 patients became either infected or colonized with an epidemic strain of vanB vancomycin-resistant Enterococcus faecium despite standard infection control procedures. The following additional interventions were then introduced to control the outbreak: (1) formation of a VRE executive group; (2) rapid laboratory identification (30 to 48 hours) using culture and polymerase chain reaction detection of vanA and vanB resistance genes; (3) mass screening of all hospitalized patients with isolation of carriers and cohorting of contacts; (4) environmental screening and increased cleaning; (5) electronic flagging of medical records of contacts; and (6) antibiotic restrictions (third-generation cephalosporins and vancomycin).
Results:A total of 19,658 patient and 24,396 environmental swabs were processed between July and December 2001. One hundred sixty-nine patients in 23 wards were colonized with a single strain of vanB vancomycin-resistant E. faecium. Introducing additional control measures rapidly brought the outbreak under control. Hospital-wide screening found 39 previously unidentified colonized patients, with only 7 more nonsegregat-ed patients being detected in the next 2 months. The outbreak was terminated within 3 months at a cost of $2.7 million (Australian dollars).
Conclusion:Despite widespread dissemination of VRE in a large acute care facility, eradication was achievable by a well-resourced, coordinated, multifaceted approach and was in accordance with good clinical governance.