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Bertoni C, Abodi M, D’Oria V, Milani GP, Agostoni C, Mazzocchi A. Alpha-Linolenic Acid and Cardiovascular Events: A Narrative Review. Int J Mol Sci 2023; 24:14319. [PMID: 37762621 PMCID: PMC10531611 DOI: 10.3390/ijms241814319] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/01/2023] [Revised: 09/12/2023] [Accepted: 09/15/2023] [Indexed: 09/29/2023] Open
Abstract
Cardiovascular diseases (CVDs) represent the leading cause of global mortality with 1.7 million deaths a year. One of the alternative systems to drug therapy to minimize the risk of CVDs is represented by alpha-linolenic acid (ALA), an essential fatty acid of the omega-3 series, known for its cholesterol-lowering effect. The main purpose of this review is to analyze the effects of ALA and investigate the relevant omega-6/omega-3 ratio in order to maintain functionally beneficial effects. Concerning the lipid-lowering preventive effects, ALA may favorably affect the values of LDL-C and triglycerides in both adult and pediatric populations. Furthermore, ALA has shown protective effects against hypertension, contributing to balancing blood pressure through customary diet. According to the 2009 EFSA statement, dietary ALA may contribute to reducing the risk of CVDs, thanks to anti-hypertensive, anti-atherosclerotic and cardioprotective effects.
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Affiliation(s)
- Camilla Bertoni
- Department of Veterinary Sciences for Health, Animal Production and Food Safety, University of Milan, 20122 Milan, Italy; (C.B.); (M.A.)
| | - Martina Abodi
- Department of Veterinary Sciences for Health, Animal Production and Food Safety, University of Milan, 20122 Milan, Italy; (C.B.); (M.A.)
| | - Veronica D’Oria
- Pediatric Area, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (V.D.); (G.P.M.)
| | - Gregorio P. Milani
- Pediatric Area, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (V.D.); (G.P.M.)
- Department of Clinical Sciences and Community Health, University of Milan, 20122 Milan, Italy;
| | - Carlo Agostoni
- Pediatric Area, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, 20122 Milan, Italy; (V.D.); (G.P.M.)
- Department of Clinical Sciences and Community Health, University of Milan, 20122 Milan, Italy;
| | - Alessandra Mazzocchi
- Department of Clinical Sciences and Community Health, University of Milan, 20122 Milan, Italy;
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2
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Sala-Vila A, Fleming J, Kris-Etherton P, Ros E. Impact of α-Linolenic Acid, the Vegetable ω-3 Fatty Acid, on Cardiovascular Disease and Cognition. Adv Nutr 2022; 13:1584-1602. [PMID: 35170723 PMCID: PMC9526859 DOI: 10.1093/advances/nmac016] [Citation(s) in RCA: 41] [Impact Index Per Article: 13.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/07/2021] [Revised: 12/31/2021] [Accepted: 02/11/2022] [Indexed: 01/28/2023] Open
Abstract
Given the evidence of the health benefits of plant-based diets and long-chain n-3 (ω-3) fatty acids, there is keen interest in better understanding the role of α-linolenic acid (ALA), a plant-derived n-3 fatty acid, on cardiometabolic diseases and cognition. There is increasing evidence for ALA largely based on its major food sources (i.e., walnuts and flaxseed); however, this lags behind our understanding of long-chain n-3 fatty acids. Meta-analyses of observational studies have shown that increasing dietary ALA is associated with a 10% lower risk of total cardiovascular disease and a 20% reduced risk of fatal coronary heart disease. Three randomized controlled trials (RCTs) [AlphaOmega trial, Prevención con Dieta Mediterránea (PREDIMED) trial, and Lyon Diet Heart Study] all showed benefits of diets high in ALA on cardiovascular-related outcomes, but the AlphaOmega trial, designed to specifically evaluate ALA effects, only showed a trend for benefit. RCTs have shown that dietary ALA reduced total cholesterol, LDL cholesterol, triglycerides, and blood pressure, and epidemiologic studies and some trials also have shown an anti-inflammatory effect of ALA, which collectively account for, in part, the cardiovascular benefits of ALA. A meta-analysis reported a trend toward diabetes risk reduction with both dietary and biomarker ALA. For metabolic syndrome and obesity, the evidence for ALA benefits is inconclusive. The role of ALA in cognition is in the early stages but shows promising evidence of counteracting cognitive impairment. Much has been learned about the health benefits of ALA and with additional research we will be better positioned to make strong evidence-based dietary recommendations for the reduction of many chronic diseases.
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Affiliation(s)
- Aleix Sala-Vila
- Fatty Acid Research Institute, Sioux Falls, SD, USA
- Cardiovascular Risk and Nutrition, Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain
| | - Jennifer Fleming
- Department of Nutritional Sciences, College of Health and Human Development, Pennsylvania State University, University Park, PA, USA
| | - Penny Kris-Etherton
- Department of Nutritional Sciences, College of Health and Human Development, Pennsylvania State University, University Park, PA, USA
| | - Emilio Ros
- Lipid Clinic, Endocrinology and Nutrition Service, Hospital Clínic, August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain
- CIBER Physiopathology of Obesity and Nutrition (CIBEROBN), Instituto de Salud Carlos III (ISCIII), Madrid, Spain
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Javed K, Rakha A, Butt MS, Faisal MN, Tariq U, Saleem M. Evaluating the anti-arthritic potential of walnut (Juglans regia L.) in FCA induced Sprague Dawley rats. J Food Biochem 2022; 46:e14327. [PMID: 35929358 DOI: 10.1111/jfbc.14327] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2022] [Revised: 06/08/2022] [Accepted: 06/17/2022] [Indexed: 01/08/2023]
Abstract
Rheumatoid arthritis (RA) is an autoimmune progressive disease, associated with many pathophysiological consequences. Owing to the adverse effects and higher costs of pharmaceuticals, people are now looking for complementary and alternative remedies. In this milieu, the present study was designed to explore the therapeutic potential of walnuts against FCA-induced arthritis in rat models. Purposely, 50 Sprague Dawley rats were housed in a well-ventilated animal room and separated into 5 groups of 10 rats each. The rats were categorized as G0 (negative control), G1 (positive control, i.e., FCA induced untreated arthritic rats), G2 (arthritic rats treated with MTX), G3 (arthritic rats treated with walnut feed), and G4 (arthritic rats treated with walnut extract), with an efficacy trial lasting for 42 days. The physical analysis explicated that paw swelling was significantly improved by 10%-12.8% in treatment groups after the intervention when compared with positive control. Moreover, biochemical analyses revealed significantly lower levels of ESR, CRP, and RF in rats treated with walnut-based interventions when compared to positive control. ESR values were decreased by 62.4% and 69.92% in G3 and G4 , whereas CRP levels were improved by 56.20% and 77.78% in G3 and G4 when compared with G1 . Likewise, RF values decreased in G2 , G3 , and G4 by 64.71%, 55.88%, and 69.24%, respectively when compared to G1 . The histological examination demonstrated the potential role of walnut-based interventions in reducing the severity of disease by decreasing cell infiltration, bone erosion, and paw inflammation. Meanwhile, the gene expression analysis revealed that walnut-based interventions protected the paw joints from damage by downregulating the RANKL-OPG pathway. Conclusively, walnut feed and extract may serve as potent anti-arthritic interventions with no side effects. PRACTICAL APPLICATIONS: Plant-based therapeutics are effective in the prevention and management of various chronic diseases. The current research explored the anti-arthritic potential of walnuts. Walnut feed and extract effectively reduced the serum arthritic biomarkers as well as downregulated the genes involved in bone destruction. Thus, the inclusion of dietary ingredients having therapeutic potential such as walnuts may be synchronized in clinical practices to ameliorate arthritis.
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Affiliation(s)
- Komal Javed
- National Institute of Food Science and Technology, Faculty of Food Nutrition and Home Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan.,Department of Human Nutrition and Dietetics, Riphah International University Faisalabad, Faisalabad, Pakistan
| | - Allah Rakha
- National Institute of Food Science and Technology, Faculty of Food Nutrition and Home Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan
| | - Masood Sadiq Butt
- National Institute of Food Science and Technology, Faculty of Food Nutrition and Home Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan
| | - Muhammad Naeem Faisal
- Institute of Pharmacy, Physiology, and Pharmacology, Faculty of Veterinary Science, University of Agriculture Faisalabad, Faisalabad, Pakistan
| | - Urwa Tariq
- National Institute of Food Science and Technology, Faculty of Food Nutrition and Home Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan.,Department of Human Nutrition and Dietetics, Riphah International University Faisalabad, Faisalabad, Pakistan
| | - Makkia Saleem
- National Institute of Food Science and Technology, Faculty of Food Nutrition and Home Sciences, University of Agriculture Faisalabad, Faisalabad, Pakistan
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Bellien J, Bozec E, Bounoure F, Khettab H, Malloizel-Delaunay J, Skiba M, Iacob M, Donnadieu N, Coquard A, Morio B, Laillet B, Rigaudière JP, Chardigny JM, Monteil C, Vendeville C, Mercier A, Cailleux AF, Blanchard A, Amar J, Fezeu LK, Pannier B, Bura-Rivière A, Boutouyrie P, Joannidès R. The effect of camelina oil on vascular function in essential hypertensive patients with metabolic syndrome: a randomized, placebo-controlled, double-blind study. Am J Clin Nutr 2022; 115:694-704. [PMID: 34791007 DOI: 10.1093/ajcn/nqab374] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/28/2021] [Accepted: 11/10/2021] [Indexed: 11/12/2022] Open
Abstract
BACKGROUND The effects of a dietary supplementation with the vegetable ω-3 α-linolenic acid (ALA) on cardiovascular homeostasis are unclear. In this context, it would be interesting to assess the effects of camelina oil. OBJECTIVE This study aimed to assess the cardiovascular and metabolic effects of camelina oil in hypertensive patients with metabolic syndrome. METHODS In a double-blind, placebo-controlled randomized study, treated essential hypertensive patients with metabolic syndrome received, during 6 mo, either cyclodextrin-complexed camelina oil containing ≈ 1.5 g ALA/d (n = 40) or an isocaloric placebo (n = 41), consisting of the same quantity of cyclodextrins and wheat starch. Anthropometric data, plasma lipids, glycemia, insulinemia, creatininemia, TBARs, high-sensitivity C-reactive protein, and n-3, n-6, and n-9 fatty acids in erythrocyte membranes were measured. Peripheral and central blood pressures, arterial stiffness, carotid intima-media thickness, and brachial artery endothelium-dependent flow-mediated dilatation (FMD) and endothelium-independent dilatation were assessed. RESULTS Compared with placebo, camelina oil increased ALA (mean ± SD: 0 ± 0.04 compared with 0.08 ± 0.06%, P <0.001), its elongation product EPA (0 ± 0.5 compared with 0.16 ± 0.65%, P <0.05), and the n-9 gondoic acid (GA; 0 ± 0.04 compared with 0.08 ± 0.04%, P <0.001). No between-group difference was observed for cardiovascular parameters. However, changes in FMD were associated with the magnitude of changes in EPA (r = 0.26, P = 0.03). Compared with placebo, camelina oil increased fasting glycemia (-0.2 ± 0.6 compared with 0.3 ± 0.5 mmol/L, P <0.001) and HOMA-IR index (-0.8 ± 2.5 compared with 0.5 ± 0.9, P <0.01), without affecting plasma lipids, or inflammatory and oxidative stress markers. Changes in HOMA-IR index were correlated with the magnitude of changes in GA (r = 0.32, P <0.01). Nutritional intake remained similar between groups. CONCLUSION ALA supplementation with camelina oil did not improve vascular function but adversely affected glucose metabolism in hypertensive patients with metabolic syndrome. Whether this adverse effect on insulin sensitivity is related to GA enrichment, remains to be elucidated.
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Affiliation(s)
- Jeremy Bellien
- Department of Pharmacology, Rouen University Hospital, Rouen, France.,Normandie Université, Rouen Normandy University (UNIROUEN), Institut National de la Santé et de la Recherche Médicale (INSERM), Fédération Hospitalo-Universitaire CArdiac Research Network on Aortic VAlve and heart faiLure (FHU CARNAVAL), Rouen, France.,Centre d'Investigation Clinique (CIC)-INSERM 1404, Rouen University Hospital, Rouen, France
| | - Erwan Bozec
- Université de Paris, Service de Pharmacologie, INSERM U970, équipe 7, Paris, France.,Université de Lorraine, Centre d'Investigations Cliniques-Plurithématique, INSERM 1433, CHRU Nancy, Inserm DCAC, and F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France
| | - Frédéric Bounoure
- Normandie Université, UNIROUEN, INSERM U1239, Pharmacie Galénique, Rouen France
| | - Hakim Khettab
- Université de Paris, Service de Pharmacologie, INSERM U970, équipe 7, Paris, France.,Service de Pharmacologie, AP-HP, HEGP, Paris, France
| | | | - Mohamed Skiba
- Service de Pharmacologie, AP-HP, HEGP, Paris, France
| | - Michèle Iacob
- Department of Pharmacology, Rouen University Hospital, Rouen, France.,Normandie Université, Rouen Normandy University (UNIROUEN), Institut National de la Santé et de la Recherche Médicale (INSERM), Fédération Hospitalo-Universitaire CArdiac Research Network on Aortic VAlve and heart faiLure (FHU CARNAVAL), Rouen, France
| | | | - Aude Coquard
- Department of Pharmacy, Rouen University Hospital, Rouen, France
| | - Béatrice Morio
- Unité de Nutrition Humaine (UNH), Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE), Université Clermont Auvergne, CRNH Auvergne, Clermont-Ferrand, France
| | - Brigitte Laillet
- Unité de Nutrition Humaine (UNH), Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE), Université Clermont Auvergne, CRNH Auvergne, Clermont-Ferrand, France
| | - Jean-Paul Rigaudière
- Unité de Nutrition Humaine (UNH), Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE), Université Clermont Auvergne, CRNH Auvergne, Clermont-Ferrand, France
| | - Jean-Michel Chardigny
- Unité de Nutrition Humaine (UNH), Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE), Université Clermont Auvergne, CRNH Auvergne, Clermont-Ferrand, France
| | | | | | - Alain Mercier
- Department of General Practice, University of Paris 13, SMBH, Bobigny, France
| | | | - Anne Blanchard
- Centre d'Investigation Clinique INSERM CIC-1418, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Européen Georges Pompidou, Paris, France
| | - Jacques Amar
- Department of Arterial Hypertension, Toulouse University III, Toulouse, France
| | - Léopold K Fezeu
- Sorbonne Paris Nord University, INSERM U1153, INRAE U1125, CNAM, Nutritional Epidemiology Research Team (EREN), Epidemiology and Statistics Research Center-University of Paris (CRESS), Bobigny, France
| | - Bruno Pannier
- Department of Nephrology, Centre Hospitalier FH Manhès, Fleury-Mérogis, France
| | | | - Pierre Boutouyrie
- Université de Paris, Service de Pharmacologie, INSERM U970, équipe 7, Paris, France.,Service de Pharmacologie, AP-HP, HEGP, Paris, France
| | - Robinson Joannidès
- Department of Pharmacology, Rouen University Hospital, Rouen, France.,Normandie Université, Rouen Normandy University (UNIROUEN), Institut National de la Santé et de la Recherche Médicale (INSERM), Fédération Hospitalo-Universitaire CArdiac Research Network on Aortic VAlve and heart faiLure (FHU CARNAVAL), Rouen, France.,Centre d'Investigation Clinique (CIC)-INSERM 1404, Rouen University Hospital, Rouen, France
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Ajabnoor SM, Thorpe G, Abdelhamid A, Hooper L. Long-term effects of increasing omega-3, omega-6 and total polyunsaturated fats on inflammatory bowel disease and markers of inflammation: a systematic review and meta-analysis of randomized controlled trials. Eur J Nutr 2021; 60:2293-2316. [PMID: 33084958 DOI: 10.1007/s00394-020-02413-y] [Citation(s) in RCA: 43] [Impact Index Per Article: 10.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2020] [Accepted: 10/06/2020] [Indexed: 02/06/2023]
Abstract
BACKGROUND AND AIM Effects of long-chain omega-3 (LCn3) and omega-6 fatty acids on prevention and treatment of inflammatory bowel diseases (IBD, including Crohn's Disease, CD and ulcerative colitis, UC), and inflammation are unclear. We systematically reviewed long-term effects of omega-3, omega-6 and total polyunsaturated fats (PUFA) on IBD diagnosis, relapse, severity, pharmacotherapy, quality of life and key inflammatory markers. METHODS We searched Medline, Embase, Cochrane CENTRAL, and trials registries, including RCTs in adults with or without IBD comparing higher with lower omega-3, omega-6 and/or total PUFA intake for ≥ 24 weeks that assessed IBD-specific outcomes or inflammatory biomarkers. RESULTS We included 83 RCTs (41,751 participants), of which 13 recruited participants with IBD. Increasing LCn3 may reduce risk of IBD relapse (RR 0.85, 95% CI 0.72-1.01) and IBD worsening (RR 0.85, 95% CI 0.71-1.03), and reduce erythrocyte sedimentation rate (ESR, SMD - 0.23, 95% CI - 0.44 to - 0.01), but may increase IBD diagnosis risk (RR 1.10, 95% CI 0.63-1.92), and faecal calprotectin, a specific inflammatory marker for IBD (MD 16.1 μg/g, 95% CI - 37.6 to 69.8, all low-quality evidence). Outcomes for alpha-linolenic acid, omega-6 and total PUFA were sparse, but suggested little or no effect where data were available. CONCLUSION This is the most comprehensive meta-analysis of RCTs investigating long-term effects of omega-3, omega-6 and total PUFA on IBD and inflammatory markers. Our findings suggest that supplementation with PUFAs has little or no effect on prevention or treatment of IBD and provides little support for modification of long-term inflammatory status.
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Affiliation(s)
- Sarah M Ajabnoor
- Norwich Medical School, University of East Anglia, Norwich, UK.
- Clinical Nutrition Department, Faculty of Applied Medical Sciences, King Abdulaziz University, P.O. Box 80324, Jeddah, 21589, Saudi Arabia.
| | - Gabrielle Thorpe
- School of Health Sciences, University of East Anglia, Norwich, UK
| | | | - Lee Hooper
- Norwich Medical School, University of East Anglia, Norwich, UK
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Mazzocchi A, De Cosmi V, Risé P, Milani GP, Turolo S, Syrén ML, Sala A, Agostoni C. Bioactive Compounds in Edible Oils and Their Role in Oxidative Stress and Inflammation. Front Physiol 2021; 12:659551. [PMID: 33995124 PMCID: PMC8119658 DOI: 10.3389/fphys.2021.659551] [Citation(s) in RCA: 25] [Impact Index Per Article: 6.3] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2021] [Accepted: 04/12/2021] [Indexed: 12/13/2022] Open
Abstract
Diet and inflammatory response are recognized as strictly related, and interest in exploring the potential of edible fats and oils for health and chronic diseases is emerging worldwide. Polyunsaturated fatty acids (PUFAs) present in fish oil (FO), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may be partly converted into oxygenated bioactive lipids with anti-inflammatory and/or pro-resolving activities. Moreover, the co-presence of phenolic compounds and vitamins in edible oils may prevent the development of chronic diseases by their anti-inflammatory, antioxidant, neuroprotective, and immunomodulatory activities. Finally, a high content in mono-unsaturated fatty acids may improve the serum lipid profile and decrease the alterations caused by the oxidized low-density lipoproteins and free radicals. The present review aims to highlight the role of lipids and other bioactive compounds contained in edible oils on oxidative stress and inflammation, focusing on critical and controversial issues that recently emerged, and pointing to the opposing role often played by edible oils components and their oxidized metabolites.
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Affiliation(s)
- Alessandra Mazzocchi
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
| | - Valentina De Cosmi
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.,Pediatric Intermediate Care Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
| | - Patrizia Risé
- Department of Pharmaceutical Sciences, University of Milan, Milan, Italy
| | - Gregorio Paolo Milani
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.,Pediatric Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
| | - Stefano Turolo
- Pediatric Nephrology, Dialysis and Transplant Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
| | - Marie-Louise Syrén
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
| | - Angelo Sala
- Department of Pharmaceutical Sciences, University of Milan, Milan, Italy.,Istituto per la Ricerca e l'Innovazione Biomedica (IRIB), Consiglio Nazionale delle Ricerche (CNR), Palermo, Italy
| | - Carlo Agostoni
- Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.,Pediatric Intermediate Care Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
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van Vliet S, Kronberg SL, Provenza FD. Plant-Based Meats, Human Health, and Climate Change. FRONTIERS IN SUSTAINABLE FOOD SYSTEMS 2020. [DOI: 10.3389/fsufs.2020.00128] [Citation(s) in RCA: 39] [Impact Index Per Article: 7.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022] Open
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Chen CG, Wang P, Zhang ZQ, Ye YB, Zhuo SY, Zhou Q, Chen YM, Su YX, Zhang B. Effects of plant oils with different fatty acid composition on cardiovascular risk factors in moderately hypercholesteremic Chinese adults: a randomized, double-blinded, parallel-designed trial. Food Funct 2020; 11:7164-7174. [PMID: 32756661 DOI: 10.1039/d0fo00875c] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]
Abstract
OBJECTIVES Plant oil for cooking typically provides 40% to 50% of dietary fat, 65% of linoleic acid, 44% of α-linolenic acid and 41% of oleic acid in the Chinese diet. However, the comparative effects of fatty acids derived from plant oil on cardiovascular risk factors in Chinese are still inconclusive. Hence, the aim of this study is to investigate whether cardiovascular risk factors are altered depending on various types of plant oils such as peanut oil rich in oleic acid, corn oil rich in linoleic acid, and blend oil fortified by α-linolenic acid. DESIGN A randomized, double-blinded, parallel-designed trial. SETTING The First and the Second Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. PARTICIPANTS A total of 251 volunteers with fasting blood total cholesterol between 5.13 and 8.00 mmol L-1 were enrolled. INTERVENTION Volunteers received peanut oil, corn oil or blend oil to use for cooking for one year. MAIN OUTCOME MEASURES The erythrocyte membrane fatty acid composition, fasting plasma lipids, glucose and insulin concentrations and high sensitivity C-reactive protein (hsCRP) levels were measured before, during and after the intervention. The level of α-linolenic acid in erythrocyte membranes was significantly increased in the blend oil group after the intervention (P < 0.001). The level of other fatty acids did not show any statistically significant differences between the three groups. No significant differences were observed in the concentrations of fasting plasma lipids, hsCRP, glucose, and insulin among the three groups using different types of plant oils. CONCLUSIONS The results suggest that although ingesting cooking oil with different fatty acid composition for one year could change erythrocyte membrane fatty acid compositions, it did not significantly modify cardiovascular risk factors in moderately hypercholesteremic people.
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Affiliation(s)
- Chao-Gang Chen
- Department of Clinical Nutrition, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510012, P. R. China
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Abdelhamid AS, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KHO, Summerbell CD, Worthington HV, Song F, Hooper L. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2020; 3:CD003177. [PMID: 32114706 PMCID: PMC7049091 DOI: 10.1002/14651858.cd003177.pub5] [Citation(s) in RCA: 120] [Impact Index Per Article: 24.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
BACKGROUND Omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3)), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) may benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. OBJECTIVES To assess the effects of increased intake of fish- and plant-based omega-3 fats for all-cause mortality, cardiovascular events, adiposity and lipids. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to February 2019, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to August 2019, with no language restrictions. We handsearched systematic review references and bibliographies and contacted trial authors. SELECTION CRITERIA We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation or advice to increase LCn3 or ALA intake, or both, versus usual or lower intake. DATA COLLECTION AND ANALYSIS Two review authors independently assessed trials for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. MAIN RESULTS We included 86 RCTs (162,796 participants) in this review update and found that 28 were at low summary risk of bias. Trials were of 12 to 88 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most trials assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet. LCn3 doses ranged from 0.5 g a day to more than 5 g a day (19 RCTs gave at least 3 g LCn3 daily). Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (risk ratio (RR) 0.97, 95% confidence interval (CI) 0.93 to 1.01; 143,693 participants; 11,297 deaths in 45 RCTs; high-certainty evidence), cardiovascular mortality (RR 0.92, 95% CI 0.86 to 0.99; 117,837 participants; 5658 deaths in 29 RCTs; moderate-certainty evidence), cardiovascular events (RR 0.96, 95% CI 0.92 to 1.01; 140,482 participants; 17,619 people experienced events in 43 RCTs; high-certainty evidence), stroke (RR 1.02, 95% CI 0.94 to 1.12; 138,888 participants; 2850 strokes in 31 RCTs; moderate-certainty evidence) or arrhythmia (RR 0.99, 95% CI 0.92 to 1.06; 77,990 participants; 4586 people experienced arrhythmia in 30 RCTs; low-certainty evidence). Increasing LCn3 may slightly reduce coronary heart disease mortality (number needed to treat for an additional beneficial outcome (NNTB) 334, RR 0.90, 95% CI 0.81 to 1.00; 127,378 participants; 3598 coronary heart disease deaths in 24 RCTs, low-certainty evidence) and coronary heart disease events (NNTB 167, RR 0.91, 95% CI 0.85 to 0.97; 134,116 participants; 8791 people experienced coronary heart disease events in 32 RCTs, low-certainty evidence). Overall, effects did not differ by trial duration or LCn3 dose in pre-planned subgrouping or meta-regression. There is little evidence of effects of eating fish. Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20; 19,327 participants; 459 deaths in 5 RCTs, moderate-certainty evidence),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25; 18,619 participants; 219 cardiovascular deaths in 4 RCTs; moderate-certainty evidence), coronary heart disease mortality (RR 0.95, 95% CI 0.72 to 1.26; 18,353 participants; 193 coronary heart disease deaths in 3 RCTs; moderate-certainty evidence) and coronary heart disease events (RR 1.00, 95% CI 0.82 to 1.22; 19,061 participants; 397 coronary heart disease events in 4 RCTs; low-certainty evidence). However, increased ALA may slightly reduce risk of cardiovascular disease events (NNTB 500, RR 0.95, 95% CI 0.83 to 1.07; but RR 0.91, 95% CI 0.79 to 1.04 in RCTs at low summary risk of bias; 19,327 participants; 884 cardiovascular disease events in 5 RCTs; low-certainty evidence), and probably slightly reduces risk of arrhythmia (NNTB 91, RR 0.73, 95% CI 0.55 to 0.97; 4912 participants; 173 events in 2 RCTs; moderate-certainty evidence). Effects on stroke are unclear. Increasing LCn3 and ALA had little or no effect on serious adverse events, adiposity, lipids and blood pressure, except increasing LCn3 reduced triglycerides by ˜15% in a dose-dependent way (high-certainty evidence). AUTHORS' CONCLUSIONS This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and low-certainty evidence suggests that increasing LCn3 slightly reduces risk of coronary heart disease mortality and events, and reduces serum triglycerides (evidence mainly from supplement trials). Increasing ALA slightly reduces risk of cardiovascular events and arrhythmia.
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Affiliation(s)
- Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Priti Biswas
- University of East AngliaMED/HSCNorwich Research ParkNorwichUKNR4 7TJ
| | - Gabrielle C Thorpe
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Helen J Moore
- Teesside UniversitySchool of Social Sciences, Humanities and LawMiddlesboroughUKTS1 3BA
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Carolyn D Summerbell
- Durham UniversityDepartment of Sport and Exercise Sciences42 Old ElvetDurhamUKDH13HN
| | - Helen V Worthington
- Division of Dentistry, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of ManchesterCochrane Oral HealthCoupland Building 3Oxford RoadManchesterUKM13 9PL
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
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Muscle protein breakdown is impaired during immobilization compared to during a subsequent retraining period in older men: no effect of anti-inflammatory medication. Pflugers Arch 2020; 472:281-292. [PMID: 32025814 PMCID: PMC7035225 DOI: 10.1007/s00424-020-02353-w] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/20/2019] [Revised: 12/29/2019] [Accepted: 01/26/2020] [Indexed: 12/25/2022]
Abstract
Muscle inactivity reduces muscle protein synthesis (MPS), whereas a subsequent period of rehabilitation resistance training (retraining) increases MPS. However, less is known regarding muscle protein breakdown (MPB) during such conditions. Furthermore, nonsteroidal anti-inflammatory drugs (NSAIDs) may have a dampening effect on MPB during periods of inactivity in older individuals. Thus, we measured the average MPB, by use of the deuterated water methodology, during an immobilization period and a subsequent retraining period in older individuals with and without NSAID treatment. Eighteen men (60–80 years: range) were randomly assigned to ibuprofen (1200 mg/d, Ibu) or placebo (Plc). One lower limb was immobilized in a cast for 2 weeks and retrained for 2 weeks, and 2 × 20 g of whey protein was ingested daily during both periods. Besides MPB, the protein expression of different muscle degradation signaling molecules was investigated. MPB was lower during immobilization compared to retraining (p < 0.01). NSAID treatment did not affect the MPB rate during immobilization or retraining (p > 0.05). The protein expression of muscle degradation signaling molecules changed during the study intervention but were unaffected by NSAID treatment. The finding that MPB was lower during immobilization than during retraining indicates that an increased MPB may play an important role in the muscle protein remodeling processes taking place within the initial retraining period. Moreover, NSAID treatment did not significantly influence the MPB rate during 2 weeks of lower limb immobilization or during 2 weeks of subsequent retraining in older individuals.
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Burak C, Wolffram S, Zur B, Langguth P, Fimmers R, Alteheld B, Stehle P, Egert S. Effect of alpha-linolenic acid in combination with the flavonol quercetin on markers of cardiovascular disease risk in healthy, non-obese adults: A randomized, double-blinded placebo-controlled crossover trial. Nutrition 2019; 58:47-56. [DOI: 10.1016/j.nut.2018.06.012] [Citation(s) in RCA: 25] [Impact Index Per Article: 4.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/29/2017] [Revised: 06/27/2018] [Accepted: 06/29/2018] [Indexed: 12/29/2022]
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Abdelhamid AS, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KHO, AlAbdulghafoor FK, Summerbell CD, Worthington HV, Song F, Hooper L. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 11:CD003177. [PMID: 30521670 PMCID: PMC6517311 DOI: 10.1002/14651858.cd003177.pub4] [Citation(s) in RCA: 95] [Impact Index Per Article: 13.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
BACKGROUND Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. OBJECTIVES To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors. SELECTION CRITERIA We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake. DATA COLLECTION AND ANALYSIS Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. MAIN RESULTS We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet. LCn3 doses ranged from 0.5g/d LCn3 to > 5 g/d (16 RCTs gave at least 3g/d LCn3).Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted.Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs) and ALA may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence with greater effects in trials at low summary risk of bias), and probably reduces risk of arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear.Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression.There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, except LCn3 reduced triglycerides by ˜15% in a dose-dependant way (high-quality evidence). AUTHORS' CONCLUSIONS This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event and arrhythmia risk.
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Affiliation(s)
- Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Priti Biswas
- University of East AngliaMED/HSCNorwich Research ParkNorwichUKNR4 7TJ
| | - Gabrielle C Thorpe
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Helen J Moore
- Durham UniversityWolfson Research InstituteDurhamUKDH1 3LE
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Fai K AlAbdulghafoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Carolyn D Summerbell
- Durham UniversityDepartment of Sport and Exercise Science42 Old ElvetDurhamUKDH13HN
| | - Helen V Worthington
- Division of Dentistry, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of ManchesterCochrane Oral HealthJR Moore BuildingOxford RoadManchesterUKM13 9PL
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
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Hooper L, Al‐Khudairy L, Abdelhamid AS, Rees K, Brainard JS, Brown TJ, Ajabnoor SM, O'Brien AT, Winstanley LE, Donaldson DH, Song F, Deane KHO. Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 11:CD011094. [PMID: 30488422 PMCID: PMC6516799 DOI: 10.1002/14651858.cd011094.pub4] [Citation(s) in RCA: 31] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/03/2023]
Abstract
BACKGROUND Omega-6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated. OBJECTIVES To assess effects of increasing omega-6 fats (linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all-cause mortality. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. SELECTION CRITERIA We included randomised controlled trials (RCTs) comparing higher versus lower omega-6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, abstracts, trials registry entries and unpublished studies. Outcomes were all-cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega-6 fat effects from those of other dietary, lifestyle or medication interventions. DATA COLLECTION AND ANALYSIS Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta-analyses used random-effects analysis, while sensitivity analyses used fixed-effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables. MAIN RESULTS We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega-6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.Primary outcomes: we found low-quality evidence that increased intake of omega-6 fats may make little or no difference to all-cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega-6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose-response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega-6 intake across outcomes.Additional key outcomes: we found increased intake of omega-6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low-quality evidence). High-quality evidence suggests increasing omega-6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) -0.33 mmol/L, 95% CI -0.50 to -0.16, I2 = 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega-6 fats probably has little or no effect on adiposity (body mass index (BMI) MD -0.20 kg/m2, 95% CI -0.56 to 0.16, 371 participants, 1 trial, moderate-quality evidence). It may make little or no difference to serum triglycerides (MD -0.01 mmol/L, 95% CI -0.23 to 0.21, 834 participants, 5 trials), HDL (MD -0.01 mmol/L, 95% CI -0.03 to 0.02, 1995 participants, 4 trials) or low-density lipoprotein (MD -0.04 mmol/L, 95% CI -0.21 to 0.14, 244 participants, 2 trials, low-quality evidence). AUTHORS' CONCLUSIONS This is the most extensive systematic assessment of effects of omega-6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega-6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega-6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega-6 fats remain to be proven, increasing omega-6 fats may be of benefit in people at high risk of MI. Increased omega-6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.
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Affiliation(s)
- Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Lena Al‐Khudairy
- Warwick Medical School, University of WarwickDivision of Health SciencesCoventryUKCV4 7AL
| | - Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Karen Rees
- Warwick Medical School, University of WarwickDivision of Health SciencesCoventryUKCV4 7AL
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Sarah M Ajabnoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Alex T O'Brien
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Lauren E Winstanley
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Daisy H Donaldson
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesColney LaneNorwichUKNR4 7UL
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Abdelhamid AS, Martin N, Bridges C, Brainard JS, Wang X, Brown TJ, Hanson S, Jimoh OF, Ajabnoor SM, Deane KHO, Song F, Hooper L. Polyunsaturated fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 11:CD012345. [PMID: 30484282 PMCID: PMC6517012 DOI: 10.1002/14651858.cd012345.pub3] [Citation(s) in RCA: 35] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/19/2022]
Abstract
BACKGROUND Evidence on the health effects of total polyunsaturated fatty acids (PUFA) is equivocal. Fish oils are rich in omega-3 PUFA and plant oils in omega-6 PUFA. Evidence suggests that increasing PUFA-rich foods, supplements or supplemented foods can reduce serum cholesterol, but may increase body weight, so overall cardiovascular effects are unclear. OBJECTIVES To assess effects of increasing total PUFA intake on cardiovascular disease and all-cause mortality, lipids and adiposity in adults. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to April 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. SELECTION CRITERIA We included randomised controlled trials (RCTs) comparing higher with lower PUFA intakes in adults with or without cardiovascular disease that assessed effects over 12 months or longer. We included full texts, abstracts, trials registry entries and unpublished data. Outcomes were all-cause mortality, cardiovascular disease mortality and events, risk factors (blood lipids, adiposity, blood pressure), and adverse events. We excluded trials where we could not separate effects of PUFA intake from other dietary, lifestyle or medication interventions. DATA COLLECTION AND ANALYSIS Two review authors independently screened titles and abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias. We wrote to authors of included trials for further data. Meta-analyses used random-effects analysis, sensitivity analyses included fixed-effects and limiting to low summary risk of bias. We assessed GRADE quality of evidence. MAIN RESULTS We included 49 RCTs randomising 24,272 participants, with duration of one to eight years. Eleven included trials were at low summary risk of bias, 33 recruited participants without cardiovascular disease. Baseline PUFA intake was unclear in most trials, but 3.9% to 8% of total energy intake where reported. Most trials gave supplemental capsules, but eight gave dietary advice, eight gave supplemental foods such as nuts or margarine, and three used a combination of methods to increase PUFA.Increasing PUFA intake probably has little or no effect on all-cause mortality (risk 7.8% vs 7.6%, risk ratio (RR) 0.98, 95% confidence interval (CI) 0.89 to 1.07, 19,290 participants in 24 trials), but probably slightly reduces risk of coronary heart disease events from 14.2% to 12.3% (RR 0.87, 95% CI 0.72 to 1.06, 15 trials, 10,076 participants) and cardiovascular disease events from 14.6% to 13.0% (RR 0.89, 95% CI 0.79 to 1.01, 17,799 participants in 21 trials), all moderate-quality evidence. Increasing PUFA may slightly reduce risk of coronary heart disease death (6.6% to 6.1%, RR 0.91, 95% CI 0.78 to 1.06, 9 trials, 8810 participants) andstroke (1.2% to 1.1%, RR 0.91, 95% CI 0.58 to 1.44, 11 trials, 14,742 participants, though confidence intervals include important harms), but has little or no effect on cardiovascular mortality (RR 1.02, 95% CI 0.82 to 1.26, 16 trials, 15,107 participants) all low-quality evidence. Effects of increasing PUFA on major adverse cardiac and cerebrovascular events and atrial fibrillation are unclear as evidence is of very low quality.Increasing PUFA intake probably slightly decreases triglycerides (by 15%, MD -0.12 mmol/L, 95% CI -0.20 to -0.04, 20 trials, 3905 participants), but has little or no effect on total cholesterol (mean difference (MD) -0.12 mmol/L, 95% CI -0.23 to -0.02, 26 trials, 8072 participants), high-density lipoprotein (HDL) (MD -0.01 mmol/L, 95% CI -0.02 to 0.01, 18 trials, 4674 participants) or low-density lipoprotein (LDL) (MD -0.01 mmol/L, 95% CI -0.09 to 0.06, 15 trials, 3362 participants). Increasing PUFA probably has little or no effect on adiposity (body weight MD 0.76 kg, 95% CI 0.34 to 1.19, 12 trials, 7100 participants).Effects of increasing PUFA on serious adverse events such as pulmonary embolism and bleeding are unclear as the evidence is of very low quality. AUTHORS' CONCLUSIONS This is the most extensive systematic review of RCTs conducted to date to assess effects of increasing PUFA on cardiovascular disease, mortality, lipids or adiposity. Increasing PUFA intake probably slightly reduces risk of coronary heart disease and cardiovascular disease events, may slightly reduce risk of coronary heart disease mortality and stroke (though not ruling out harms), but has little or no effect on all-cause or cardiovascular disease mortality. The mechanism may be via TG reduction.
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Affiliation(s)
- Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Nicole Martin
- University College LondonInstitute of Health Informatics Research222 Euston RoadLondonUKNW1 2DA
| | - Charlene Bridges
- University College LondonInstitute of Health Informatics Research222 Euston RoadLondonUKNW1 2DA
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Xia Wang
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Sarah Hanson
- University of East AngliaSchool of Health SciencesEdith Cavell BuildingNorwichUKNR4 7TJ
| | - Oluseyi F Jimoh
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Sarah M Ajabnoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesEdith Cavell BuildingNorwichUKNR4 7TJ
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
| | - Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichNorfolkUKNR4 7TJ
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15
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DiNicolantonio JJ, O'Keefe JH. Importance of maintaining a low omega-6/omega-3 ratio for reducing inflammation. Open Heart 2018; 5:e000946. [PMID: 30564378 PMCID: PMC6269634 DOI: 10.1136/openhrt-2018-000946] [Citation(s) in RCA: 87] [Impact Index Per Article: 12.4] [Reference Citation Analysis] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 11/15/2018] [Indexed: 01/11/2023] Open
Affiliation(s)
| | - James H O'Keefe
- Saint Luke's Mid America Heart Institute, Kansas, Missouri, USA
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DiNicolantonio JJ, O'Keefe JH. Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis. Open Heart 2018; 5:e000898. [PMID: 30364556 PMCID: PMC6196963 DOI: 10.1136/openhrt-2018-000898] [Citation(s) in RCA: 48] [Impact Index Per Article: 6.9] [Reference Citation Analysis] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 08/22/2018] [Indexed: 12/31/2022] Open
Affiliation(s)
- James J DiNicolantonio
- Department of Preventive Cardiology, Saint Luke's Mid America Heart Institute, Kansas City, Missouri, USA
| | - James H O'Keefe
- Department of Preventive Cardiology, Saint Luke's Mid America Heart Institute, Kansas City, Missouri, USA
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Abdelhamid AS, Martin N, Bridges C, Brainard JS, Wang X, Brown TJ, Hanson S, Jimoh OF, Ajabnoor SM, Deane KHO, Song F, Hooper L. Polyunsaturated fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 7:CD012345. [PMID: 30019767 PMCID: PMC6513571 DOI: 10.1002/14651858.cd012345.pub2] [Citation(s) in RCA: 49] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
BACKGROUND Evidence on the health effects of total polyunsaturated fatty acids (PUFA) is equivocal. Fish oils are rich in omega-3 PUFA and plant oils in omega-6 PUFA. Evidence suggests that increasing PUFA-rich foods, supplements or supplemented foods can reduce serum cholesterol, but may increase body weight, so overall cardiovascular effects are unclear. OBJECTIVES To assess effects of increasing total PUFA intake on cardiovascular disease and all-cause mortality, lipids and adiposity in adults. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to April 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. SELECTION CRITERIA We included randomised controlled trials (RCTs) comparing higher with lower PUFA intakes in adults with or without cardiovascular disease that assessed effects over 12 months or longer. We included full texts, abstracts, trials registry entries and unpublished data. Outcomes were all-cause mortality, cardiovascular disease mortality and events, risk factors (blood lipids, adiposity, blood pressure), and adverse events. We excluded trials where we could not separate effects of PUFA intake from other dietary, lifestyle or medication interventions. DATA COLLECTION AND ANALYSIS Two review authors independently screened titles and abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias. We wrote to authors of included trials for further data. Meta-analyses used random-effects analysis, sensitivity analyses included fixed-effects and limiting to low summary risk of bias. We assessed GRADE quality of evidence. MAIN RESULTS We included 49 RCTs randomising 24,272 participants, with duration of one to eight years. Eleven included trials were at low summary risk of bias, 33 recruited participants without cardiovascular disease. Baseline PUFA intake was unclear in most trials, but 3.9% to 8% of total energy intake where reported. Most trials gave supplemental capsules, but eight gave dietary advice, eight gave supplemental foods such as nuts or margarine, and three used a combination of methods to increase PUFA.Increasing PUFA intake probably has little or no effect on all-cause mortality (risk 7.8% vs 7.6%, risk ratio (RR) 0.98, 95% confidence interval (CI) 0.89 to 1.07, 19,290 participants in 24 trials), but probably slightly reduces risk of coronary heart disease events from 14.2% to 12.3% (RR 0.87, 95% CI 0.72 to 1.06, 15 trials, 10,076 participants) and cardiovascular disease events from 14.6% to 13.0% (RR 0.89, 95% CI 0.79 to 1.01, 17,799 participants in 21 trials), all moderate-quality evidence. Increasing PUFA may slightly reduce risk of coronary heart disease death (6.6% to 6.1%, RR 0.91, 95% CI 0.78 to 1.06, 9 trials, 8810 participants) andstroke (1.2% to 1.1%, RR 0.91, 95% CI 0.58 to 1.44, 11 trials, 14,742 participants, though confidence intervals include important harms), but has little or no effect on cardiovascular mortality (RR 1.02, 95% CI 0.82 to 1.26, 16 trials, 15,107 participants) all low-quality evidence. Effects of increasing PUFA on major adverse cardiac and cerebrovascular events and atrial fibrillation are unclear as evidence is of very low quality.Increasing PUFA intake slightly reduces total cholesterol (mean difference (MD) -0.12 mmol/L, 95% CI -0.23 to -0.02, 26 trials, 8072 participants) and probably slightly decreases triglycerides (MD -0.12 mmol/L, 95% CI -0.20 to -0.04, 20 trials, 3905 participants), but has little or no effect on high-density lipoprotein (HDL) (MD -0.01 mmol/L, 95% CI -0.02 to 0.01, 18 trials, 4674 participants) or low-density lipoprotein (LDL) (MD -0.01 mmol/L, 95% CI -0.09 to 0.06, 15 trials, 3362 participants). Increasing PUFA probably causes slight weight gain (MD 0.76 kg, 95% CI 0.34 to 1.19, 12 trials, 7100 participants).Effects of increasing PUFA on serious adverse events such as pulmonary embolism and bleeding are unclear as the evidence is of very low quality. AUTHORS' CONCLUSIONS This is the most extensive systematic review of RCTs conducted to date to assess effects of increasing PUFA on cardiovascular disease, mortality, lipids or adiposity. Increasing PUFA intake probably slightly reduces risk of coronary heart disease and cardiovascular disease events, may slightly reduce risk of coronary heart disease mortality and stroke (though not ruling out harms), but has little or no effect on all-cause or cardiovascular disease mortality. The mechanism may be via lipid reduction, but increasing PUFA probably slightly increases weight.
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Affiliation(s)
- Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Nicole Martin
- University College LondonFarr Institute of Health Informatics Research222 Euston RoadLondonUKNW1 2DA
| | - Charlene Bridges
- University College LondonFarr Institute of Health Informatics Research222 Euston RoadLondonUKNW1 2DA
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Xia Wang
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Sarah Hanson
- University of East AngliaSchool of Health SciencesEdith Cavell BuildingNorwichUKNR4 7TJ
| | - Oluseyi F Jimoh
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Sarah M Ajabnoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesEdith Cavell BuildingNorwichUKNR4 7TJ
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
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Abdelhamid AS, Brown TJ, Brainard JS, Biswas P, Thorpe GC, Moore HJ, Deane KHO, AlAbdulghafoor FK, Summerbell CD, Worthington HV, Song F, Hooper L. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 7:CD003177. [PMID: 30019766 PMCID: PMC6513557 DOI: 10.1002/14651858.cd003177.pub3] [Citation(s) in RCA: 122] [Impact Index Per Article: 17.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
BACKGROUND Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. OBJECTIVES To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors. SELECTION CRITERIA We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake. DATA COLLECTION AND ANALYSIS Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. MAIN RESULTS We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted.Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear.Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression.There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence). AUTHORS' CONCLUSIONS This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.
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Affiliation(s)
- Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Priti Biswas
- University of East AngliaMED/HSCNorwich Research ParkNorwichUKNR4 7TJ
| | - Gabrielle C Thorpe
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Helen J Moore
- Durham UniversityWolfson Research InstituteDurhamUKDH1 3LE
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesEarlham RoadNorwichUKNR4 7TJ
| | - Fai K AlAbdulghafoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Carolyn D Summerbell
- Durham UniversityDepartment of Sport and Exercise Science42 Old ElvetDurhamUKDH13HN
| | - Helen V Worthington
- Division of Dentistry, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of ManchesterCochrane Oral HealthJR Moore BuildingOxford RoadManchesterUKM13 9PL
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
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Hooper L, Al‐Khudairy L, Abdelhamid AS, Rees K, Brainard JS, Brown TJ, Ajabnoor SM, O'Brien AT, Winstanley LE, Donaldson DH, Song F, Deane KHO. Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev 2018; 7:CD011094. [PMID: 30019765 PMCID: PMC6513455 DOI: 10.1002/14651858.cd011094.pub3] [Citation(s) in RCA: 41] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/01/2023]
Abstract
BACKGROUND Omega-6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated. OBJECTIVES To assess effects of increasing omega-6 fats (linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all-cause mortality. SEARCH METHODS We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. SELECTION CRITERIA We included randomised controlled trials (RCTs) comparing higher versus lower omega-6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, abstracts, trials registry entries and unpublished studies. Outcomes were all-cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega-6 fat effects from those of other dietary, lifestyle or medication interventions. DATA COLLECTION AND ANALYSIS Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta-analyses used random-effects analysis, while sensitivity analyses used fixed-effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables. MAIN RESULTS We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega-6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.Primary outcomes: we found low-quality evidence that increased intake of omega-6 fats may make little or no difference to all-cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega-6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose-response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega-6 intake across outcomes.Additional key outcomes: we found increased intake of omega-6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low-quality evidence). High-quality evidence suggests increasing omega-6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) -0.33 mmol/L, 95% CI -0.50 to -0.16, I2 = 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega-6 fats probably has little or no effect on adiposity (body mass index (BMI) MD -0.20 kg/m2, 95% CI -0.56 to 0.16, 371 participants, 1 trial, moderate-quality evidence). It may make little or no difference to serum triglycerides (MD -0.01 mmol/L, 95% CI -0.23 to 0.21, 834 participants, 5 trials), HDL (MD -0.01 mmol/L, 95% CI -0.03 to 0.02, 1995 participants, 4 trials) or low-density lipoprotein (MD -0.04 mmol/L, 95% CI -0.21 to 0.14, 244 participants, 2 trials, low-quality evidence). AUTHORS' CONCLUSIONS This is the most extensive systematic assessment of effects of omega-6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega-6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega-6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega-6 fats remain to be proven, increasing omega-6 fats may be of benefit in people at high risk of MI. Increased omega-6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.
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Affiliation(s)
- Lee Hooper
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Lena Al‐Khudairy
- Warwick Medical School, University of WarwickDivision of Health SciencesCoventryUKCV4 7AL
| | - Asmaa S Abdelhamid
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Karen Rees
- Warwick Medical School, University of WarwickDivision of Health SciencesCoventryUKCV4 7AL
| | - Julii S Brainard
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Tracey J Brown
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Sarah M Ajabnoor
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Alex T O'Brien
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Lauren E Winstanley
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Daisy H Donaldson
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Fujian Song
- University of East AngliaNorwich Medical SchoolNorwich Research ParkNorwichUKNR4 7TJ
| | - Katherine HO Deane
- University of East AngliaSchool of Health SciencesColney LaneNorwichUKNR4 7UL
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Tiwari-Heckler S, Gan-Schreier H, Stremmel W, Chamulitrat W, Pathil A. Circulating Phospholipid Patterns in NAFLD Patients Associated with a Combination of Metabolic Risk Factors. Nutrients 2018; 10:nu10050649. [PMID: 29883377 PMCID: PMC5986528 DOI: 10.3390/nu10050649] [Citation(s) in RCA: 63] [Impact Index Per Article: 9.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/10/2018] [Revised: 05/11/2018] [Accepted: 05/15/2018] [Indexed: 12/13/2022] Open
Abstract
Background: Non-alcoholic fatty liver disease (NAFLD) is associated with inefficient macro- and micronutrient metabolism, and alteration of circulating phospholipid compositions defines the signature of NAFLD. This current study aimed to assess the pattern of serum phospholipids in the spectrum of NAFLD, and its related comorbidities and genetic modifications. Methods: 97 patients with diagnosed NAFLD were recruited at a single center during 2013–2016. Based on histological and transient elastography assessment, 69 patients were divided into non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver (NAFL) subgroups. 28 patients served as healthy controls. Serum phospholipids were determined by liquid-chromatography mass spectrometry (LC-MS/MS). Results: The total content of phosphatidylcholine (PC) and sphingomyelin in the serum was significantly increased in NAFL and NASH patients, compared to healthy controls. In addition, serum lysophospatidylethanolamine levels were significantly decreased in NAFL and NASH individuals. Circulating PC species, containing linoleic and α-linolenic acids, were markedly increased in NAFLD patients with hypertension, compared to NAFLD patients without hypertension. The pattern of phospholipids did not differ between NAFLD patients with diabetes and those without diabetes. However, NAFLD patients with hyperglycemia (blood glucose level (BGL) >100 mg/dL) exhibited significantly a higher amount of monounsaturated phosphatidylethanolamine than those with low blood glucose levels. In addition, NAFLD patients with proven GG-genotype of PNPLA3, who were at higher risk for the development of progressive disease with fibrosis, showed lower levels of circulating plasmalogens, especially 16:0, compared to those with CC- and CG-allele. Conclusions: Our extended lipidomic study presents a unique metabolic profile of circulating phospholipids associated with the presence of metabolic risk factors or the genetic background of NAFLD patients.
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Affiliation(s)
- Shilpa Tiwari-Heckler
- Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
| | - Hongying Gan-Schreier
- Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
| | - Wolfgang Stremmel
- Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
| | - Walee Chamulitrat
- Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
| | - Anita Pathil
- Department of Internal Medicine IV, Gastroenterology and Hepatology, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany.
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de Oliveira PA, Kovacs C, Moreira P, Magnoni D, Saleh MH, Faintuch J. Unsaturated Fatty Acids Improve Atherosclerosis Markers in Obese and Overweight Non-diabetic Elderly Patients. Obes Surg 2018; 27:2663-2671. [PMID: 28470492 DOI: 10.1007/s11695-017-2704-8] [Citation(s) in RCA: 33] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/21/2023]
Abstract
BACKGROUND Several studies have demonstrated the benefits of replacing trans and saturated fats with unsaturated fatty acids on cardiovascular diseases. We aimed to demonstrate the effect of polyunsaturated and monounsaturated fat supplementation on the biochemical and endothelial markers of atherosclerotic disease in obese or overweight non-diabetic elderly patients. METHOD Seventy-nine patients were randomly divided into three groups: flaxseed oil, olive oil, and sunflower oil; patients in each group received 30 mL of oil for 90 days. Patients were subjected to anthropometric and bioimpedance assessments; biochemical and endothelial evaluations were performed through ultrasonography of the brachial artery and carotid artery for endothelium-dependent dilation and intima-media thickness assessment, respectively, before and after the intervention. The participants' usual diet remained unchanged. RESULTS The flaxseed oil group had improved ultra-sensitive C-reactive protein levels (p = 0.074) and reduced carotid intima-media thickness (CIMT) (p = 0.028); the olive oil group exhibited an improved apolipoprotein (Apo)B/ApoA ratio (p = 0.021), reduced CIMT (p = 0.028), and improved flow-mediated vasodilation (FMV) (p = 0.054); and similarly, the sunflower oil group showed an improved ApoB/ApoA ratio (p = 0.024), reduced CIMT (p = 0.048), and improved FMV (p = 0.001). CONCLUSION Unsaturated fatty acid supplementation using the three vegetable oils attenuated pro-inflammatory properties and improved prothrombotic conditions. Therefore, introducing or replacing saturated and trans fat with unsaturated fatty acids is beneficial for cardiovascular risk reduction in obese or overweight non-diabetic elderly people. Further studies are needed to determine which unsaturated fat best prevents cardiovascular disease in elderly patients.
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Affiliation(s)
- Patrícia Amante de Oliveira
- Department of Gastroenterology, Hospital das Clínicas, São Paulo, 05403-900, Brazil. .,, Rua Abílio Soares, 250 - 3° andar - Paraíso, São Paulo, CEP: 04005-909, Brazil. .,Dante Pazzanese Institute of Cardiology, São Paulo, 04012-909, Brazil.
| | - Cristiane Kovacs
- Dante Pazzanese Institute of Cardiology, São Paulo, 04012-909, Brazil
| | - Priscila Moreira
- Dante Pazzanese Institute of Cardiology, São Paulo, 04012-909, Brazil
| | - Daniel Magnoni
- Dante Pazzanese Institute of Cardiology, São Paulo, 04012-909, Brazil
| | | | - Joel Faintuch
- Department of Gastroenterology, Hospital das Clínicas, São Paulo, 05403-900, Brazil
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Steffen BT, Guan W, Stein JH, Tattersall MC, Kaufman JD, Sandfort V, Szklo M, Tsai MY. Plasma n-3 and n-6 Fatty Acids Are Differentially Related to Carotid Plaque and Its Progression: The Multi-Ethnic Study of Atherosclerosis. Arterioscler Thromb Vasc Biol 2018; 38:653-659. [PMID: 29326315 PMCID: PMC5823763 DOI: 10.1161/atvbaha.117.310366] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/11/2017] [Accepted: 01/02/2018] [Indexed: 01/09/2023]
Abstract
OBJECTIVE ω-3 (n-3) fatty acids (FAs) have long been considered healthful dietary components, yet recent clinical trials have questioned their cardiovascular benefits. By contrast, the ω-6 (n-6) FAs have been considered harmful, proatherogenic macronutrients, despite an absence of empirical evidence supporting this hypothesis. We aimed to determine whether plasma n-3 and n-6 FAs are related to risk of carotid plaque and its progression in 3327 participants of MESA (Multi-Ethnic Study of Atherosclerosis). APPROACH AND RESULTS Carotid plaque was assessed using ultrasonography at baseline and after a median period of 9.5 years. Plasma phospholipid n-3 and n-6 FAs were determined using gas chromatography-flame ionization detection. Relative risk regression analyses assessed the relations of FAs with the presence or progression of carotid plaque adjusted for typical cardiovascular disease risk factors. At baseline, it was found that participants in the fourth quartile of n-3 docosahexaenoic acid showed a 9% lower risk of carotid plaque (P=0.05), whereas those in the second quartile of n-3 α-linolenic acid showed an 11% greater risk compared with respective referent quartiles (P=0.02). In prospective analyses, individuals in the top quartile of docosahexaenoic acid showed a 12% lower risk of carotid plaque progression during 9.5 years compared with those in the referent quartile (P=0.002). No significant relations were observed among n-6 FAs and plaque outcomes. No significant race/ethnicity interactions were found. CONCLUSIONS These findings support docosahexaenoic acid as an atheroprotective macronutrient, whereas null findings for n-6 FAs challenge the view that they promote atherosclerosis.
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Affiliation(s)
- Brian T Steffen
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Weihua Guan
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - James H Stein
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Mathew C Tattersall
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Joel D Kaufman
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Veit Sandfort
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Moyses Szklo
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.)
| | - Michael Y Tsai
- From the Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (B.T.S., M.Y.T.); Division of Biostatistics, University of Minnesota School of Public Health, Minneapolis (W.G.); Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison (J.H.S., M.C.T.); Department of Epidemiology, School of Public Health, University of Washington, Seattle (J.D.K.); Department of Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, MD (V.S.); and Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (M.S.).
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Haghighatdoost F, Nobakht M. Gh BF. Effect of conjugated linoleic acid on blood inflammatory markers: a systematic review and meta-analysis on randomized controlled trials. Eur J Clin Nutr 2017; 72:1071-1082. [DOI: 10.1038/s41430-017-0048-z] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/14/2017] [Revised: 10/10/2017] [Accepted: 11/06/2017] [Indexed: 01/05/2023]
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Effect of dietary alpha-linolenic acid on blood inflammatory markers: a systematic review and meta-analysis of randomized controlled trials. Eur J Nutr 2017; 57:877-891. [DOI: 10.1007/s00394-017-1386-2] [Citation(s) in RCA: 28] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2016] [Accepted: 01/24/2017] [Indexed: 12/14/2022]
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Lacasse MC, Tang A, Dubois J, Alvarez F, Spahis S, Chagnon M, Deschênes S, Levy E. Monitoring the efficacy of omega-3 supplementation on liver steatosis and carotid intima-media thickness: a pilot study. Obes Sci Pract 2017; 3:201-211. [PMID: 28702213 PMCID: PMC5478813 DOI: 10.1002/osp4.91] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2016] [Revised: 11/13/2016] [Accepted: 11/16/2016] [Indexed: 12/12/2022] Open
Abstract
Purpose To determine the effects of omega‐3 supplementation on liver fat and carotid intima–media thickness (IMT) and to assess accuracy of ultrasound (US) for grading liver steatosis. Materials and Methods In this one‐way crossover pilot study, we assigned children with obesity and liver steatosis to receive 1.2 g daily of omega‐3 supplementation vs. inactive sunflower oil for 24 or 12 weeks. Liver fat content was assessed by magnetic resonance spectroscopy (MRS), magnetic resonance imaging (MRI) and US, and common carotid IMT by US. Statistical analysis included Chi‐square, Student's t‐tests, ANOVA tests and receiver operating characteristic (ROC) curves. Results Omega‐3 supplementation was associated with a trend towards decrease in MRS‐determined liver fat fraction (0.7% and 2.1% decrease in the 24‐week and 12‐week omega‐3 group, respectively) compared with the sunflower oil group (1.0% increase). These changes were not significant, whether assessed by MRS (P = 0.508), MRI (P = 0.508) or US (P = 0.678). Using US, the area under the ROC curves were 0.964, 0.817 and 0.783 for distinguishing inferred steatosis grades 0 vs. 1–2–3, 0–1 vs. 2–3 and 0–1–2 vs. 3, respectively, indicating good accuracy of US‐based fat grading. Omega‐3 supplementation was associated with a decrease in US‐determined IMT (0.05‐mm decrease in the 24‐week omega‐3 group. A 0.015‐mm increase was found in the 12‐week omega‐3 group, and a 0.007‐mm decrease in the sunflower oil group (P = 0.003). Conclusion Omega‐3 supplementation had no significant effect on liver fat fraction, but led to carotid IMT decrease in children with obesity and liver steatosis.
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Affiliation(s)
- M-C Lacasse
- Department of Radiology Centre Hospitalier de l'Université de Montréal (CHUM) Montréa Québec Canada
| | - A Tang
- Department of Radiology Centre Hospitalier de l'Université de Montréal (CHUM) Montréa Québec Canada.,Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM) Montréal Québec Canada
| | - J Dubois
- Department of Radiology Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Centre de Recherche du Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada
| | - F Alvarez
- Centre de Recherche du Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Department of Gastroenterology, Hepatology and NutritionCentre Hospitalier Universitaire Ste-Justine Montréal Québec Canada
| | - S Spahis
- Centre de Recherche du Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Department of Gastroenterology, Hepatology and NutritionCentre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Department of Nutrition Université de Montréal Québec Canada
| | - M Chagnon
- Department of Mathematics and Statistics, Pavillon André-Aisenstadt Université de Montréal Montréal Québec Canada
| | - S Deschênes
- Department of Radiology Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Centre de Recherche du Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada
| | - E Levy
- Centre de Recherche du Centre Hospitalier Universitaire Ste-Justine Montréal Québec Canada.,Department of Gastroenterology, Hepatology and NutritionCentre Hospitalier Universitaire Ste-Justine Montréal Québec Canada
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26
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Best practices for design and implementation of human clinical trials studying dietary oils. Prog Lipid Res 2017; 65:1-11. [DOI: 10.1016/j.plipres.2016.10.003] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/03/2016] [Accepted: 10/24/2016] [Indexed: 12/19/2022]
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Baker EJ, Miles EA, Burdge GC, Yaqoob P, Calder PC. Metabolism and functional effects of plant-derived omega-3 fatty acids in humans. Prog Lipid Res 2016; 64:30-56. [DOI: 10.1016/j.plipres.2016.07.002] [Citation(s) in RCA: 224] [Impact Index Per Article: 24.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2016] [Revised: 07/28/2016] [Accepted: 07/29/2016] [Indexed: 12/17/2022]
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Metaflammatory responses during obesity: Pathomechanism and treatment. Obes Res Clin Pract 2015; 10:103-13. [PMID: 26614484 DOI: 10.1016/j.orcp.2015.10.012] [Citation(s) in RCA: 29] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/25/2015] [Revised: 10/07/2015] [Accepted: 10/30/2015] [Indexed: 12/11/2022]
Abstract
Obesity induced inflammation acts as a reflex produced due to altered metabolic homeostasis in accordance to the nutrient overload on the metabolic cells. It involves up-regulation of the genes encoding for cytokines, chemokines and other inflammatory mediators through activated transcription factors - nuclear factor-kB, activator protein-1, nuclear factor of activated T cells and signal transducer and activator of transcription 3. These execute macromolecular innate immune cell sensor - inflammasome to activate caspase-1 pathway resulting in proteolytic maturation. Secretion of pro-inflammatory cytokines including TNF-α, IL-6, CRP, IL-1β, etc. from the M1 macrophages of white adipose tissue is increased, whereas there occurs a steep decline in the production of anti-inflammatory cytokines like IL-10, IL-Ra, adiponectin. Not only the adipose tissue, but also the immune cells, liver, brain, muscles and pancreas suffers from the inflammatory insult during obese condition and are exaggeratedly affected. The inflammatory kinases like JNK and IKK apart from inhibiting insulin action and glucose uptake, down-regulate transcriptional process resulting in increased expression of pro-inflammatory cytokines. Macrophage-like Kupffer cells initiate the inflammatory process in the liver preceding the inflammatory signals produced by the white adipose tissue which may further lead to hepatic-necro-inflammation. The muscle-fibre is affected by the cytokines and therefore results in decreased glycogen synthesis. The triggered hypothalamic-pituitary-adrenal axis further affects the expression of inflammatory cytokines thus altering insulin homeostasis and initiating glucose intolerance. Anti-inflammatory treatment so as to curb the severity of inflammatory responses includes administration of synthetic drugs to target the actual inflammatory molecules and various therapeutic interventions.
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Al-Khudairy L, Hartley L, Clar C, Flowers N, Hooper L, Rees K. Omega 6 fatty acids for the primary prevention of cardiovascular disease. Cochrane Database Syst Rev 2015:CD011094. [PMID: 26571451 DOI: 10.1002/14651858.cd011094.pub2] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/22/2022]
Abstract
BACKGROUND Omega 6 plays a vital role in many physiological functions but there is controversy concerning its effect on cardiovascular disease (CVD) risk. There is conflicting evidence whether increasing or decreasing omega 6 intake results in beneficial effects. OBJECTIVES The two primary objectives of this Cochrane review were to determine the effectiveness of:1. Increasing omega 6 (Linoleic acid (LA), Gamma-linolenic acid (GLA), Dihomo-gamma-linolenic acid (DGLA), Arachidonic acid (AA), or any combination) intake in place of saturated or monounsaturated fats or carbohydrates for the primary prevention of CVD.2. Decreasing omega 6 (LA, GLA, DGLA, AA, or any combination) intake in place of carbohydrates or protein (or both) for the primary prevention of CVD. SEARCH METHODS We searched the following electronic databases up to 23 September 2014: the Cochrane Central Register of Controlled Trials (CENTRAL) on the Cochrane Library (Issue 8 of 12, 2014); MEDLINE (Ovid) (1946 to September week 2, 2014); EMBASE Classic and EMBASE (Ovid) (1947 to September 2014); Web of Science Core Collection (Thomson Reuters) (1990 to September 2014); Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment Database, and Health Economics Evaluations Database on the Cochrane Library (Issue 3 of 4, 2014). We searched trial registers and reference lists of reviews for further studies. We applied no language restrictions. SELECTION CRITERIA Randomised controlled trials (RCTs) of interventions stating an intention to increase or decrease omega 6 fatty acids, lasting at least six months, and including healthy adults or adults at high risk of CVD. The comparison group was given no advice, no supplementation, a placebo, a control diet, or continued with their usual diet. The outcomes of interest were CVD clinical events (all-cause mortality, cardiovascular mortality, non-fatal end points) and CVD risk factors (changes in blood pressure, changes in blood lipids, occurrence of type 2 diabetes). We excluded trials involving exercise or multifactorial interventions to avoid confounding. DATA COLLECTION AND ANALYSIS Two review authors independently selected trials for inclusion, extracted the data, and assessed the risk of bias in the included trials. MAIN RESULTS We included four RCTs (five papers) that randomised 660 participants. No ongoing trials were identified. All included trials had at least one domain with an unclear risk of bias. There were no RCTs of omega 6 intake reporting CVD clinical events. Three trials investigated the effect of increased omega 6 intake on lipid levels (total cholesterol, low density lipoprotein (LDL-cholesterol), and high density lipoprotein (HDL-cholesterol)), two trials reported triglycerides, and two trials reported blood pressure (diastolic and systolic blood pressure). Two trials, one with two relevant intervention arms, investigated the effect of decreased omega 6 intake on blood pressure parameters and lipid levels (total cholesterol, LDL-cholesterol, and HDL-cholesterol) and one trial reported triglycerides. Our analyses found no statistically significant effects of either increased or decreased omega 6 intake on CVD risk factors.Two studies were supported by funding from the UK Food Standards Agency and Medical Research Council. One study was supported by Lipid Nutrition, a commercial company in the Netherlands and the Dutch Ministry of Economic Affairs. The final study was supported by grants from the Finnish Food Research Foundation, Finnish Heart Research Foundation, Aarne and Aili Turnen Foundation, and the Research Council for Health, Academy of Finland. AUTHORS' CONCLUSIONS We found no studies examining the effects of either increased or decreased omega 6 on our primary outcome CVD clinical endpoints and insufficient evidence to show an effect of increased or decreased omega 6 intake on CVD risk factors such as blood lipids and blood pressure. Very few trials were identified with a relatively small number of participants randomised. There is a need for larger well conducted RCTs assessing cardiovascular events as well as cardiovascular risk factors.
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Affiliation(s)
- Lena Al-Khudairy
- Division of Health Sciences, Warwick Medical School, University of Warwick, Coventry, UK, CV4 7AL
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Probst Y, Zammit G. Predictors for Reporting of Dietary Assessment Methods in Food-based Randomized Controlled Trials over a Ten-year Period. Crit Rev Food Sci Nutr 2015. [DOI: 10.1080/10408398.2013.816653] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/23/2022]
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Should the pharmacological actions of dietary fatty acids in cardiometabolic disorders be classified based on biological or chemical function? Prog Lipid Res 2015. [PMID: 26205317 DOI: 10.1016/j.plipres.2015.07.002] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
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No positive influence of ingesting chia seed oil on human running performance. Nutrients 2015; 7:3666-76. [PMID: 25988762 PMCID: PMC4446772 DOI: 10.3390/nu7053666] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/03/2015] [Revised: 04/29/2015] [Accepted: 05/12/2015] [Indexed: 11/17/2022] Open
Abstract
Runners (n = 24) reported to the laboratory in an overnight fasted state at 8:00 am on two occasions separated by at least two weeks. After providing a blood sample at 8:00 am, subjects ingested 0.5 liters flavored water alone or 0.5 liters water with 7 kcal kg−1 chia seed oil (random order), provided another blood sample at 8:30 am, and then started running to exhaustion (~70% VO2max). Additional blood samples were collected immediately post- and 1-h post-exercise. Despite elevations in plasma alpha-linolenic acid (ALA) during the chia seed oil (337%) versus water trial (35%) (70.8 ± 8.6, 20.3 ± 1.8 μg mL−1, respectively, p < 0.001), run time to exhaustion did not differ between trials (1.86 ± 0.10, 1.91 ± 0.13 h, p = 0.577, respectively). No trial differences were found for respiratory exchange ratio (RER) (0.92 ± 0.01), oxygen consumption, ventilation, ratings of perceived exertion (RPE), and plasma glucose and blood lactate. Significant post-run increases were measured for total leukocyte counts, plasma cortisol, and plasma cytokines (Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-10 (IL-10), and Tumor necrosis factors-α (TNF-α)), with no trial differences. Chia seed oil supplementation compared to water alone in overnight fasted runners before and during prolonged, intensive running caused an elevation in plasma ALA, but did not enhance run time to exhaustion, alter RER, or counter elevations in cortisol and inflammatory outcome measures.
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Fleming JA, Kris-Etherton PM. The evidence for α-linolenic acid and cardiovascular disease benefits: Comparisons with eicosapentaenoic acid and docosahexaenoic acid. Adv Nutr 2014; 5:863S-76S. [PMID: 25398754 PMCID: PMC4224228 DOI: 10.3945/an.114.005850] [Citation(s) in RCA: 67] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022] Open
Abstract
Our understanding of the cardiovascular disease (CVD) benefits of α-linolenic acid (ALA, 18:3n-3) has advanced markedly during the past decade. It is now evident that ALA benefits CVD risk. The expansion of the ALA evidence base has occurred in parallel with ongoing research on eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) and CVD. The available evidence enables comparisons to be made for ALA vs. EPA + DHA for CVD risk reduction. The epidemiologic evidence suggests comparable benefits of plant-based and marine-derived n-3 (omega-3) PUFAs. The clinical trial evidence for ALA is not as extensive; however, there have been CVD event benefits reported. Those that have been reported for EPA + DHA are stronger because only EPA + DHA differed between the treatment and control groups, whereas in the ALA studies there were diet differences beyond ALA between the treatment and control groups. Despite this, the evidence suggests many comparable CVD benefits of ALA vs. EPA + DHA. Thus, we believe that it is time to revisit what the contemporary dietary recommendation should be for ALA to decrease the risk of CVD. Our perspective is that increasing dietary ALA will decrease CVD risk; however, randomized controlled clinical trials are necessary to confirm this and to determine what the recommendation should be. With a stronger evidence base, the nutrition community will be better positioned to revise the dietary recommendation for ALA for CVD risk reduction.
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Monteiro J, Leslie M, Moghadasian MH, Arendt BM, Allard JP, Ma DWL. The role of n - 6 and n - 3 polyunsaturated fatty acids in the manifestation of the metabolic syndrome in cardiovascular disease and non-alcoholic fatty liver disease. Food Funct 2014; 5:426-35. [PMID: 24496399 DOI: 10.1039/c3fo60551e] [Citation(s) in RCA: 60] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]
Abstract
Cardiovascular disease (CVD) and non-alcoholic fatty liver disease (NAFLD) are manifestations of the metabolic syndrome. CVD remains the number one cause of mortality in the West, while NAFLD is the most common liver disease. Growing evidence suggests that polyunsaturated fatty acids (PUFA) influence risk factors including circulating lipids and inflammation on the development of CVD and NAFLD. N - 6 and n - 3 PUFA are comprised of distinct family members, which are increasingly recognized for their individual effects. Therefore, this review examines what is currently known about the specific effects of the major n - 3 and n - 6 PUFA on CVD and NAFLD. Overall, this review supports a beneficial effect of n - 3 PUFA and highlights distinctive effects between alpha-linolenic acid found in plant oils relative to marine derived eicosapentaenoic acid and docosahexaenoic acid. This review also highlights contrasting health effects between the n - 6 PUFA, linoleic and arachidonic acid.
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Affiliation(s)
- Jessica Monteiro
- Department of Human Health and Nutritional Sciences, College of Biological Science, 491 Gordon Street, University of Guelph, Animal Science/Nutrition Building, Room 342, Guelph, Ontario N1G 2W1, Canada.
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Khan SA, Ali A, Khan SA, Zahran SA, Damanhouri G, Azhar E, Qadri I. Unraveling the complex relationship triad between lipids, obesity, and inflammation. Mediators Inflamm 2014; 2014:502749. [PMID: 25258478 PMCID: PMC4166426 DOI: 10.1155/2014/502749] [Citation(s) in RCA: 38] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/22/2014] [Revised: 06/21/2014] [Accepted: 07/05/2014] [Indexed: 01/14/2023] Open
Abstract
Obesity today stands at the intersection between inflammation and metabolic disorders causing an aberration of immune activity, and resulting in increased risk for diabetes, atherosclerosis, fatty liver, and pulmonary inflammation to name a few. Increases in mortality and morbidity in obesity related inflammation have initiated studies to explore different lipid mediated molecular pathways of attempting resolution that uncover newer therapeutic opportunities of anti-inflammatory components. Majorly the thromboxanes, prostaglandins, leukotrienes, lipoxins, and so forth form the group of lipid mediators influencing inflammation. Of special mention are the omega-6 and omega-3 fatty acids that regulate inflammatory mediators of interest in hepatocytes and adipocytes via the cyclooxygenase and lipoxygenase pathways. They also exhibit profound effects on eicosanoid production. The inflammatory cyclooxygenase pathway arising from arachidonic acid is a critical step in the progression of inflammatory responses. New oxygenated products of omega-3 metabolism, namely, resolvins and protectins, behave as endogenous mediators exhibiting powerful anti-inflammatory and immune-regulatory actions via the peroxisome proliferator-activated receptors (PPARs) and G protein coupled receptors (GPCRs). In this review we attempt to discuss the complex pathways and links between obesity and inflammation particularly in relation to different lipid mediators.
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Affiliation(s)
- Shahida A. Khan
- Department of Applied Nutrition, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
| | - Ashraf Ali
- Department of Medical Biotechnology, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
| | - Sarah A. Khan
- National Brain Research Center, Manesar, Gurgaon District, Haryana 122 051, India
| | - Solafa A. Zahran
- Department of Applied Nutrition, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
| | - Ghazi Damanhouri
- King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
| | - Esam Azhar
- Special Infectious Agents Unit, Biosafety Level 3, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
- Medical Laboratory Technology Department, Faculty of Applied Medical Sciences, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
| | - Ishtiaq Qadri
- Department of Medical Biotechnology, King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589, Saudi Arabia
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Petersen KS, Clifton PM, Keogh JB. The association between carotid intima media thickness and individual dietary components and patterns. Nutr Metab Cardiovasc Dis 2014; 24:495-502. [PMID: 24374005 DOI: 10.1016/j.numecd.2013.10.024] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/05/2013] [Revised: 10/14/2013] [Accepted: 10/16/2013] [Indexed: 12/13/2022]
Abstract
AIMS To review: 1) the correlation between individual dietary components and carotid intima media thickness (cIMT); 2) the relationship between dietary patterns and cIMT; 3) the effect of dietary interventions on cIMT progression. DATA SYNTHESIS An electronic search for epidemiological and intervention trials investigating the association between dietary components or patterns of intake and cIMT was performed in PUBMED, EMBASE and the Cochrane Library. Epidemiological data shows that a higher intake of fruit, wholegrains and soluble fibre and lower consumption of saturated fat in favour of polyunsaturated fat is associated with lower cIMT. In people at high risk of cardiovascular disease >93 g/day of fruit is associated with lower cIMT. Lower cIMT has also been observed when >0.79 serves/day of wholegrains and >25 g/day of fibre, predominately in the soluble form is consumed. Saturated fat is positively associated with cIMT, for every 10 g/day increase in saturated fat cIMT is 0.03 mm greater. Olive oil is inversely associated with cIMT, with a benefit seen when >34 g/day is consumed. While there are many epidemiological studies exploring the association between dietary intake and cIMT there are few intervention studies. Intervention studies show that a Mediterranean diet may reduce cIMT progression, especially in those with a higher cIMT. CONCLUSIONS A Mediterranean style dietary pattern, which is high in fruits, wholegrains, fibre and olive oil and low in saturated fat, may reduce carotid atherosclerosis development and progression. However further research from randomised controlled trials is required to understand the association between diet and cIMT and the underlying mechanisms.
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Affiliation(s)
- K S Petersen
- School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, GPO Box 2471, Adelaide, SA 5000, Australia
| | - P M Clifton
- School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, GPO Box 2471, Adelaide, SA 5000, Australia
| | - J B Keogh
- School of Pharmacy and Medical Sciences, Division of Health Sciences, University of South Australia, GPO Box 2471, Adelaide, SA 5000, Australia.
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Chiva-Blanch G, Estruch R. Circulating immune cell activation and diet: A review on human trials. World J Immunol 2014; 4:12-19. [DOI: 10.5411/wji.v4.i1.12] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/21/2013] [Revised: 12/05/2013] [Accepted: 02/18/2014] [Indexed: 02/05/2023] Open
Abstract
Protein energy malnutrition is the main cause of immunodeficiency and, secondarily, of several infections. However, immune cell activation is involved in several pathophysiological processes that play a crucial role in the appearance of cardiovascular disease (CVD) or cancer. The aim of this review is to update the knowledge of the modulation of immune cell activation by different dietary patterns and its components focusing on CVD or cancer. While a westernized high-saturated fat high-carbohydrate diet is positively associated with low-grade inflammation, vegetable- and fruit-based diets rich in monounsaturated fatty acids, polyunsaturated fatty acids and polyphenols, key nutrients of Mediterranean diet, decrease the levels of cellular and circulating inflammatory biomarkers thereby reducing the risk of related chronic diseases.
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Mayengbam S, Yang H, Barthet V, Aliani M, House JD. Identification, characterization, and quantification of an anti-pyridoxine factor from flaxseed using ultrahigh-performance liquid chromatography-mass spectrometry. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY 2014; 62:419-426. [PMID: 24354394 DOI: 10.1021/jf404786v] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 06/03/2023]
Abstract
In the present study, the anti-pyridoxine compounds linatine (1-[(n-γ-L-glutamyl)amino]-D-proline) and 1-amino-D-proline (1ADP) were quantified following extraction from defatted flaxseed using aqueous isopropanol as a solvent, with extraction variables including time, temperature, and the solid/solvent ratio. Both linatine and 1ADP were identified, characterized, and quantified via UPLC/ESI-MS using authentic standards. To optimize the extraction conditions for these anti-pyridoxine compounds, a response surface methodology was applied using a second-order polynomial to describe the experimental data. The predicted model for the optimal extraction was significant (P < 0.05) with a R(2) of 0.82. A varietal analysis showed that the amount of anti-pyridoxine present in flaxseed ranged from 177 to 437 μg 1ADPE/g of whole seed. The current study establishes the content of specific anti-pyridoxine factors in flaxseed and positions the data for use in subsequent risk assessment modeling.
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Affiliation(s)
- Shyamchand Mayengbam
- Department of Human Nutritional Sciences, ‡Richardson Centre for Functional Foods and Nutraceuticals, and #Department of Animal Science, University of Manitoba , Winnipeg, Manitoba R3T 2N2, Canada
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Fares H, Lavie CJ, DiNicolantonio JJ, O’Keefe JH, Milani RV. Omega-3 Fatty Acids: A Growing Ocean of Choices. Curr Atheroscler Rep 2014; 16:389. [DOI: 10.1007/s11883-013-0389-6] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
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Dai XW, Zhang B, Wang P, Chen CG, Chen YM, Su YX. Erythrocyte membrane n-3 fatty acid levels and carotid atherosclerosis in Chinese men and women. Atherosclerosis 2014; 232:79-85. [DOI: 10.1016/j.atherosclerosis.2013.10.028] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/24/2013] [Revised: 10/17/2013] [Accepted: 10/24/2013] [Indexed: 10/26/2022]
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Mauritia flexuosa Presents In Vitro and In Vivo Antiplatelet and Antithrombotic Activities. EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE 2013; 2013:653257. [PMID: 24454503 PMCID: PMC3878763 DOI: 10.1155/2013/653257] [Citation(s) in RCA: 11] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 04/30/2013] [Revised: 11/04/2013] [Accepted: 11/04/2013] [Indexed: 12/28/2022]
Abstract
Fruit from the palm Mauritia flexuosa is one of the most important species in Peru, Venezuela, Brazil, Colombia, Bolivia, and Guyana. The present study aimed to investigate the antiplatelet and antithrombotic activities of oil extracted from Mauritia flexuosa. The fatty acid contents were determined by gas chromatography—mass spectrometry. Oil extract of peel of Mauritia flexuosa was extracted by soxhlet extraction. The oil extract inhibited platelet secretion and aggregation induced by ADP, collagen, and TRAP-6 by a concentration-dependent way (0.1 to 1 mg/mL) without the participation of the adenylyl cyclase pathway and diminished platelet rolling and firm adhesion under flow conditions. Furthermore, the oil extract induced a marked increase in the rolling speed of leukocytes retained on the platelet surface, reflecting a reduction of rolling and less adhesion. At the concentrations used, the oil extract significantly decreased platelet release of sP-selectin, an atherosclerotic-related inflammatory mediator. Oil extract inhibited thrombus growth at the same concentration as that of aspirin, a classical reference drug. Finally, the data presented herein also demonstrate for the first time to our knowledge the protective effect of oil extracted from Mauritia flexuosa on platelet activation and thrombosis formation.
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Supplementation with n-3 polyunsaturated fatty acids to lipopolysaccharide-induced rats improved inflammation and functional properties of renal Na,K-ATPase. Nutr Res 2013; 33:772-9. [DOI: 10.1016/j.nutres.2013.06.001] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/06/2012] [Revised: 06/05/2013] [Accepted: 06/13/2013] [Indexed: 11/17/2022]
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Bloedon LT, Balikai S, Chittams J, Cunnane SC, Berlin JA, Rader DJ, Szapary PO. Flaxseed and Cardiovascular Risk Factors: Results from a Double Blind, Randomized, Controlled Clinical Trial. J Am Coll Nutr 2013; 27:65-74. [DOI: 10.1080/07315724.2008.10719676] [Citation(s) in RCA: 134] [Impact Index Per Article: 11.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/26/2022]
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Almario RU, Karakas SE. Lignan Content of the Flaxseed Influences Its Biological Effects in Healthy Men and Women. J Am Coll Nutr 2013; 32:194-9. [DOI: 10.1080/07315724.2013.791147] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/26/2022]
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Rodríguez-Hernández H, Simental-Mendía LE, Rodríguez-Ramírez G, Reyes-Romero MA. Obesity and inflammation: epidemiology, risk factors, and markers of inflammation. Int J Endocrinol 2013; 2013:678159. [PMID: 23690772 PMCID: PMC3652163 DOI: 10.1155/2013/678159] [Citation(s) in RCA: 275] [Impact Index Per Article: 22.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/14/2013] [Accepted: 03/27/2013] [Indexed: 12/23/2022] Open
Abstract
Obesity is a public health problem that has reached epidemic proportions with an increasing worldwide prevalence. The global emergence of obesity increases the risk of developing chronic metabolic disorders. Thus, it is an economic issue that increased the costs of the comorbidities associated. Moreover, in recent years, it has been demonstrated that obesity is associated with chronic systemic inflammation, this status is conditioned by the innate immune system activation in adipose tissue that promotes an increase in the production and release of pro-inflammatory cytokines that contribute to the triggering of the systemic acute-phase response which is characterized by elevation of acute-phase protein levels. On this regard, low-grade chronic inflammation is a characteristic of various chronic diseases such as metabolic syndrome, cardiovascular disease, diabetes, hypertension, non-alcoholic fatty liver disease, and some cancers, among others, which are also characterized by obesity condition. Thus, a growing body of evidence supports the important role that is played by the inflammatory response in obesity condition and the pathogenesis of chronic diseases related.
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Affiliation(s)
- Heriberto Rodríguez-Hernández
- Biomedical Research Unit of the Mexican Social Security Institute at Durango, Predio Canoas 100, Los Angeles, 34067 Durango, DGO, Mexico
- Faculty of Medicine and Nutrition, Juárez University of Durango State, Av. Universidad and Fanny Anitúa s/n, Zona Centro, 34000 Durango, DGO, Mexico
| | - Luis E. Simental-Mendía
- Biomedical Research Unit of the Mexican Social Security Institute at Durango, Predio Canoas 100, Los Angeles, 34067 Durango, DGO, Mexico
- *Luis E. Simental-Mendía:
| | - Gabriela Rodríguez-Ramírez
- Biomedical Research Unit of the Mexican Social Security Institute at Durango, Predio Canoas 100, Los Angeles, 34067 Durango, DGO, Mexico
| | - Miguel A. Reyes-Romero
- Faculty of Medicine and Nutrition, Juárez University of Durango State, Av. Universidad and Fanny Anitúa s/n, Zona Centro, 34000 Durango, DGO, Mexico
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Substitution of TAG oil with diacylglycerol oil in food items improves the predicted 10 years cardiovascular risk score in healthy, overweight subjects. J Nutr Sci 2012; 1:e17. [PMID: 25191546 PMCID: PMC4153080 DOI: 10.1017/jns.2012.18] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/23/2012] [Revised: 08/24/2012] [Accepted: 09/04/2012] [Indexed: 01/07/2023] Open
Abstract
Dietary fat is normally in TAG form, but diacylglycerol (DAG) is a natural component of
edible oils. Studies have shown that consumption of DAG results in metabolic
characteristics that are distinct from those of TAG, which may be beneficial in preventing
and managing obesity. The objective of the present study was to investigate if food items
in which part of the TAG oil is replaced with DAG oil combined with high α-linolenic acid
(ALA) content would influence metabolic markers. A 12-week double-blinded randomised
controlled parallel-design study was conducted. The participants (n 23)
were healthy, overweight men and women, aged 37–67 years, BMI 27–35 kg/m2, with
waist circumference >94 cm (men) and >88 cm (women). The two groups received
20 g margarine, 11 g mayonnaise and 12 g oil per d, containing either high ALA and
sn-1,3-DAG or high ALA and TAG. Substitution of TAG oil with DAG oil in
food items for 12 weeks led to an improvement of the predicted 10 years cardiovascular
risk score in overweight subjects by non-significantly improving markers of health such as
total body fat percentage, trunk fat mass, alanine aminotransferase, systolic blood
pressure, γ-glutamyl transferase, alkaline phosphatase and total fat-free mass. This may
suggest that replacing TAG oil with DAG oil in healthy, overweight individuals may have
beneficial metabolic effects.
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Key Words
- ALA, α-linolenic acid
- ALAT, alanine aminotransferase
- ALP, alkaline phosphatase
- ASAT, aspartame aminotransferase
- CRP, C-reactive protein
- DAG, diacylglycerol
- Diacylglycerol
- FFM, fat-free mass
- HOMA-IR, homeostatic model assessment for insulin resistance
- Liver markers
- Overweight human subjects
- TAG
- hsCRP, high-sensitivity CRP
- γ-GT, γ-glutamyl transferase
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Chiang YL, Haddad E, Rajaram S, Shavlik D, Sabaté J. The effect of dietary walnuts compared to fatty fish on eicosanoids, cytokines, soluble endothelial adhesion molecules and lymphocyte subsets: a randomized, controlled crossover trial. Prostaglandins Leukot Essent Fatty Acids 2012; 87:111-7. [PMID: 22959886 DOI: 10.1016/j.plefa.2012.07.007] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/22/2012] [Revised: 07/26/2012] [Accepted: 07/27/2012] [Indexed: 12/20/2022]
Abstract
We tested the hypothesis that walnut consumption can exert effects on markers of inflammation and endothelial activation similar to those produced by fish consumption. In a crossover dietary intervention trial, 25 normal to mildly hyperlipidemic men and women were randomly assigned to one of three isoenergetic diets: a walnut diet incorporating 42.5 g of walnuts per 10.1 mJ 6 times per week (1.8% of energy n-3 fat); a fish diet providing 113 g of fatty fish per 10.1 mJ 2 times per week (0.8% of energy n-3 fat), or a control diet (no nuts or fish, 0.4% of energy n-3 fat) for 4 weeks on each diet. Both the walnut and fish diets inhibited circulating concentrations of prostaglandin E metabolite (PGEM) and 11-dehydro thromboxane B2, but demonstrated no effect on blood interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α¯ (TNF-α¯), and C-reactive protein (CRP) or the number of circulating lymphocyte subsets. On the walnut diet the proportion of plasma phospholipid α¯-linolenic acid (ALA) increased 140% and arachidonic acid (AA) decreased 7% compared to both the control and fish diets. The proportion of plasma phospholipid eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased about 200% and 900% respectively on the fish diet relative to either the control or walnut diet. The walnut diet inhibited E-selectin by 12.7% relative to the fish diet, and the fish diet inhibited secretory intercellular adhesion molecule-1 (s-ICAM-1) by 4.5% relative to the control diet. Both walnuts and fish in commonly consumed amounts may have modest albeit distinct effects on circulating adhesion molecules.
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Affiliation(s)
- Yu-Lan Chiang
- Department of Nutrition, Loma Linda University, Nichol Hall 1102, Loma Linda, CA 92354, USA
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Dietary flaxseed oil reduces adipocyte size, adipose monocyte chemoattractant protein-1 levels and T-cell infiltration in obese, insulin-resistant rats. Cytokine 2012; 59:382-91. [DOI: 10.1016/j.cyto.2012.04.004] [Citation(s) in RCA: 39] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/14/2011] [Revised: 03/13/2012] [Accepted: 04/06/2012] [Indexed: 12/14/2022]
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Egert S, Stehle P. Impact of n-3 fatty acids on endothelial function: results from human interventions studies. Curr Opin Clin Nutr Metab Care 2011; 14:121-31. [PMID: 21252652 DOI: 10.1097/mco.0b013e3283439622] [Citation(s) in RCA: 74] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
PURPOSE OF REVIEW Dysfunction of the endothelium plays an integral role in atherogenesis. This review summarizes recent findings on the effects of marine [eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA)] and plant [alpha-linolenic acids (ALA)] n-3 polyunsaturated fatty acids (PUFAs) on endothelial function in healthy individuals and in patients with cardiovascular disease (CVD) risk factors or manifest CVD. RECENT FINDINGS We identified 33 intervention trials investigating the effects of n-3 PUFA on fasting and/or postprandial endothelial function. In healthy individuals regular supplementation of EPA/DHA or ALA shows inconsistent results on endothelial function, whereas markers of endothelial function seem to be improved in overweight dyslipidaemic patients and type 2 diabetics. Conflicting results are observed in CVD patients. Reasons for discrepancies between the study results include the health status and age of participants, duration of supplementation, dose and fatty acid composition of the administered n-3 PUFAs as well as methods used to assess endothelial function. SUMMARY In individuals with CVD risk factors including overweight, dyslipidemia and type 2 diabetes n-3 PUFAs may improve endothelial function. However, the evidence for a clinical efficacy is not strong enough to make final recommendations with respect to a specific dose and the duration of supplementation.
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Affiliation(s)
- Sarah Egert
- Department of Nutrition and Food Science, Nutritional Physiology, University of Bonn, Bonn, Germany.
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Effects on markers of inflammation and endothelial cell function of three ad libitum diets differing in type and amount of fat and carbohydrate: a 6-month randomised study in obese individuals. Br J Nutr 2011; 106:123-9. [PMID: 21320366 DOI: 10.1017/s0007114510005829] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
Abstract
Diet is important for the prevention of CVD, and diets high in MUFA might be more cardioprotective than low-fat diets. We hypothesise that inflammation and endothelial cell function will be improved most favourably by a high-MUFA diet compared with a low-fat diet. This was tested in a parallel randomised intervention trial on overweight individuals (aged 28·2 (SD 4·6) years) assigned to a diet moderate in the amount of fat (35-45% of energy; >20% of fat as MUFA; MUFA diet, n 39), a low-fat (20-30% of energy) diet (LF diet, n 43) or a control diet (35 % of energy as fat, n 24) for 6 months after weight loss. Protein constituted 10-20 % of energy in all diets. Food was provided free of charge. Fasting blood samples were collected before and after the intervention and analysed for C-reactive protein (CRP), IL-6, intercellular adhesion molecule, von Willebrand factor (vWF) and tissue factor pathway inhibitor. vWF concentrations tended to fall on the LF diet (4·78 (SD 16·44) %; P = 0·07). Concentrations of IL-6 were reduced by the MUFA (0·37 (SD 0·74) pg/ml; P < 0·01) and LF (0·47 (SD 0·69) pg/ml; P < 0·001) diets, and CRP was reduced on all diets (MUFA: 0·48 (SD 1·93) mg/l (P < 0·01); LF: 1·46 (SD 2·89) mg/l (P < 0·001); control: 1·20 (SD 1·97) mg/l (P < 0·01)). No significant differences were observed between changes induced by the different diets. Our findings suggest that in overweight subjects after weight loss, the MUFA and LF diets have similar long-term effects on inflammation and endothelial cell function.
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