Modern Dietary Fat Intakes in Disease Promotion (Nutrition and Health)

Modern Dietary Fat Intakes in Disease Promotion

Nutrition and Health Adrianne Bendich, PhD, FACN, Series Editor

For other titles published in this series, go to www.springer.com/series/7659

Modern Dietary Fat Intakes in Disease Promotion Edited by

Fabien De Meester, phd DMF Ltd Company, Marche/Famenne, Belgium

Sherma Zibadi, md, phd University of Arizona, College of Medicine, Sarver Heart Center, Tucson, AZ and

Ronald Ross Watson, phd University of Arizona, Mel and Enid Zuckerman College of Public Health, Tucson, AZ

Editors Fabien De Meester, PhD Managing Director DMF Ltd Company Luxembourg Str 46 6900 Marche/Famenne Belgium [email protected]

Sherma Zibadi, MD, PhD University of Arizona Mel & Enid Zuckerman College of Public Health P.O. Box 245163 Tucson, AZ 85724-5163 USA [email protected]

Ronald Ross Watson, PhD Department of Health Promotion Sciences University of Arizona Health Sciences Center 1295 N. Martin Ave. P.O. Box 245155 Tucson, AZ 85724-5155 USA [email protected]

Series Editor Adrianne Bendich, PhD, FACN GlaxoSmithKline Consumer Healthcare Parsippany, NJ USA

ISBN 978-1-60327-570-5 e-ISBN 978-1-60327-571-2 DOI 10.1007/978-1-60327-571-2 Springer New York Dordrecht Heidelberg London Library of Congress Control Number: 2010921817 © Springer Science+Business Media, LLC 2010 All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Humana Press, c/o Springer Science+Business Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein. Printed on acid-free paper Humana Press is part of Springer Science+Business Media (www.springer.com)

Series Preface

The Nutrition and Health series of books have had great success because each volume has the consistent overriding mission of providing health professionals with texts that are essential because each includes (1) a synthesis of the state of the science, (2) timely, in-depth reviews by the leading researchers in their respective fields, (3) extensive, up-to-date fully annotated reference lists, (4) a detailed index, (5) relevant tables and figures, (6) identification of paradigm shifts and the consequences, (7) virtually no overlap of information between chapters, but targeted, inter-chapter referrals, (8) suggestions of areas for future research, and (9) balanced, data-driven answers to patient as well as health professionals questions which are based upon the totality of evidence rather than the findings of any single study. The series volumes are not the outcome of a symposium. Rather, each editor has the potential to examine a chosen area with a broad perspective, both in subject matter and in the choice of chapter authors. The editor(s), whose training(s) is (are) both research and practice oriented, has(ve) the opportunity to develop a primary objective for their book, define the scope and focus, and then invite the leading authorities to be part of their initiative. The authors are encouraged to provide an overview of the field, discuss their own research, and relate the research findings to potential human health consequences. Because each book is developed de novo, the chapters are coordinated so that the resulting volume imparts greater knowledge than the sum of the information contained in the individual chapters. Modern Dietary Fat Intakes in Disease Promotion, edited by Fabien De Meester, Sherma Zibadi, and Ronald Ross Watson, clearly exemplifies the goals of the Nutrition and Health series. The editors are leaders in their fields of expertise. Fabien De Meester, Ph.D., was until recently President and CEO of BNLfood. He recently decided to step down from his position at BNLfood to establish a new and innovative international platform of DMF (Development & Management Frontiers) companies focused on educational aspects of the Columbus Concept as the new standard in lipid nutrition. Dr. De Meester and Dr. Watson have published a recent volume for Humana Press entitled Wild-Type Food in Health Promotion and Disease Prevention: the Columbus Concept. Dr. De Meester has published over 50 research articles, patents, and communications on topics related to organic chemistry, enzymology, biochemistry, molecular biology, food science, and business, and has organized a series of international workshops on the Columbus Concept. Dr. Sherma Zibadi, M.D., Ph.D., has completed postgraduate training in medicine and has concentrated on metabolic diseases. Dr. Watson is a well-known editor of more than 65 volumes on a wide range of biomedically related nutrition topics over the past 25 years and has published over 250 peer-reviewed research articles. He is professor of Public Health at the University of Arizona and the director of the NIH-funded Alcohol Research Center. The book chapters are logically organized to provide the reader with a basic understanding of the interactions between behavioral aspects of eating and the critical importance of what we v

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eat with specific emphasis on the types and qualities of the fats that are consumed. The volume is divided into five sections including the section on the behavioral aspects of eating; a second section on dietary fats; the third section examines the clinical relevance of fats and cardiovascular disease. The fourth section contains novel chapters on the potential for contaminants in fats and oils to increase risk of illnesses. The fifth section looks at dietary and pharmaceutical approaches to modify fat-induced disease and ill-health. Each section contains chapters that address treatment options as well as prevention strategies. This logical sequence of chapters provides the latest information on the current standards of practice for clinicians, related health professionals including the dietician, nurse, pharmacist, physical therapist, behaviorist, psychologist, and others involved in the team effort required for successful treatment of lipid disorders, cardiac and cerebrovascular diseases as well as conditions that adversely affect normal metabolic processes. This comprehensive volume also has great value for academicians involved in the education of graduate students and post-doctoral fellows, medical students and allied health professionals who plan to interact with patients with lipid disorders as well as those who are overweight or obese. Cutting edge discussions of the roles of growth factors, hormones, cellular and nuclear receptors, adipose tissue, and all of the cells directly involved in fat metabolism are included in well-organized chapters that put the molecular aspects into clinical perspective. Of great importance, the editor and authors have provided chapters that balance the most technical information with discussions of its importance for clients and patients as well as graduate and medical students, health professionals, and academicians. There are numerous chapters that are devoted to the treatment of obesity and its related comorbidities. These include an overview of current treatment options as well as a discussion of future treatments that are already in development. Critical to any weight reduction program is exercise, and there is a comprehensive chapter on the role of physical activity, exercise, and nutrition in weight control. The importance of a team approach to the treatment of obesity as a chronic disease is extensively discussed in chapters on social interactions, lifestyles as well as behavioral modification in the treatment of obesity. Unique to this volume are chapters that examine the development of obesity in Asian populations including an examination of factors including social class and genetics. Specific treatment modalities are reviewed in separate chapters on pharmacotherapies, combination therapies, potential for behavioral interventions, and the effects of different fat types on feelings of hunger and satiety. Each of these chapters presents an objective evaluation of the treatment and identifies the positives and negatives that have been seen during clinical studies as well as cumulative data derived from clinical practice. There is a clear, data-driven message throughout the volume that there are important debates that are ongoing between researchers concerning the value of weight reduction, statins, fish consumption, consumption of meats, and the use of feedlots versus free-range feeding of domesticated animals. There are also thought-provoking chapters that examine whether all saturated fats are “bad” and whether there are sufficient studies to warrant a recommendation of consumption of conjugated linoleic acid; there are two novel chapters on the effects of modifying milk fats and/or other dairy constituents. Of particular interest to the consumer and the patient are answers to their questions about food contaminants. Chapters examine the health effects of inadequate storage, processing, and/or cooking of foods including those with potentially oxidizable fats. Another chapter reviews the complex area of mycotoxins that have been in the human food supply since the beginning of civilization. Women of child-bearing potential are anxious to know about the benefits and/or

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risks of eating fish that are rich in long-chain polyunsaturated fats, yet may also contain contaminants from the sea. Two in-depth chapters provide guidance to the reader in the value of fish consumption. Detailed tables and figures assist the reader in comprehending the complexities of the chemistry of fats and their effects on eating behaviors. Modulators of eating responses and the role of Western diets in the development of the diseases associated with overconsumption of total calories, total fats, specific fats, and other dietary constituents are covered in the last section that also includes discussions of chronic fatigue syndrome, attention-deficit hyperactivity, insulin resistance and type 2 diabetes, micronutrients including selenium, folic acid, and vitamins B12 and B6; chapters include discussions of the relevance of bioactive compounds such as polyphenols, resveratrol, tocotrienols, phytosterols, soy, sulfur compounds from cruciferous vegetables, and other relevant plant constituents. Thus, this volume is focused on answering questions commonly asked by clients and patients about why some diets do not work and why some “professional” sources advocate certain products that are available over the counter but may not “work.” The over-riding goal of this volume is to provide the health professional with balanced documentation and awareness that their clients’/patients’ metabolic conditions are complex states that transcend the simplistic view of just losing a few pounds. Hallmarks of the 29 chapters include bulleted key points at the beginning of each chapter, complete definitions of terms with the abbreviations fully defined for the reader, and consistent use of terms between chapters. There are more than 75 relevant tables, graphs, and figures as well as over 2,200 up-to-date references; all chapters include a conclusion section that provides the highlights of major findings. The volume contains a highly annotated index and within chapters, readers are referred to relevant information in other chapters. This important text provides practical, data-driven resources based upon the totality of the evidence to help the reader understand the basics, treatments, and preventive strategies that are involved in balancing the fats in one’s diet as well as within one’s body. The overarching goal of the editors is to provide fully referenced information to health professionals so that they may have a balanced perspective on the value of various treatment options that are available today as well as in the foreseeable future. In conclusion, Modern Dietary Fat Intake in Disease Promotion, edited by Fabien De Meester, Sherma Zibadi, and Ronald Ross Watson, provides health professionals in many areas of research and practice with the most up-to-date, well-referenced, and easy-to-understand volume on the importance of identifying and treating as well as providing strategies to prevent the development of chronic, serious metabolic diseases. This volume will serve the reader as the most authoritative resource in the field to date and is a very welcome addition to the Nutrition and Health series. Adrianne Bendich, Ph.D., FACN Parsippany, NJ

Preface

Modern Dietary Fat Intakes in Disease Promotion is the follow-up book to the original one published in 2008 under the running title Wild-Type Food in Health Promotion and Disease Prevention: The Columbus Concept, 2008 Humana Press Inc, ISBN 978-1-58829-668-9, E-ISBN 978-1-59745-330-1. It shifts focus from examining the beneficial effects of dietary fat intake to targeting the disease-promoting aspects of fat in the human diet. A review of both disease promotion and disease prevention reveals many diet–health relationships and paradoxes reported regularly in the scientific literature. Perhaps the most frequently neglected family of essential nutrients in contemporary diets is polyunsaturated fatty acids or PUFAs. Their two subgroups omega-6 and omega-3 compete against each other for substrates, intermediaries, and end products in many biological pathways involved in physiological inflammatory processes. A consensus is growing in the modern scientific community about their public health burden through the promotion of chronic degenerative diseases whose incidences and severity continue to increase. Recent attempts at increasing dietary omega-3 fatty acids in foods to reduce disease have met with limited enthusiasm and acceptance by producers, retailers, and consumers—essentially due to the oxidative instability of these acids. Simultaneously, there is a return to plant and animal foods that reflect the wild standard—in other words, which include healthy omega-6/3 fatty acids with an ω6:ω3 PUFA ratio of 1:1 and/or a 25% proportion of ω6 highly unsaturated fatty acids (HUFAs). The goal is to have more balance in blood serum/plasma total lipids in association with a balanced mixture of naturally occurring antioxidant vitamins and minerals. This is the basis of the Columbus Concept, referred to as a new standard in lipid nutrition; it implies a reduction in the relative contribution of omega-6 fatty acids and favors an absolute increase in the contribution of omega-3 fatty acids to the modern dietary pattern. Modern Dietary Fat Intakes in Disease Promotion was a challenging but critical book to edit and publish, as the twentieth century has seen food become readily available due to remarkable advances in agricultural and food-processing technologies. There are both benefits and adverse health consequences to removing cholesterol and omega-3 fats from natural foods, hydrogenating PUFAs from vegetable and fish oils/fats by chemical means, designing high-fat/carbohydrate empty-calorie diets, and spreading around non-biodegradable agrochemicals and pesticides. Such practices today appear to belong to a regrettable era of (1) free-market excitement, probably fueled by a lack of humility in recognizing the historical importance of humanity’s adjustment to wild-type foods, and (2) over-confidence in scientific knowledge. Now, at the beginning of the twenty-first century, we have learned from the cholesterol craze that nature-designed foods may not need to be altered to improve their beneficial health effects, save perhaps in subgroups of the world population that are genetically predisposed to specific diseases and for whom a ix

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nutrigenetic/genomic approach is more appropriate. Therefore, the twenty-first century appears to be focusing on nutritional sciences based on wisdom and the following basic principles: 1. Appropriate balanced intake of essential nutrients. 2. Energy intake = energy expenditure. 3. Whole foods and/or least-processed foods including the following: a. Non-chemically hydrogenated saturated and mono-unsaturated fats for cooking. b. Cold-pressed, non-refined, antioxidant-rich polyunsaturated oils for dressing. c. Extracted, refined, antioxidant-rich highly unsaturated oils for supplementing. Modern Dietary Fat Intakes in Disease Promotion calls for a three-level grasp of the feed– food–fork value chain that includes the following reviewed critical aspects: 1. Behavior: social, cultural, economic, and educational aspects. 2. Composition: fat/protein, triglycerides/phospholipids, and omega-6/-3 ratios. 3. Contamination: peroxides, agrochemicals, and microorganisms.

Volume Contents The first chapters include discussions of the behavioral aspects of eating. Wilczy´nska-Kwiatek, De Meester, Singh, and Łapi´nski review nutrition as modified by behavior on brain function. They point out that the high-carbohydrate diets promoted by Western food guidelines are associated with clinical manifestations of affective disorders leading to depression. This disease is ranked by WHO as the leading degenerative disease in developed countries. A parallel is made between the increased intake of carbohydrate-rich, refined, grain-based fast foods and lower proportional intake of essential nutrients including omega-3 fats, antioxidant vitamins, and minerals. This observation led the authors to review the effects of dietary essential nutrients, primarily omega-3 fatty acids, on psychological function and mental health. The authors found strong evidence that EPA (eicosapentaenoic acid, C20:5ω3) is a promising dietary supplement for the prevention of mental decay in healthy individuals. Puri adds two papers on the potential role of modern lifestyles in myalgic encephalomyelitis and attention-deficit hyperactivity disorder. He shows how a deficiency of and/or imbalance between omega-6 and omega-3 at the tissue level—caused by Western diets and environmental (viral infection, organophosphate) factors— could lead to the rising prevalence of neuron-degenerative diseases in the Western world. Puri concludes that a change in diet should be considered by physicians prior to prescribing a synthetic drug to children and adults newly diagnosed with such disorders. Going and Hingle review data that correlate the health effects of diet and exercise. They define the beneficial influences of regular-to-moderate physical activity and moderate energy-dense, nutrient-rich diets to help control weight and regulate metabolism. O’Hara and Gregg emphasize that focusing health recommendations only on body weight (the weight-centered health paradigm) may not be health promoting. First, it is ineffective as a means to improving health or controlling body weight, and second, the attitudes, behaviors, and practices arising from such a paradigm are harmful to health and well-being. In particular, this paradigm is associated with dissatisfaction, dieting,

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discrimination, and death. Dokken and Boucher test the hypothesis that excessive caloric intake of any kind versus any specific dietary components, including fats, explains the strong relationship between obesity associated with insulin resistance and type 2 diabetes. Dube and Stanton report on the social context of dietary behavior. They suggest that a multi-faceted approach targeting the home-cooking role model, increasing the availability of fruits and vegetables, and decreasing the availability of snacks is necessary to encourage lifetime healthy dietary practices in children and adults, lower the burden on health-care systems, and to reduce health disparities. Bartholomew and Jowers review strategies for modifying school-based foods and conclude that restricting access to calorie-dense foods by manipulating the price structures of their healthy counterparts (i.e., salad bars versus snack foods) has great potential for success. Singh, Rastogi, Goyal, Vajpayee, Fedacko, Pella, and De Meester review data suggesting that populations of developing countries are more sensitive to modern chronic diseases of affluence than are those of developed countries, suggesting a maladaptive process in the latter. They cite data showing that southeast Asians suffer more diabetes and coronary artery disease than do Caucasians, especially at younger ages, whereas their fat intake is less than 25% and obtained from plant rather than animal food. Vaghefi, Watkins, and Brown define how modern Western low-cost and time-saving diets are finding their ways throughout the planet through economic development and technological progress. The high fat content and the low nutritional value of such diets are discussed from the standpoint of their contribution to promoting diseases globally. There are important chapters that review the composition of fats, oils, and other constituents in the diet. Vituru and Gormley explain how the oil-seed industry resulted from the ability to hydrogenate oil produced by extraction from seeds. This generalized processing of plant fats thereafter led to the appearance of trans-unsaturated fats and the disappearance of ω3 fats in the twentieth-century diet, a double trend that mirrors the dramatic global increase in modern degenerative diseases. Crawford, Lehane, and Ghebremeskel revisit health effects as modified by dietary animal fat. Feeding intensively reared, domesticated animals with growth-promoting oil grains has facilitated artificially fat animals presenting high fat/protein and increased omega6/3 and triglyceride/phospholipid ratios in their carcasses. Using such animals as food has little in common with using wild animals or game historically as food—and is a possible modulator of human physiology from an evolutionary standpoint. Surai, Pappas, Karadas, Papazyan, and Fisinin point out that modern, land-based agriculture has washed essential micronutrients away from the food supply. Their review focuses on the removal of selenium as a striking example of a lost essential mineral in plants due to low soil pH and high concentrations of sulfur and phosphorus from the massive use of fertilizer. Enrichment of chickens, cattle, and pig feed with selenomethionine appears to be a sustainable transitory solution to the problem until soil composition can be restored, which is appropriate to animal/man feeding requirements. Sabetisoofyani, Larson, and Watson address the primary role of homocysteine in the inception and progression of endothelial dysfunction with accelerated atherosclerosis from both a dietary perspective (a deficiency in essential B vitamins) and a genomic perspective (mutations in cystathione βsynthase or 5,10-methylenetetrahydrofolate reductase). Ravnskov’s review summarizes much of his lifetime effort at re-establishing the facts behind lipid nutrition. He concludes that cholesterol and saturated fats are not primary risk factors of cardiovascular disease, claiming that both the market place and limited understanding of research on fats and cholesterol have helped encourage previous misconceptions about cholesterol and heart disease. Ravnskov calls for an urgent revision of modern dietary guidelines based on a more educated approach to dietary lipids.

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Jahreis and Hengst provide evidence that dietary fats do not represent a health issue per se. They suggest that fats obtained from ruminants fed grass-type, omega-3-rich fodder promote positive effects on established risk factors of CVD. Jacques, Leblanc, and Bergeron review the different options available to the dairy industry for increasing the understanding of both scientists and the lay public about the health roles of certain fats, particularly in terms of the many misconceptions about cholesterol and saturated fats. Modifications of milk-fat composition through cow feeding, enzymatic inter-esterification, and physical fractionation appear to be among the most promising options. De Lorgeril corroborates Ravnskov’s review by summarizing recent cholesterol-lowering (absorption, synthesis) trials. He concludes with a similar recommendation that medical (in addition to food) guidelines should be carefully re-examined. He describes how reducing blood cholesterol increases atherosclerotic progression as measured by changes in carotid intima-media thickness. Sharma, Singh, and Katz explain the role of statins in modern and modernizing societies where blood cholesterol and triglyceride lowering has become a health-care priority, notwithstanding the potential side effects of such a preventive approach in what they refer to as cardiovascular incapability. Careful selection as to statin types and dosage appears to minimize their side effects on hepatic and renal functions, muscular impairments, and other physical properties while providing sought-after preventive benefits. Vasanthi, Kartal-Özer, Azzi, and Das summarize the recent literature on the efficacy and mechanisms of popular cholesterol-lowering dietary supplements. Zibadi, Larson, and Watson explore how obesity induces maladaptive remodeling of the cardiac muscle through alterations in myocyte shape and number and the extracellular matrix, resulting in cardiac hypertrophy and fibrosis. Leptin, an adipokine overproduced in obesity, appears to play a major role in the remodeling process and therefore to provide an avenue of treating obesity and other hyperleptinemic-related cardiac dysfunctions. Cordova et al. present the genetically modified rodent animal models that are developed to test the maladaptive remodeling hypothesis in the human obesity, cardiac structural, and functional changes relationship. Togni presents the non-deficiency malnutrition syndrome that results from the characteristic load of empty calories in advanced Western diets. In this context, he shows that plant extracts including polyphenols may be recommended as dietary supplements. Kelley, Hubbard, and Erickson review the currently available literature on the influence of conjugated linoleic acid (CLA) isomers on human body composition and tumorigenesis. They conclude that at present it is too early for CLA to be labeled as a health-promoting dietary supplement. Vemuri and Kelley warn that t10,c12-CLA may cause lipodystrophy, insulin resistance, non-alcoholic fatty liver disease, fat mass, and increased body weight in animals and humans. A unique feature of this volume is the extensive information pertaining to major sources of food contaminants. Surai and Fisinin describe how food processing can affect dietary lipids and eventually promote ill-health effects when not protected from peroxidation. They emphasize the need for improving the conditions of food processing, storage, and cooking at a time when fat hydrogenation is increasingly perceived as detrimental to foods. Surai, Mezes, Fotina, and Denev report on the global endemic contamination of the feed–food–fork chain by fungal metabolites: mycotoxins. These food contaminants have detrimental biological effects on both animal and human health through their organ toxicity, including immunomodulation, neurotoxicity, mutagenicity, carcinogenicity, and teratogenicity. As 25% of the current world crop production is potentially contaminated, it is essential to find sustainable solutions to this fungal-persistent presence in the animal and human food chain. Sioen, De Henauw, and Van Camp review a conflict of interest in establishing dietary recommendations for fish as a source of long-chain, ω3 fatty acids. Modern agro-food and environmental practices translate into loading oceans with all kinds

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of persistent and potentially toxic residues that accumulate in fish, in particular fish fats. Their statistical evaluation proposes a balance that can be approached in terms of nutritional benefits versus toxicological aspects of fish consumption. Covaci and Dirtu extend this discussion to naturally produced, organo-brominated compounds from marine micro-organisms present in fish and fish fats. Their review presents evidence that refined fish-oil dietary supplements might be a suitable alternative to fish consumption. The Columbus Concept, defined by this book and the previous one, still has a long way to go to establish itself in the market place. The way lipid standards are taught and implemented in dietary and medical practices within culinary and medical schools, agro-food and pharmaceutical industries, and legislatures has to be changed. In the balance, the burden and cost of chronic diseases on both modern and modernizing societies is exploding, and currently there is no single critical environmental factor identified other than a dietary omega-6/3 PUFA imbalance. Fabien De Meester Marche/Famenne, Belgium Sherma Zibadi Tucson, AZ Ronald Ross Watson Tucson, AZ

Acknowledgments Modern Dietary Fat Intakes in Disease Promotion is positioned as a complementary rationale to the previously published Wild-Type Food in Health Promotion and Disease Prevention: The Columbus Concept. As with the previous volume, this book is the result of long-term, committed teamwork aimed at translating an ever more robust new standard in lipid nutrition into a market reality. In 2008, the Sixth International Congress on the Columbus Concept (ICCC) coincided with the Second Congress of the International Society of Nutrigenetics & Nutrigenomics (ISNN) in Geneva, Switzerland, where a satellite session on dietary PUFAs and cholesterol was organized and sponsored by the Columbus Paradigm Institute (www.columbus-concept.com), a BNLfood company. A special note of thanks should be extended to Artemis P Simopoulos from the Center for Genetics, Nutrition, and Health (CGNH, Washington DC) for her continuous support for the development of the Columbus Concept. Dr. De Meester extends his most sincere gratitude to all contributors of this second tome on the Columbus Concept and confirms his uncompromised support to taking it to market for the health benefits of human societies at large. In this respect, he wishes to emphasize the outstanding contributions of Michael Crawford, Michel de Lorgeril, Ram B. Singh, Peter Surai, Basant Puri, Uffe Ravnskov, and Ronald Ross Watson to the Columbus venture so far. Dr. Watson acknowledges the vital work of our editorial assistants Bethany L. Stevens and Leslie Dupont. Bethany has kept the editors and the authors on task over most of the previous 2 years, answering questions, reviewing manuscripts, dealing with idiosyncrasies of the publishing process, and providing calm assurance that the work would get done. Without her efforts the book would not have appeared and certainly would not have achieved its current quality. Leslie was instrumental in reviewing and editing the preface and Chapter 1.

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Dr. De Meester and Dr. Watson also appreciate the continuing financial support for the editing team efforts by BNLfood and others developing the Columbus concept. Finally, the volume editors would like to extend their appreciation to Humana Publishing Company and their staff for providing a professional platform of communication for new, challenging ideas and hypotheses in nutritional sciences and to the series editor Adrianne Bendich, on the one hand, for her personal input in positioning the book toward the right audience and, on the other, her incisive and pertinent comments, suggestions, and recommendations for improving the content, coherence, and presentation.

Acknowledgments

The work of editorial assistant Bethany L. Stevens in communicating with authors, working with the manuscripts and the publisher was critical to the successful completion of the book and is much appreciated. Her daily responses to queries and collection of manuscripts and documents were extremely helpful. Support for her work was graciously provided by DMF Ltd Company Belgium. Finally Nguyen T. Nga of the Arizona Health Sciences library was instrumental in finding the authors and their addresses in the early stages of the book’s preparation.

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Contents

Part I

Behavioral Aspects of Eating

1 Western Diet and Behavior: The Columbus Concept . . . . . . . . . . . . . . . Agnieszka Wilczy´nska-Kwiatek, Fabien De Meester, Ram B. Singh, and Łukasz Łapi´nski 2 The Social Context of Dietary Behaviors: The Role of Social Relationships and Support on Dietary Fat and Fiber Intake . . . . . . . . . . Anish R. Dube and Cassandra A. Stanton 3

Social Class, Food Intakes and Risk of Coronary Artery Disease in the Developing World: The Asian Paradox . . . . . . . . . . . . . . . . . . . Ram B. Singh, S.S. Rastogi, R.K. Goyal, S. Vajpayee, Jan Fedacko, Daniel Pella, and Fabien De Meester

4 Social, Cultural, Economical, and Practical Factors . . . . . . . . . . . . . . . Simin B. Vaghefi, Julia Watkins, and Karri Brown Part II 5

3

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Dietary Fats

Partially Hydrogenated Fats in the US Diet and Their Role in Disease . . . . . James J. Gormley and Vijaya Juturu

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6 Fatty Acid Ratios in Free-Living and Domestic Animals . . . . . . . . . . . . . Michael A. Crawford, Y. Wang, C. Lehane, and K. Ghebremeskel

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7 Is Saturated Fat Bad? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Uffe Ravnskov

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8

9

Alteration of Human Body Composition and Tumorigenesis by Isomers of Conjugated Linoleic Acid . . . . . . . . . . . . . . . . . . . . . . Nirvair S. Kelley, Neil E. Hubbard, and Kent L. Erickson

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Insulin Resistance and Non-alcoholic Fatty Liver Disease Induced by Conjugated Linoleic Acid in Humans . . . . . . . . . . . . . . . . . . . . . Madhuri Vemuri and Darshan S. Kelley

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Contents

Part III Fats and Cardiovascular Disease 10 Dietary Fat Intake: Promotion of Disease in Carotid Artery Disease: Lipid Lowering Versus Side Effects of Statins . . . . . . . . . . . . . . . . . . Rakesh Sharma, Ram B. Singh, Robert J. Moffatt, and Jose Katz

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11 Recent Cholesterol-Lowering Drug Trials: New Data, New Questions . . . . . Michel de Lorgeril

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12

Leptin and Obesity: Role in Cardiac Structure and Dysfunction . . . . . . . . Sherma Zibadi, Douglas F. Larson, and Ronald Ross Watson

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Cardiac Structural and Functional Changes in Genetically Modified Models of Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Felina Cordova, Sherma Zibadi, Douglas F. Larson, and Ronald Ross Watson

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Fat-Modified Dairy Products and Blood Lipids in Humans . . . . . . . . . . . Gerhard Jahreis and Christin Hengst

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15 Modified Milk Fat Reduces Plasma Triacylglycerol Concentrations: Health and Disease Effects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hélène Jacques, Nadine Leblanc, and Nathalie Bergeron

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Dietary Supplements, Cholesterol and Cardiovascular Disease . . . . . . . . . Hannah R. Vasanthi, Nesrin Kartal-Özer, Angelo Azzi, and Dipak K. Das

Part IV 17

Contaminants in Fats and Oils: Role in Illness

Ill Health Effects of Food Lipids: Consequences of Inadequate Food Processing, Storage and Cooking . . . . . . . . . . . . . . . . . . . . . . . . . Peter Surai and V.I. Fisinin

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18 Mycotoxins in Human Diet: A Hidden Danger . . . . . . . . . . . . . . . . . . Peter Surai, Miklos Mezes, T.I. Fotina, and S.D. Denev

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19 Nutrition–Toxicological Dilemma on Fish Consumption . . . . . . . . . . . . . Isabelle Sioen, Stefaan De Henauw, and Johan Van Camp

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Anthropogenic and Naturally Produced Contaminants in Fish Oil: Role in Ill Health . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Adrian Covaci and Alin C. Dirtu

Part V

Dietary and Pharmaceutical Approaches to Modify Fat-Induced Disease and Ill-Health

21 Do Modern Western Diets Play a Role in Myalgic Encephalomyelitis? . . . . . Basant K. Puri 22

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The Role of Modern Western Diets in Attention-Deficit Hyperactivity Disorder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Basant K. Puri

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The Role of Dietary Fat in Insulin Resistance and Type 2 Diabetes . . . . . . . Betsy Dokken and Jackie Boucher

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Strategies to Modify School-Based Foods to Lower Obesity and Disease Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . John B. Bartholomew and Esbelle M. Jowers

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Selenium Enigma: Health Implications of an Inadequate Supply . . . . . . . . Peter Surai, A.C. Pappas, F. Karadas, T.T. Papazyan, and V.I. Fisinin

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26 Homocysteine: Role in Cardiovascular Disease . . . . . . . . . . . . . . . . . . Arash Sabetisoofyani, Douglas F. Larson, and Ronald Ross Watson

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27

Dietary Plant Extracts to Modify Effects of High Fat Modern Diets in Health Promotion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Stefano Togni

28 Don’t Diet: Adverse Effects of the Weight Centered Health Paradigm . . . . . Lily O’Hara and Jane Gregg 29

417 431

Physical Activity in Diet-Induced Disease Causation and Prevention in Women and Men . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Scott Going and Melanie Hingle

443

Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

455

Contributors

Angelo Azzi Vascular Biology Laboratory, JM USDA-HNRCA, Tufts University, Boston, MA, USA John B. Bartholomew Department of Kinesiology and Health Education, The University of Texas, 1 University Station, D3700, Austin, TX 78712-1204, USA Nathalie Bergeron College of Pharmacy, Touro University California, 1310 Johnson Lane, Mare Island, Vallejo, CA 94592 USA Jackie Boucher Minneapolis Heart Institute Foundation, 920 East 28th Street, Suite 100, Minneapolis, MN 55407, USA, [email protected] Karri Brown Department of Nutrition and Dietetics, College of Health, University of North Florida, Jacksonville, FL, USA Felina Cordova Mel and Enid Zuckerman College of Public Health, University of Arizona, 1295 N. Martin, Tucson, AZ 85724-5155, USA Adrian Covaci Department of Pharmaceutical Sciences, Toxicological Center, University of Antwerp, Universiteitsplein 1, 2610, Antwerp, Belgium M.A. Crawford Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, England Dipak K. Das Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA Stefaan De Henauw Department of Public Health, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium Michel De Lorgeril Laboratoire TIMC-IMAG, UMR 5525, Cœur and Nutrition, Faculté de Médecine, Université Joseph Fourier—Grenoble 1, CNRS, Grenoble, France; Domaine de la Merci, 38706 La Tronche, France Fabien De Meester Managing Director, DMF Ltd Company, Luxembourg Str 46, 6900 Marche/Famenne, Belgium, [email protected] S.D. Denev Trakia University, Stara Zagora, Bulgaria xxi

xxii

Contributors

Alin C. Dirtu Department of Pharmaceutical Sciences, Toxicological Center, University of Antwerp, Universiteitsplein 1, 2610, Antwerp, Belgium; Department of Chemistry, “Al. I. Cuza” University of Iasi, Carol I Bvd., No. 11, 700506, Iasi, Romania Betsy B. Dokken Department of Medicine, Section of Endocrinology, Diabetes and Hypertension, University of Arizona, 1656 East Mabel St, Tucson, AZ, USA, [email protected] Anish R. Dube Program in Public Health at Brown University, Providence, RI, USA Kent L. Erickson Department of Cell Biology and Human Anatomy, School of Medicine, University of California, One Shields Ave., Davis, CA 95616-8643, USA, [email protected] Jan Fedacko PJ Safaric University, Kosice, Slovakia V.I. Fisinin All-Russian Research and Technology Institute of Poultry Production, Sergiev Posad, Russia T.I. Fotina Sumy National Agrarian University, Sumy, Ukraine K. Ghebremeskel Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, England Scott Going Department of Nutritional Sciences, The University of Arizona, 2549 N Santa Rita Ave, #1, Tucson, AZ 85719, USA, [email protected] James J. Gormley Gormley NPI Consulting, Riverdale, NY 10463, USA, gormleyconsulting.blogspot.com R.K. Goyal Government Medical College, MS University of Baroda, Surat, Gujarat, India Jane Gregg Health Promotion, School of Health and Sport Sciences, University of the Sunshine Coast, Sippy Downs, QLD, Australia Christin Hengst Department of Nutritional Physiology, Institute of Nutrition, Friedrich Schiller University, Dornburger Str. 24, D-07743 Jena, Germany, [email protected] Melanie Hingle USDA-ARS Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX, USA Neil E. Hubbard Department of Cell Biology and Human Anatomy, School of Medicine, University of California, One Shields Ave., Davis, CA 95616-8643, USA Helene Jacques Department of Food Science and Nutrition, Institute of Nutraceuticals and Functional Foods, Laval University, 2425 Agriculture St., Paul-Comtois Building, Quebec, QC, G1V 0A6 Canada, [email protected]

Contributors

xxiii

Gerhard Jahreis Department of Nutritional Physiology, Institute of Nutrition, Friedrich Schiller University, Dornburger Str. 24, D-07743 Jena, Germany, [email protected] Esbelle M. Jowers Exercise and Sport Psychology Laboratory, Department of Kinesiology and Health Education, The University of Texas, 1 University Station, D3700, Austin, TX 78712-1204, USA, [email protected] Vijaya Juturu UnitedBio-Med Inc, 102 Hunters Run, DobbsFerry, NY 10522, USA F. Karadas Department of Animal Science, Faculty of Agriculture, University of Yuzuncu Yil, Van, Turkey Nesrin Kartal-Özer Department of Biocemistry, Faculty of Medicine, Marmara University, 34668, Istanbul, Turkey Jose Katz Department of medicine, Columbia University, New York 10033, USA Darshan S. Kelley Department of Nutrition, Western Human Nutrition Research Center, ARS, USDA, University of California, Davis, CA 95616, USA, [email protected] Nirvair S. Kelley Department of Cell Biology and Human Anatomy, School of Medicine, University of California, One Shields Ave., Davis, CA 95616-8643, USA ´ Łukasz Łapinski Psychological Center PARTNER, Wieczorka 22 Str, Gliwice, Poland, [email protected] Douglas F. Larson College of Medicine, Sarver Heart Center, The University of Arizona, Tucson, AZ 85724, USA Nadine Leblanc Department of Food Science and Nutrition, Institute of Nutraceuticals and Functional Foods, Laval University, 2425 Agriculture St., Paul-Comtois Building, Quebec, QC, G1V 0A6 Canada C. Lehane Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, England M. Mezes Szent István University, Gödöll˝o, Hungary Robert J. Moffatt Department of Exercise Science, Nutrition and Food, Florida State University, Tallahassee, FL 32306 Lily O’Hara Public Health in the School of Health and Sport Sciences, University of the Sunshine Coast, Sippy Downs, QLD, Australia, [email protected]. T.T. Papazyan Alltech Russia, Moscow, Russia A.C. Pappas Laboratory of Nutritional Physiology and Feeding, Faculty of Animal Science and Aquaculture, Agricultural University of Athens, Athens, Greece Daniel Pella PJ Safaric University, Kosice, Slovakia

xxiv

Contributors

Basant K. Puri MRI Unit, Hammersmith Hospital, Du Cane Road, London, W12 0HS, UK, [email protected] S.S. Rastogi Halberg Hospital and Research Institute, Moradabad, UP 244001, India Uffe Ravnskov Magle Stora Kyrkogata 9, 22350 Lund, Sweden, [email protected] Arash Sabetisoofyani College of Medicine, Sarver Heart Center, The University of Arizona, Tucson, AZ 85724, USA Rakesh Sharma Department of medicine, Columbia University, New York 10033, USA; Center of Nanomagnetics and Biotechnology, Florida State University, Tallahassee, FL 32304, USA, [email protected] Ram B. Singh Helberg Research Institute, Moradabad, Uttar Pradesh, India Isabelle Sioen Department of Public Health, Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium, [email protected] Cassandra Stanton Transdisciplinary Research Group, Department of Psychiatry and Human Behavior, Butler Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA, [email protected] P.F. Surai Avian Science Research Centre, Scottish Agricultural College, Ayr, UK; Division of Environmental and Evolutionary Biology, University of Glasgow, Glasgow, UK; Szent István University, Gödöll˝o, Hungary; Sumy National Agrarian University, Sumy, Ukraine; Trakia University, Stara Zagora, Bulgaria, [email protected] Stefano Togni DVM—Indena SpA, Viale Ortles, 12, Milano, 20139 MI, Italy, [email protected] Simin B. Vaghefi Department of Nutrition and Dietetics, College of Health, University of North Florida, Jacksonville, FL, USA S. Vajpayee Government Medical College, MS University of Baroda, Surat, Gujarat, India Johan Van Camp Department of Food Safety and Food Quality, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium, [email protected] Hannah R. Vasanthi Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA; Department of Biochemistry, Sri Ramachandra Medical College and Research Institute, Sri Ramachandra University, Chennai, India Madhuri Vemuri Department of Nutrition, Western Human Nutrition Research Center, ARS, USDA, University of California, Davis, CA 95616, USA Y. Wang Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, England Julia Watkins Department of Nutrition and Dietetics, College of Health, University of North Florida, Jacksonville, FL, USA

Contributors

xxv

Ronald Ross Watson College of Medicine, Sarver Heart Center, The University of Arizona, Tucson, AZ 85724, USA; College of Public Health, The University of Arizona, Tucson, AZ 85724, USA ´ Agnieszka Wilczynska-Kwiatek Institute of Psychology, University of Silesia, ul. ˙ Grazy´nskiego 53, 40-126 Katowice, Poland, [email protected]; [email protected] Sherma Zibadi College of Medicine, Sarver Heart Center, The University of Arizona, Tucson, AZ 85724, USA; College of Public Health, The University of Arizona, Tucson, AZ 85724, USA

Part I

Behavioral Aspects of Eating

Chapter 1

Western Diet and Behavior: The Columbus Concept ´ Agnieszka Wilczynska-Kwiatek, Fabien De Meester, Ram B. Singh, ´ and Łukasz Łapinski

Key Points • Increased intake of refined grains and fast foods is associated with a lower intake of ω-3 fatty acids, vitamins, and antioxidants, and associated with a sequence in the emergence of chronic diseases of affluence. • Increased consumption of refined carbohydrates may also increase the risk of mental disorders: not only depression, anxiety, stress, personality, and behavioral disorders but also general cognitive impairment in older people. • Dietary intake of ω-3 fatty acids, antioxidant vitamins A, E, C, and beta-carotene is inversely associated with these psychological disorders. • There is some evidence that increased intake of linoleic acid, saturated fat, and trans fat as well as refined carbohydrates is proinflammatory, leading to increased plasma levels of transcription factors of proinflammatory cytokines. • As cytokines may be positively associated with affective and anxiety-related disorders and type A behavior, available clinical trials indicate that treatment with ω-3 fatty acids can modulate depression and behavioral disorders. Keywords Diets · Food · Nutrients · Fatty acids · Depression · Anxiety · Psychological disorders · Cognitive impairment

1 Introduction Research has indicated that brain function is highly sensitive to variations in diet. Probably the best known example is the consumption of caffeine, which is present in tea, coffee, chocolate, and other foods. Caffeine is a stimulant that improves mental alertness and performance. It has become clear that many other dietary components—from vitamins to macro-elements— influence brain function. For some, biochemical effects, and for others, behavioral and functional

A. Wilczy´nska-Kwiatek () Institute of Psychology, University of Silesia, ul. Graz˙ y´nskiego 53, 40-126 Katowice, Poland e-mails: [email protected]; [email protected] F. De Meester et al. (eds.), Modern Dietary Fat Intakes in Disease Promotion, Nutrition and Health, DOI 10.1007/978-1-60327-571-2_1, © Springer Science+Business Media, LLC 2010

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effects have been reported. As the study of nutrition, behavior, and brain function is relatively new, it is not surprising that huge gaps exist in the biochemical, physiological, psychological, and behavioral aspects of our knowledge of how diet affects brain function. However, some accurate and relevant data are available. Clear functional effects seem evident although underlying mechanisms are still inadequately understood. The aim of this chapter is to identify the effects of dietary constituents and functional food components (particularly ω-3 fatty acids) on psychological function and mental health.

2 Changing Patterns of Food Consumption in Western Societies As with all organisms, people are dependent on food in order to live and function, yet the nature of this relationship has gone through continual change. Hunter–gatherer cultures were forced to cope with the limited amount of food available in their surroundings. On the other hand, life in most Western civilizations allows for consumption of a considerably higher quantity of calories than what the human body actually requires [1], and the food eaten may come from the furthest reaches of the planet. Barry M. Popkin [2, 1] emphasized that the underlying shifts in demographic, economic, cultural, and related forces that affect fertility, mortality, and disease patterns also affect the structure of diet, physical activity, and body-composition trends. Popkin claimed that nutrition transition has followed five general patterns (see Table 1.1), which are not necessarily restricted to particular periods of human history: (1) hunting and gathering, (2) famine, (3) receding famine, (4) degenerative disease, and (5) behavioral change. The first pattern is found in hunter–gatherer societies, whose diets might be acknowledged to be very healthy. Those societies are nonetheless generally characterized by a very low life expectancy, usually as a result of infectious diseases and other natural causes. As new techniques for gathering food developed, hunter–gatherer societies moved away from a diet based on game, fruits, and vegetables and became more dependent on farming; therefore, grains and cereals became predominant features of their diets. The second pattern is found in simple farming cultures that experience alternating periods of famine and harvest. The Industrial Revolution brought with it colossal dietary changes, and the influx of an enormous labor force into cities required a large amount of inexpensive food to feed them. These requirements were met in part by dramatic changes in the manner of processing and preserving food, for example, canning, freezing, increasingly cheap methods of grinding grains (removing many of their nutrients), and the production of sugar and vegetable oil. Finally, the twentieth century increased the pace of change in food processing in hitherto unimaginable ways. One of the effects, besides increased health and shifting lifestyles, is the fact that current widespread diets differ considerably from those of our ancestors in both quantity and quality. The three consecutive patterns described by Popkin concern the contemporary world to a great degree. In pattern 3, famine begins to recede as income rises. In pattern 4, changes in nutrition as a result of quick economic and industrial development are connected with different diseases such as CVD, depression, and cancer. This pattern may be considered typical of most Western societies. Western diets are becoming increasingly energy dense and sweet. In addition, high-fiber foods are being replaced by processed versions of the same foods [2, 1]. The increased intake of refined grains and fast foods is associated with a lower intake of ω-3 fatty acids, leading to a sequence in the emergence of chronic diseases of affluence: obesity, diabetes, metabolic syndrome, heart attack, and bone and joint diseases. Such dietary changes

Robust, lean population; few nutritional deficiencies

Hunter–gatherers

Primitive, onset of fire

Subsistence, primitive stone tools

Economy

Household production

Income and assets

Plants, low-fat wild animals, varied diet

Nutritional status

Nutrition profile Diet

Labor intensive, primitive technology begins (clay cooking vessels) Subsistence, few tools

Children and women suffer most from low fat intake, nutritional deficiency diseases emerge, stature declines Agriculture, animal husbandry, homemaking begin; shift to monocultures

Cereals predominant, diet less varied

Table 1.1 Characteristics of the five patterns of the nutrition transition by Popkin Transition profile (1) Collecting food (2) Famine

Increases in income disparity and agricultural tool industrialization

Fewer starchy staples; more fruit, vegetables, animal protein; low variety continues Continued MCH1 nutrition problems, many deficiencies disappear, weaning diseases emerge, stature grows Second agricultural revolution (crop rotation, fertilizer), Industrial Revolution, women join labor force Primitive water systems, clay stoves, cooking technology advances

(3) Receding famine

Rapid growth in income and income disparities, technology proliferation

Fewer jobs with heavy physical activity, service sector and mechanization, household technology revolution Household technology mechanizes and proliferates

More fat (especially from animal products), sugar, processed foods; less fiber Obesity, problems for elderly (bone health, etc.), many disabling conditions

(4) Degenerative disease

Service sector mechanization and industrial robotization dominate, increase in leisure exercise offsets sedentary jobs Significant reduction in food preparation costs as a result of technologic change Decrease in income growth, increase in home, and leisure technologies

Higher quality fats, reduced refined carbohydrates, more whole grains, fruit, vegetables Reduction in body fat and obesity, improvement in bone health

(5) Behavioral change

1 Western Diet and Behavior: The Columbus Concept 5

Much infectious disease, no epidemics

Young population

Rural, low density

Nonexistent

Age structure

Residency patterns

Food processing

Low fertility, high mortality, low life expectancy

(1) Collecting food

Morbidity

Demographic profile Mortality and fertility

Table 1.1 (continued) Transition profile

Food storage begins

Rural, a few small, crowded cities

Young, very few elderly

Epidemics, endemic disease (plague, smallpox, polio, tuberculosis), deficiency disease begins, starving common

Age of Malthus; high natural fertility, short life expectancy, high infant and maternal mortality

(2) Famine

Chiefly rural, move to cities increases, international migration begins, megacities develop Storage processes (drying, salting) begin, canning and processing technologies emerge, increases in food refining and milling

Chiefly young, shift to older population begins

Mortality declines slowly, then rapidly; fertility static, then declines; small, cumulative population growth, which later explodes Tuberculosis, smallpox infection, parasitic disease, polio, weaning disease (diarrhea, retarded growth) expand, later decline

(3) Receding famine

Numerous food-transforming technologies

Lower density cities rejuvenate, increase in urbanization of rural areas encircling cities Technologies create foods and food constituent substitutes (e.g., macronutrient substitutes)

Increases in health promotion (preventive and therapeutic), rapid decline in cardiovascular disease, slower change in age-specific cancer profile Increases in the proportion of elderly >75 years of age Chronic disease related to diet and pollution (heart disease, cancer), decline in infectious disease

Rapid decline in fertility, rapid increase in proportion of elderly person Dispersal of urban population decreases in rural green space

Life expectancy extends to ages 70 and 80 years, disability-free period increases

(5) Behavioral change

Life expectancy hits unique levels (ages 60–70), huge decline and fluctuations in fertility (e.g., postwar baby boom)

(4) Degenerative disease

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may also increase the risk of mental disorders and dysfunctions, like depression, stress, anxiety, and personality and behavioral disorders—in addition to general cognitive impairment in the aged [3–5]. Recent studies (ibid. [6, 7–29]) contain advanced research on the influence of foods on individuals’ mental conditions. A crucial role has been ascribed to ω-3 fatty acids, which are particularly important for the normal functioning of most human organs. A deficiency in essential fatty acids can cause intensification of cardio-, cerebro-, and retinal–vascular diseases; brain and autoimmune diseases; cancers; obesity; diabetes; bone loss; and so forth. The researchers also emphasize the role of fatty acids in treating mental disorders such as depression, bipolar disorders, and schizophrenia, as well as aggression prevention and support in the treatment of Alzheimer’s disease (ibid. [30]). With further research the cycle of civilization-based nutritional changes can be viewed optimistically. The fifth and final pattern indicated by Popkin represents another change in thinking and behavior. However, Western societies must take precise action to promote healthy lifestyles. Pattern 5 is a positive model based on rejecting negative trends characteristic of earlier patterns. It is a conscious step toward healthy lifestyles and nutrition, with all modern knowledge and technology available as a basis for healthier choices. Such an approach is promoted by the recently developed Columbus Concept, which refers to a return of modern dietary patterns to their Paleolithic standards, with particular attention to essential fatty acids (www.columbusconcept.com).

3 A Healthful Change in Behavior A healthful change in behavior is associated with human developmental change and increased human consciousness and intentional behaviors [31]. Ajzen and Fishbein [32] explain the undertaking of health-oriented decisions by rational action theory. A change expected in the area of dietary behavior may occur when an individual has proper motivation and intention, which mark the beginning of change implementation. Changes in behavior are preconditioned by the knowledge and awareness of the direction and scale of necessity. A change in dietary behavior is equivalent to adopting a new attitude toward one’s own diet. Being complex in nature, a change in attitude must concern all of its aspects: cognitive (acquisition of knowledge and identification of benefits), emotional (positive approach, satisfaction, etc.), and behavioral (taking specific actions). Obstacles to diet-related human behavioral change are determined by dietary habits originating in socializing processes, cultural influences, and, to a significant extent, tradition. A major enemy of health is Western societies’ demands for fast and easily available food (e.g., sweets, French fries) to satisfy cravings. As a rule, the internally motivated modification of improper dietary habits and the adoption of healthful dietary behavior are determined by one’s individually perceived susceptibility to a given disease or the gravity of an already developed illness. External stimuli that favor undertaking healthful actions include health-promoting campaigns organized by mass media, other people’s advice, physicians’ indications, friends’ or family members’ diseases, and news articles [33]. According to a study conducted in 1981 by Mark Condiotte and Edward Lichtenstein [34], it is the sense of self-efficacy that plays a major role in maintaining healthful habits. It should be emphasized that everyday human functioning (including nutritional) is in a dynamic state of fragile balance [35, 36].

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Even if consumers aim to modify their nutritional and dietary habits and make them more health-oriented, the Western diet offers foods that are difficult to recognize as healthful. Maintaining a balance in human health requires returning to traditional dietary solutions by means of modern science and available technologies. This optimal approach seems well supported by the Columbus Concept as a market initiative.

4 The Columbus Concept The Columbus Concept surmises that humans evolved on a diet that was low in saturated fat with equal amounts of ω6 and ω-3 fatty acids. In nature, lipid and fatty-acid fractions are grossly balanced (polyunsaturated:saturated or P:S = ω6:ω-3 = 1:1) and rich in monounsaturated fatty acids (P:M:S=1:6:1). These ratios represent the overall distribution of fats in a natural, untamed environment (www.columbus-concept.com). The Columbus foods include eggs, milk, meat, oil, and bread, all rich in ω-3 fatty acids, similar to wild foods consumed before the agricultural revolution. Blood-lipid composition reflects one’s health status: (a) circulating serum lipoproteins and their ratio provide information on their atherogenicity to blood vessels and (b) circulating plasma fatty acids, such as the ω6:ω-3 fatty-acid ratio, indicate the proinflammatory status of blood vessels. Both (a) and (b) are phenotype related and depend on genetic, environmental, and developmental factors. As such, they appear as universal markers for holistic health. Blood cholesterol is central to this approach; blood lipoproteins affect blood-vessel integrity when circulating throughout the body. Of major importance to a healthy dietary regimen appear to be both the essential dietary nutrients (essential amino acids, fatty acids, antioxidant vitamins, and minerals) and the functional components (diet, sport, spiritualism, etc.). Dietary patterns rich in the preceding nutrients protect against chronic diseases of affluence such as CVD, diabetes, and cancer, as well as mental diseases such as depression, type-A behavior, anxiety, and stress.

5 Omega-3 and Omega-6 Polyunsaturated Fatty Acids (PUFAs) The ω6 and ω-3 PUFAs linoleic and linolenic acid are essential fatty acids in humans (and many other mammals), as they cannot be synthesized by organisms but instead have to be obtained from one’s diet. PUFAs are composed of hydrocarbon chains of variable length with a methyl group at one end (omega), a carboxyl group at the other, and several double bonds. The position of the first double bond differentiates ω-3 fatty acids (such as α-linolenic acid or C18:3ω-3) and ω6 (like linoleic acid or C18:2ω6) [37]; ω-3 PUFAs have a double bond at the third carbon, while ω6 PUFAs have one at the sixth. The chemical structures of linoleic acid (LA), α-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) are shown in Figs. 1.1, 1.2, 1.3, and 1.4, respectively. ALA, which is often called a short-chain ω-3 PUFA (C18:3ω-3), can be metabolized to longer chain PUFAs such as EPA (C20:5ω-3) and DHA (C22:6ω-3). LA can be converted to arachidonic acid or AA (C20:4ω6). The metabolism of essential fatty acids is shown in Fig. 1.5.

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Western Diet and Behavior: The Columbus Concept

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Fig. 1.1 Chemical structure of LA

Fig. 1.2 Chemical structure of ALA

Fig. 1.3 Chemical structure of EPA

Fig. 1.4 Chemical structure of DHA

n-6 Series 18:2 n-6 Linolenic Acid Δ-6 Desaturation ↓ 18:3 n-6 γ-Linolenic Acid Elongation ↓ 20:3 n-6 Dihomogammalinolenic Acid Δ-5 Desaturation ↓ 20:4 n-6 Arachidonic Acid Elongation ↓ 22:4 n-6Adrenic Acid Δ-4 Desaturation ↓ 22:5 n-6 Docosapentaenoic Acid (n-6)

n-3 Series α-Linolenic Acid ↓ Stearidonic Acid ↓ Eicosatetraenoic Acid (n-3) ↓ Eicosapentaenoic Acid ↓ Docosapentaenoic Acid (n-3) ↓ Docosahexaenoic Acid

18:3 n-3 18:4 n-3 20:4 n-3 20:5 n-3 22:5 n-3 22:6 n-3

Fig. 1.5 The metabolism of essential fatty acids

Omega-3 PUFAs are present in linseed oil, walnuts, wheat, soybeans, and particularly in game, river and coldwater algae, and sea fish (tuna, salmon, herring, etc); omega-6 PUFAs are primarily found in maize, sunflower, sesame oils, modern meat, and eggs. Some biochemical data suggest that ω-3 PUFAs play an important role in neural structure and function. The brain and the central nervous system (CNS) contain high concentrations of ω-3

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PUFAs, and several studies suggest a role for ω-3 PUFAs in neurotransmitter synthesis, degradation, release, reuptake, and binding [38–40]. Fatty acids constitute part of all phospholipids and consequently of all biological membranes. Membrane fluidity, of crucial importance for healthy membrane functioning, depends on lipidic components. In addition, membrane fluidity is determined by the phospholipids to free cholesterol ratio, as cholesterol increases membrane viscosity [41]. DHA deficit is associated with dysfunctions in neuronal membrane stability and the transmission of serotonin, norepinephrine, and dopamine, which might relate to the etiology of mood and the cognitive dysfunction of depression. A diet rich in essential polyunsaturated fatty acids allows for a higher incorporation of cholesterol in the membranes to balance their fluidity, which, in turn, contributes to lower blood-cholesterol levels [37]. The significant factor in fatty-acid efficacy does not seem to be its absolute level but instead the ratio between various groups of fatty acids. It is known, for instance, that the relative amounts of ω6 and ω-3 PUFAs in the cell membrane are responsible for affecting cellular function [42, 43]. The types of fatty acids that are available to the composition of cell membranes depend upon diet. The retina and the brain, particularly the cerebral cortex, are rich in ω-3 fatty acids [44, 45], and the role of ω-3 PUFAs in visual and cognitive development has been widely examined [46–49]. Any dietary deficits of essential PUFAs have consequences on cerebral development, modifying the activity of enzymes in the cerebral membranes. In addition, it has been ascertained that maternal intake of ω-3 PUFAs during pregnancy and lactation may positively influence the later visual and mental development of children [49, 50]. The essential PUFAs are precursors of eicosanoids—prostaglandins and leukotrienes—which are involved in inflammation and immune response, and a diet rich in fish oil reduces the production of PGE2. Furthermore, an increase in EPA intake leads to a reduction in the production of inflammatory cytokines. Therefore, it might be important to use ω-3 PUFAs in the treatment of chronic inflammatory diseases like rheumatoid arthritis. Finally, it was reported that ω-3 PUFAs might prevent the onset of hormone-dependent tumors (i.e., prostatic cancer) [51]. To sum up, DHA and EPA play roles in numerous cellular functions, including membrane fluidity, membrane enzyme activities, and eicosanoid synthesis, all of which are essential for brain development in infants and required for maintaining normal brain function in all humans [52]. On the other hand, large multi-gram amounts of ω-3 PUFAs may cause excessively prolonged bleeding, possibly resulting in hemorrhagic strokes and oxidative damage to various tissues [3]. For this reason it is often suggested to accompany ω-3 PUFA supplementation with various antioxidants such as vitamins E and C, flavonoids, and polyphenols. In fact, much evidence indicates that antioxidants are also essential in maintaining neurophysiologic conditions [53].

6 Nutrients and Brain Function Polyunsaturated fatty acids (PUFAs) constitute key structural components of the phospholipid membranes in body tissues, being especially rich in the human brain and the central nervous system (CNS) [54]. They are known to play a role in nervous system activity, neuroplasticity of nerve membranes [55], synaptogenesis [56], synaptic transmission [44], and neurotransmitter uptake. Most neurotransmitters, catecholamines, acetylcholines, serotonin, and dopamine can also affect the function of the cardiovascular system, in addition to their effects on neuropsychiatric

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systems and behaviors [57–60]. The synthesis of these neurotransmitters has been shown to depend on dietary precursors such as tryptophan, choline, tyrosine, and arginine [57, 58]. Some evidence suggests that total and saturated fat, linoleic acid, trans fat, sugar, salt, alcohol, and obesity may have adverse effects on brain and heart function as well as mental function. In contrast, ω-3 fatty acids, monounsaturated fatty acids, antioxidant vitamins, flavonoids, coenzyme Q10, potassium, magnesium, calcium, and moderate alcohol consumption may have beneficial effects. There is evidence that ω-3 fatty acids and other nutrients can affect cognitive function, mood, behavior, personality disorders, and depression (see below). Table 1.2 shows nutrients having possible effects on brain and psychological function, and Fig. 1.6 presents nutrient-related psychological disorders. Figure 1.7 illustrates the effects of lifestyle factors on biomarkers leading to cardiovascular disease and psychological problems. Table 1.2 Nutrients having possible effects on brain and psychological function

Beneficial effects

Adverse effects

Omega-3 fatty acids Monounsaturated fatty acids Vegetable proteins Soluble fiber Vitamins: A, E, C, beta-carotenes B vitamins and folic acid Coenzyme Q10 Flavonoids Potassium Magnesium Calcium Zinc Copper Selenium Chromium

Excess of total fat Excess of saturated fat trans fat Excess of linoleic acid Excess of sodium

The brain is responsible for approximately one-fifth of the body’s basal metabolism, which is provided by glucose and oxygen. Nitrogenous and lipid materials are essential to the growth and regeneration of myelin sheaths and axis cylinders as well as for enzyme systems needed for cellular metabolism and neuroprotection. Vitamins, minerals, electrolytes, ω-3 fatty acids, and coenzyme Q10 in the neurons may influence the excitability of nerve centers. These vitamins, minerals, antioxidants, flavonoids, and ω-3 fatty acids should be adequately available, as dietary deficiencies in them are associated with psychological disorders [53, 61, 62]. Epidemiological studies indicate that diets rich in antioxidants and anti-inflammatory compounds (i.e., polyphenols), such as those found in fruits and vegetables, may lower the risk of developing age-related, neurodegenerative diseases such as Alzheimer’s or Parkinson’s disease [53].

7 Nutrients and Affective Function A lack of ω-3 long-chain polyunsaturated fatty acids is implicated in the development of several human conditions and diseases, including dementia, schizophrenia, and depression [4, 5, 61]; however, ω-3 treatment of these diseases often shows positive results [63–67]. Descriptions of

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•

Affective disorders i.e. major depressive disorder, bipolar disorder, postpartum depression

•

Anxiety disorders i.e. obsessive compulsive disorder, substance abuse

• • • • • •

Stress-related disorders Schizophrenia Personality disorders Behavioral disorders and dysfunctions Attention deficit hyperactivity disorder Cognitive impairment in aging, dementia, Alzheimer’s Disease

Fig. 1.6 Psychological disorders related to nutrients

ω-3-related effects on depression, although they might be considered controversial, have led to the conclusion that ω-3 PUFAs can affect both cognitive and affective function, and may even act as “mood stabilizers.” Several lines of evidence suggest a relationship between dietary intake of ω-3 PUFAs and depressed moods in humans. In this section we aim to list the findings of published randomized controlled trials investigating the effects of dietary supplementation with ω-3 PUFAs on affective function, mainly in the treatment of mental disorders. A summary and comparison of a number of investigations in this area allows us to evaluate whether or not available data support the hypothesis that ω-3 PUFAs play a role in alleviating depression and/or anxiety. In an exhaustive search of databases (among them PubMed and EBSCO) through February 2009, we have found several clinical trials of ω-3 PUFAs in relation to affective functions1 [6, 7–29] (see Table 1.3). As can be seen in Table 1.3, the list of available clinical trials in this area makes it difficult to unambiguously affirm or reject the hypothesis about the influence of ω-3 PUFAs on emotional function. The trials vary widely, not only in terms of approach or quality of design but also in terms of groups tested, sample size, composition and quantity of PUFAs taken, length of supplementation period, and psychometric instruments used. The results of particular investigations are also ambiguous. Early studies of the relationships between ω-3 PUFAs and affective function in doubleblind, placebo-controlled trials were published by researchers at the Department of Neurology,

1 The search terms for n–3 PUFAs (n–3, omega-3, α-linolenic, eicosapentaenoic, docosahexaenoic, EPA, DHA, ALA, fish, etc.) were combined with terms for mental disorders and psychological function (depression, depressed mood, depressive disorder, affective, cognitive, anxiety, bipolar, personality, etc.).

1

Western Diet and Behavior: The Columbus Concept

13

Fig. 1.7 Effect of lifestyle factors on biomarkers leading to cardiovascular disease and psychological problems

Keck et al.

Nemets et al.

Peet and Horrobin

Llorente et al. Marangell et al.

Su et al.

Zanarini and Frankenburg

4

5

6

7 8

9

10

2003

2003

2003 2003

2002

2002

2002

1999

Borderline personality disorder

Major depression

Postpartum depression Major depression

Unipolar depressive disorder Major depression

Bipolar disorder 2.0 g e-EPA

6.0 g e-EPA

30: 20/10

28: 14/14

4.4 g EPA 2.2 g DHA 1.0 g E-EPA

70: 17→1 g/day 1, 2, 4 g EPA 18→2 g/day 17→4 g/day 99: 44/45 Ok. 0.2 g DHA 36: 18/18 2.0 g DHA

20: 10/10

116: 59/57

30: 14/16

56

56

120 42

84

28

120

112

90

MADRS MOAS

HDRS MADRS BDI BDI MADRS HDRS HDRS

HDRS YMRS CGI GAS IDS YMRS HDRS

BDI

Yes

Yes

No No

Yes

Yes

No

Yes

No

Stoll et al.

50: 24/26

Likert scale

3

1999

90

Warren et al.

0.14 g EPA 0.09 g DHA 0.14 g EPA 0.09 g DHA 6.2 g EPA 3.4 g DHA

2

63: 39/24

Yes

Chronic fatigue syndrome Chronic fatigue syndrome Bipolar disorder

Behan et al.

1

1990

Statistical significant difference

Table 1.3 Chronological list of clinical trials investigating effects of omega-3 PUFA on depressed mood and other affective manifestations Intervention No. of subjects, total: treatDuration Outcome No. Study Year Group ment/placebo Daily dose (d) measures

14 ´ A. Wilczynska-Kwiatek et al.

Study

Post et al. Fux et al.

Hirashima et al.

Silvers et al.

Fontani et al.

Osher et al. Freeman et al.

Frangou et al.

Nemets et al.

Hallahan et al.

No.

11 12

13

14

15

16 17

18

19

20

Table 1.3 (continued)

Year

2007

2006

2006

2005 2005

2005

2005

2004

2003 2004

49: 33/16

77: 40/37

21: 12/9

121 11

Patients with recurrent self-harm

49: 22/27

12 16: 6→0.5 g EPA + DHA 3→1.4 g EPA + DHA 7→2.8 g EPA + DHA Bipolar disorder 75: 24→1 g/d 25→2 g/d 26→placebo (Children) [6–12 years] 28: 13/15 Major depression

Bipolar disorder Postpartum depression

Healthy subjects

Major depression

Bipolar disorder Obsessive–compulsive disorder Bipolar disorder

Group

No. of subjects, total: treatment/placebo

HDRS-SF BD POMS

– HDRS YBOCS T2 time HDRS

Outcome measures

112

84

HDRS CGI YMRS CDRS CDI CGI BDI HDRS MOAS IMT/DMT PSS

Up to 168 HDRS 56 EPDS CGI HRSD

35

84

28

112 42

Duration (d)

1.2 g EPA + 0.9 g DHA 84

0.38–0.4 g EPA 0.18–0.2 g DHA

1, 2 g/day e-EPA

5.0–5.2 g EPA 3.0–3.4 DHA or 1.3 g EPA 0.7 g DHA 0.6 g EPA 2.4 g DHA 1.6 g EPA 0.8 g DHA 0.4 g other n – 3 PUFAs 1.5–2 g EPA 0.5 g EPA + DHA 1.4 g EPA + DHA 2.8 g EPA + DHA Ratio EPA:DHA→1.5:1

6 g EPA 2.0 g E-EPA

Daily dose

Intervention

Yes

Yes

Yes

Yes Lack of placebo control group

Yes

No

Yes

No No

Statistical significant difference

1 Western Diet and Behavior: The Columbus Concept 15

van de Rest et al.

Buydens-Branchey et al. 2008

Lucas et al.

22

23

24

Year

Rogers et al.

21

22: 11/11

302

190: 96/94

120: 59/61 Middle-aged women with moderate-to severe psychological distress (with and without MDE diagnosis) Middle-aged women 91: 46/45 with moderate-to-severe psychological distress (without MDE diagnosis)

Substance abusers

Older subjects (≥65 years) independently living

Mild-to-moderate depressive disorder

Group

No. of subjects, total: treatment/placebo

1.05 g E-EPA 0.15 g E-DHA

2.25 g EPA + 0.5 g DHA + 0.25 other PUFAs 1.05 g E-EPA 0.15 g E-DHA

1.8 g EPA + DHA or 0.4 g EPA + DHA

0.63 g EPA 0.85 g DHA

Daily dose

Intervention

56

56

84

182

84

Duration (d)

PGWB HSCL-D-20 HDRS

PGWB HSCL-D-20 HDRS

DASS BDI GHQ STAI CES-D MADRS GDS-15 HADS-A POMS

Outcome measures

Yes

No

Yes

No

No

Statistical significant difference

EPA Eicosapentaenoic acid; e-EPA, ethyl eicosapentaenoate; DHA, docosahexaenoic acid; MDE. major depressive episode; BDI, Beck Depression Inventory; HDRS, Hamilton Depression Rating Scale; HDRS-SF, HDRS Short Form; YMRS, Young Mania Rating Scale; CGI, Clinical Global Impression; GAS, Global Assessment Scale; IDS, Inventory of Depressive Symptomatology; MADRS, Montgomery-Asberg Depression Rating Scale; MOAS, Modified Overt Aggression Scale; YBOCS, Yale-Brown Obsessive–Compulsive Scale; POMS, Profile of Mood States; EPDS, Edinburgh Postnatal Depression Scale; CDRS; Children’s Depression Rating Scale; CDI, Children Depression Inventory, IMT/DMT, Immediate and Delayed Memory Tasks; PSS, Perceived Stress Scale; DASS, Depression Anxiety and Stress Scales; GHQ, General Health Questionnaire; STAI, State-Trait Anger Inventory; CES-D, Center for Epidemiologic Studies Depression Scale; GDS-15, Geriatric Depression Scale; HADS-A, Hospital Anxiety and Depression Scale; PGWB, Psychological General Well-Being Schedule; HSCL-D-20, 20-item Hopkins Symptom Checklist Depression Scale.

2009

2008

2008

Study

No.

Table 1.3 (continued)

16 ´ A. Wilczynska-Kwiatek et al.

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Western Diet and Behavior: The Columbus Concept

17

University of Glasgow [7]. In 1990, a group of 63 adults with the diagnosis of post-viral fatigue syndrome were enrolled in a clinical trial of essential fatty-acid therapy involving daily administration of small doses of ω-3 PUFAs over a 3-month period. In consultation with the patients and using a Likert scale, doctors assessed overall condition, fatigue, depression, myalgia, dizziness, and poor concentration. At 1 month, 74% of patients on active treatment and 23% of those on placebos assessed themselves as improved over the baseline. At 3 months the corresponding figures were 85 and 17% (P 140/90 mmHg Authors Year Age State subjects (%) Pre-hypertension Rural Hussain et al. Gupta et al. Singh et al. Singh et al.

1988 1994 1997 1997

Urban Wasir et al. 1995 Gupta et al. 1997 Singh et al. 1997 Singh et al. 1997 Singh et al. 1998 Begum et al. 1998 Singh et al. 1998 Singh et al. 1998 Singh et al. 1998 Source: Singh et al. [44, 23].

20–70 20–80 20–65 25–64

Rajasthan Rajasthan UP UP

5,142 3,148 162 1,702

6.8 21.2 12.9 17.3

20–75 20–65 20–65 25–64 25–64 25–64 25–64 25–64 25–64

Delhi Rajasthan Moradabad Moradabad Moradabad Trivandrum Calcutta Nagpur Mumbai

679 2,212 152 1,806 3,212 1,497

6.2 31 32.8 22.3 25.3 30.7 19.1 24.2 28.0

Table 3.3 Prevalence of type 2 diabetes in India Year Author Place 1971 Tripathi et al. 1972 Ahuja et al. 1979 Gupta et al. 1984 Murthy et al. 1986 Patel 1988 Ramchandran et al. 1989 Kodall et al. 1989 Rao et al. 1991 Ahuja et al. 1992 Ramchandran et al. 1995 Singh et al. 1997 Ramchandran et al. 1998 Singh et al. 2000 Rammurthy et al. 2001 Ramchandran et al. 2001 Iyer et al. 2004 Sadokot et al. 2006 Mohan et al. 2006 Menon et al. 2008 Kumar et al. Source: Modified from Singh et al. [23].

Cuttack (central) New Delhi (north) Multicentre Tenali (south) Bhadran (west) Kudremukh (south) Gangavathi (south) Eluru (south) New Delhi (north) Madras (south) Moradabad Madras (south) Moradabad Kerala (south) National (DESI) Dombivill National Chennai Chennai Kolkata

Urban (%) 1.2 2.3 3.0 4.7 3.8 5.0 – – 6.7 8.2 7.9 11.6 6.0 12.4 12.1 6.2 5.9(4.3) 14.3 19.5 11.5

24.6 24.6 21.3 25.7 30.1

Rural (%) – – 1.9 – – – 2.2 1.6 – 2.4 2.5 – 2.9 2.5 – – 2.7 – – –

50

R.B. Singh et al. Table 3.4 Prevalence percentage of coronary artery disease and coronary risk factors in south Asians and British North Indians South Indians, Sri Lanka, UK South British Rural Urban urban urban Asians native Coronary artery disease 3.0 9.0 13.9 Smoking (men) (%) 30 25.6 44.6 Diabetes (%) 2.3 6.0 12.0 Hypertension (140/90 mm Hg) was significantly greater in south India and west India compared to east, central, and north India. The overall prevalence of hypertension in the five cities was 25.6% (n = 823) among women (Table 3.2). Data among men are not yet available. The prevalence of various types of hypertension was as follows: isolated systolic hypertension 2.9% (n = 96), borderline 14.9%, isolated diastolic hypertension 50.5%, definite hypertension 18.6%. Risk factors of hypertension were age [years mean (SD)] 44.2 [15] vs. 36.8 [12], BMI (kg/m2 ) 24.2 (2.7) vs. 22.2 (2.7) as well as sedentary behavior (89.9 vs. 40.9%), salt intake (87.9 vs. 47.8%), and alcohol consumption (20.5 vs. 5.2%). These observations indicate that the hypertension as well as its risk factors has become a public health problem in India as revealed by the Five City Study [23–25]. The prevalence of hypertension among subjects above 20 years varies between 25 and 30% in various countries of Asia [20–25].

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3.2 Blood Pressure Variability There is a great need of conducting population surveys with ambulatory blood pressure monitoring to demonstrate vascular variability disorders (VVDs) as proposed by Franz Halberg, Germaine Cornelissen, and Othild S. from Halberg Chronobiology Center, University of Minnesota Medical School, Minneapolis, USA, and Kuniaki Otsuka, Tokyo Women’s Medical University, Tokyo, Japan, for the diagnosis of circadian-hyperamplitude tension, mesor hypertension, and ecphasia because south Asians living in the United States appear to have significantly greater risk of these problems compared to Caucasians. Collaborators may contact Dr. Germaine Cornelissen (e-mail: [email protected]).

3.3 Type 2 Diabetes Mellitus It is clear from Table 3.3 that the prevalence of type 2 diabetes mellitus was quite low before 1984 among both rural (1.6–2.4%) and urban (3.4–4.5%) populations of India. There has been a marked increase in the prevalence of diabetes in the last two decades. In rural populations it became 1.6% at Eluru in Andhra Pradesh to 2.9% at Moradabad in UP. In urban populations, the prevalence of type 2 diabetes was 5% at Kudremukh as observed by Ramchandran et al. in 1988, which increased to 14.3% in Madras as reported by Mohan and coworkers in 2006 (Table 3.5). Type 2 diabetes, hypertension, and CAD appear to be a manifestation of metabolic syndrome among Indians [36–38]. The prevalence of metabolic syndrome has been estimated to be between 20 and 25% among subjects above 20 years of age in south Asia [23–25]. Table 3.5 Genetic and other specific risk factors common in south Asians for unexplained heart disease Genetic or environmental Other risk factors 1. Insulin resistance and hyperinsulinemia 2. Poor beta-cell function 3. Increased prevalence of type II diabetes 4. Increased lipoprotein(a) 5. Increased angiotensin-converting enzyme 6. High Apo-B

1. Increased plasminogen activator inhibitor-1 2. Decreased tissue plasminogen activator 3. Decreased antioxidant vitamins A, C, β-carotene, E, Se, Zn, flavonoids, other polyphenolic substances 4. Low high-density lipoprotein cholesterol 5. Elevated homocysteines 6. Low Apo A1 7. Increased heart rate and BP variability 8. Increased small dense LDL cholesterol 9. Increased ω-6/ω-3 ratio in the diet. 50:1 due to increased intake of sun flower, corn, and soya bean oils

3.4 Coronary Artery Disease The risk factor-adjusted CAD rates are twofold greater among overseas south Asians compared to Caucasians [1–4, 17–38] (Table 3.4). South Asians develop clinical manifestations such as myocardial infarction (MI) at a young age and often follow a malignant course [39, 40]. Approximately 50% of the first MI among south Asian men occurs before the age of 55 years

52

R.B. Singh et al.

and 25% occurs before 40 years of age. The CAD mortality among south Asians younger than 30 years of age has been described to be threefold higher than that in whites in the United Kingdom and 10-fold higher than that in Chinese in Singapore. The same pattern of CAD is observed among all south Asians—whether living abroad or within Indian subcontinent—which include persons of Indian, Pakistani, Bangladeshi, and Sri Lankan origin. In urban population of south Asia, there has been a 10-fold increase in the prevalence of CAD in the last three decades. CAD appears to be more common in urban areas than in developed countries. Studies from rural areas have reported a threefold lower prevalence of CAD compared to cities; however, a threefold increase has been observed in these populations, in the last few decades, particularly in south India and Punjab. CAD prevalence has been studied in the urban populations of Chandigarh, Haryana, Delhi, UP, Rajasthan, and Kerala. The prevalence was lowest of 4% in Rohtak in the 1970s and highest of 14% in Trivandrum, as reported by Beegom and Singh [35]. The prevalence of CAD and its risk factors is significantly higher in south India compared to north India, in both rural and urban areas. The Five City Study provided most interesting evidence that CAD has become an important concern in India. CAD was threefold more common in the urban north India at Moradabad (9.0%), fourfold more common in urban south India at Trivandrum (13.9%), Mumbai (11.6%) in west India, Nagpur (10.0%) in central India, and Kolkata (8.0%) in east India, compared to rural populations. The risk of CAD, type 2 diabetes, and hypertension is higher in higher social classes 1–3, than among lower social classes in both rural and urban subjects.

4 Social Class, Coronary Risk Factors, and the Asian Paradox Social class has become an important determinant of CVD and diabetes in the industrialized countries. In south Asian countries, such as India, Pakistan, Bangladesh, Nepal, and Sri Lanka, as well as other Asian countries, such as Thailand, Malaysia, Philippines, Indonesia, Myanmar, North Korea, higher social classes 1–3 have greater prevalence of hypertension, CAD, and diabetes compared to lower social classes [20–26]. However, in industrialized countries of Asia, lower social classes have greater burden of CVD and diabetes [20–22]. While tobacco consumption is as common in Asia as in the Western world, other conventional risk factors, such as hypercholesterolemia, hypertriglyceridemia, obesity, central obesity, diabetes mellitus, and hypertension, are not that common and severe as in the industrialized countries. The paradox is that dietary intakes and physical activity explain only a part of differences in prevalence and risk of CVD and diabetes in these population groups (Tables 3.4 and 3.5). However, these risk factors have become a public health problem in these countries and would soon become more common than in Western countries. The Asian paradox is that the risk of risk factors is greater at relatively lower levels of risk factors, resulting in increased susceptibility and severity of atherosclerosis and rapid emergence of CAD at a younger age [20–22, 41–44]. This phenomenon occurs in all developing populations due to nutritional transition from poverty to affluence among populations that are adapted to survive on low nutrient intake and physically demanding occupations, which may be the cause of the Asian paradox [41–45]. It is a paradox in south Asia that serum cholesterol, body fat, dietary fat intake are higher among higher social classes, whereas in the Western populations, these risk factors are greater among lower social classes, causing a greater

3

The Asian Paradox

53

increase in CAD [43–45]. Such observations have also been reported from other countries of Asia [46–51]. In one study [46], the prevalence of risk factors in relation to social class was studied. Body mass index >25 and >27, central obesity, and sedentary lifestyle were significantly more common among higher social classes 1–3 compared to lower social classes (Table 3.6). Salt intake and tobacco consumption showed no social class difference. Table 3.6 Prevalence of risk factors (n, %) of chronic diseases in relation to social class Central BMI BMI obesity Sedentary Salt intake Social classes (>27 kg/m) (>25 kg/m) (WHR>0.85) lifestyle (>6 g/day) Social class 1 209(21.2) (n = 985) Social class 2 130(16.4) (n = 790) Social class 3 60(8.9) (n = 774) Social class 4 18(3.0) (n = 602) Social class 5 8(3.8) (n = 206) Total 425(13.0) (n = 3357) Mantel-Haenzel 7.55 χ2 P-value once/week)

612(62.1)

955(96.9)

908(92.2)

496(50.3)

81(8.1)

395(50.0)

452(57.2)

564(71.4)

421(53.3)

47(5.9)

331(19.5)

265(39.3)

285(42.3)

451(66.9)

45(6.7)

39(6.4)

72(11.9)

90(14.9)

398(66.1)

48(7.9)

12(5.8)

18(8.7)

18(8.7)

123(59.7)

18(8.7)

1189(36.5)

1762(54.0)

1865(57.2)

1889(58.0)

241(7.4)

12.17

11.66

12.65

3.14

3.16