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Teaching a very low fat semi-vegitarian diet vs. the standard modified fat diet : effects on cardiac… Johnson, Frances Nakauchi 2000

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TEACHING A VERY LOW FAT SEMI-VEGETARIAN DIET VS THE STANDARD MODIFIED FAT DIET: EFFECTS ON CARDIAC RISK FACTORS AND NUTRITION-RELATED QUALITY OF L I F E by FRANCES NAKAUCHI. JOHNSON B.H.E., U n i v e r s i t y o f B r i t i s h C o lumbia, 1975 A THESIS SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE i n THE FACULTY OF GRADUATE STUDIES (Human N u t r i t i o n Graduate Program i n t h e F a c u l t y o f A g r i c u l t u r a l S c i e n c e s ) We a c c e p t t h i s t h e s i s as c o n f o r m i n g t o t h e r e q u i r e d s t a n d a r d s THE UNIVERSITY OF BRITISH COLUMBIA September, 2000 © F r a n c e s N a k a u c h i Johnson, 2000 I n p r e s e n t i n g t h i s t h e s i s i n p a r t i a l f u l f i l m e n t o f t h e r e q u i r e m e n t s f o r an advanced degree a t t h e U n i v e r s i t y o f B r i t i s h C o l u m b i a , I agree t h a t t h e L i b r a r y s h a l l make i t f r e e l y a v a i l a b l e f o r r e f e r e n c e and s t u d y . I f u r t h e r agree t h a t p e r m i s s i o n f o r e x t e n s i v e c o p y i n g o f t h i s t h e s i s f o r s c h o l a r l y p u r p o s e s may be g r a n t e d by t h e head o f my department o r by h i s o r h e r r e p r e s e n t a t i v e s . I t i s u n d e r s t o o d t h a t c o p y i n g o r p u b l i c a t i o n o f t h i s t h e s i s f o r f i n a n c i a l g a i n s h a l l not be a l l o w e d w i t h o u t my w r i t t e n p e r m i s s i o n . Department o f ^jUusryxJCvL/ ^f^uX^^Uy^J The U n i v e r s i t y o f B r i t i s h Columbia Vancouver, Canada Date ,ALJ%CJ*KJUAS } 2 OOP \ Abstract The effect of instructing adults with cardiovascular disease on a lacto-ovo-vegetarian plus fish diet (15% total fat, <6% saturates, <100 mg cholesterol) or the standard diet (30% fat, 7-10% saturates, 200-300 mg cholesterol) was studied. Thirty-nine subjects were randomly assigned to the experimental or the control diet for 12 weeks. Measurements of weight, waist circumference, serum lipids and nutrition-related quality of life were taken before and after the intervention. Diets were monitored by 3-day food records and analyzed using the Nutritionist IV™ for Windows Version 4.1 diet analysis program. Adherence was self-reported by completion of a daily calendar. Statistical analyses were performed using SPSS 9.0 for Windows. The General Linear Model repeated measures procedure was used to compare the effects of the intervention on the two groups. Correlation analysis and multiple linear regression analysis were also conducted. There was no difference between the two groups in actual diet followed during the intervention (17.4% total fat, 4.4% saturated fat, 135 mg cholesterol per day) nor in outcome measures. Both groups benefited equally from diet intervention. Weight decreased by 2.1% (pO.OOl), waist circumference by 1.7% (pO.Ol), total cholesterol by 3.7% (p<0.05), and low density lipoprotein (LDL)-cholesterol by 5.3% (p<0.001). Scores for nutrition-related health perceptions improved significantly by 21 ± 35% (p=.002). Multiple linear regression analysis showed that 26% of the difference in L D L -cholesterol (p=.003) and 45% of the % difference in weight (p<.001) were accounted for by difference in energy intake and nutrition-related perceptions of health. Adherence i i scores showed significant inverse relationships with total (p=.002) and saturated fat (p=.001) intake. Nutrition-related health perceptions emerged as the predictor for adherence (p=.002). In conclusion, there appears to be no difference in short-term outcome by teaching a more restricted diet to subjects already on a low fat diet in a cardiac rehabilitation program. However, these results suggest that perceptions regarding one's health impact significantly on factors that affect energy intake, weight changes, and overall adherence to diet. Therefore, dietitians could emphasize the health benefits of dietary changes to encourage greater adherence to dietary principles. i i i Table of Contents P A G E A B S T R A C T ii T A B L E OF CONTENTS iv LIST OF T A B L E S vii A C K N O W L E D G E M E N T S ix CHAPTER I INTRODUCTION .- 1 CHAPTER II LITERATURE REVIEW 1. Introduction 4 2. Dyslipidemia and C V D 5 3. Dyslipidemia in Women vs Men 9 4. The Efficacy of Conventional Dietary Guidelines in Controlling Dyslipidemia.... 11 5. The Efficacy of Very Low Fat Diets in Controlling Dyslipidemia and C V D Risk 15 6. The Evidence for Vegetarian Diets in Reducing Cardiovascular Risk 19 7. The Evidence for Including Fish in a Diet for Reducing C V D Risk 21 8. Low Fat Diets and Body Weight Change - Their Effect on Blood Lipids 25 9. Implications for Planning the Optimal Diet in Controlling Blood Lipids and C V D Risk 27 10. Summary 29 11. Statement of the Problem 30 CHAPTER III M E T H O D O L O G Y 1. Overview of Design 32 2. Setting 32 3. Sample size 33 4. Recruitment 34 5. Diets a. Description of Diets Used 36 b. Diet Instruction 37 c. Diet Monitoring 37 6. Anthropometric Measurements a. Body Weight and Body Mass Index. 38 b. Waist Circumference 39 7. Lipid Measurements 39 8. Nutrition-related Quality of Life Measurements 40 9. Other Records Used 41 10. Data Analyses 41 a. Food Intake Data 41 iv b. Nutrition-related Quality of Life 42 c. Analysis of Adherence 42 d. Statistical Analysis 43 11. Miscellaneous 44 CHAPTER IV RESULTS 1. Recruitment 45 2. Subject Characteristics 46 3. Intervention - Diet During Study 48 4. Outcome Measurements 52 5. Correlation Between Diet and Outcome Measures a. Correlation Between Diet Changes and Changes in Outcome Variables... 57 b. Correlation Between Diet Followed During the Study and Outcome Measures 60 6. Correlation Among Outcome Measures 64 a. Correlation Among Changes in Outcome Measures 64 b. Correlation Between Quality of Life Measurements and Changes in Outcome Measures 68 7. Adherence in Relation to Diet and Outcome Measurements 71 a. Correlation Between Adherence and Diet 71 b. Correlation Between Adherence and Outcome Measures 73 8. Multiple Linear Regression: 75 CHAPTER V DISCUSSION 1. Overview 80 2. Effect of Experimental Diet vs Control Diet on Outcome Measures 81 3. Diet and Outcome of Both Groups as a Whole 86 4. Effect of Fish in the Experimental Diet 91 5. Feasibility of Experimental Diet 92 6. Relationship Between Diet and Quality of Life 94 7. Nutrition-related Health Perceptions and Adherence to Diet 96 8. Limitations 98 9. Implications for Dietetic Practice. 104 10. Directions for Further Research 105 11. Conclusions 106 REFERENCES 108 APPENDICES Appendix A. Ethics Approval, University of British Columbia 119 Appendix B. Ethics Approval, St. Paul's Hospital 120 Appendix C. Information Sheet for Interested Subjects 121 Appendix D. Subject Consent Form 122 Appendix E. The Experimental Diet 126 V Appendix F. The Control Diet 134 Appendix G. Diet History 139 Appendix H. Food Records 141 Appendix I. Adherence Chart 143 Appendix J. Nutrition-related Quality of Life Questionnaires 144 Appendix K. Time Line Record 150 Appendix L . Cookbook 151 v i List of Tables Page Table 1. Subject characteristics 46 Table 2. Comparison of initial diet of subjects in the control and experimental groups 47 Table 3. Comparison of initial diet to diet followed during study by the two groups, analyzed by repeated-measures A N O V A (time = within-subject factor, group = between-subject factor) 49 Table 4. Comparison of diets instructed and actual diet followed 51 Table 5. Outcome of teaching the conventional or semi-vegetarian diet (repeated-measures A N O V A , time=within-subject factor, group=between-subject factor) a. anthropometric measurements b. lipid measurements c. quality of life measurements 54 Table 6. Correlation between changes in diet and changes in anthropometric measures 58 Table 7. Correlation between changes in diet and changes in lipid measurements 59 Table 8. Correlation between changes in diet and changes in quality of life measurements 60 Table 9. Correlation between diet followed during study and anthropometric outcome measurements 61 Table 10. Correlation between diet followed during study and lipid measurement outcome 62 Table 11. Correlation between quality of life measurement outcome and diet followed during study 63 Table 12. Correlation between changes in anthropometric measures and changes in lipid measurements 65 Table 13. Correlation between changes in quality of life measurements and changes in anthropometric measures 67 Table 14. Correlation between quality of life during the study and changes in anthropometric measurements 69 Table 15. Correlation between quality of life measurements during the study and changes in lipid outcome....' 70 Table 16. Correlation between adherence and diet variables during study 72 v i i Page Table 17. Correlation between adherence and changes in diet variables 73 Table 18. Correlation between adherence and changes in outcome measures.. 74 Table 19. Correlation of adherence with outcome measures 75 Table 20. Step wise entry multiple linear regression of significantly related variables to changes in outcome measures 78 Vlll Acknowledgments So much has happened in the past five years since I have been back to university, and I know that I could not have come this far without the help and support of many many people. I am grateful to the Healthy Heart Program at St. Paul's Hospital and the Human Nutrition Program at U.B.C. in enabling me to pursue my studies. I cannot say enough thank yous to my advisor, Dr. Susan Barr for her expert guidance and encouragement throughout my entire university time. I must thank my colleagues at work, especially Shauna Ratner who recruited subjects, and to Donald Barker and Shauna who, despite their busy schedules, counseled and followed their patients who had agreed to be in this study. I am grateful to the study participants in the Healthy Heart Program, without whom this study would not have been possible. I am also very thankful for the members of my committee, Dr. Jiri Frohlich and Dr. Ryna Levy-Milne for their guidance and support in implementing the study and completing my thesis. I must mention that Dr. Frohlich has been my mentor in lipid management over the past almost 20 years, giving me incentive to further my studies in this area. I would like to express my appreciation to Dr. Gwen Chapman for giving me an appetite for research in her Human Nutrition 500 class, and for reviewing my thesis. Finally, I know that returning to school after so many years would have been impossible without the complete support and patience of my family. So, Michael, Terumi, and Mika - it's done, thanks to you all! ix CHAPTER I Introduction Cardiovascular disease (CVD) remains the number one cause of death in North America, claiming 79,457 lives in Canada in 1997 (Heart and Stroke Foundation of Canada, 1999). Modifying diet can reduce some of the major risk factors for heart disease such as obesity and elevated cholesterol levels (Forrester et al., 1996). However, the optimal diet for controlling cardiac risk factors has not yet been found. Major national and provincial health organizations such as the American Heart Association (AHA), the National Cholesterol Education Program (NCEP), and the Working Group on Hypercholesterolemia and Other Dyslipidemias recommend similar diet principles for primary and secondary prevention of heart disease and reduction of serum cholesterol levels (American Heart Association Nutrition Committee, 1996; Fodor, Frohlich, Genest, Jr., McPherson, 2000; National Cholesterol Education Program Adult Treatment Panel II, 1994; Stone, Nicolosi, Kris-Etherton, Ernst, Krauss & Winston, 1996). The diet generally recommended is a modified fat, low cholesterol diet consisting of 30% of energy as fat, 7 - 10% as saturated fat, and 200 - 300 mg of cholesterol per day. Although the conventional diet has been shown to be effective in controlling blood lipid levels, some researchers suggest that a more aggressive dietary approach that further restricts total and saturated fat intake may be required to maximize the effects of dietary manipulation, especially in those people who are at high risk for C V D . Such very low fat diets, especially when accompanied by weight loss have been shown to reduce blood cholesterol levels and other cardiac risk factors beyond what is achieved by the 1 conventional diet in some clinical trials (Lichtenstein and Van Home, 1998). One example of such a diet is that used in the Lifestyle Heart Trial (Ornish et al., 1990). Twenty-eight patients randomly assigned to a lifestyle modification program along with a very low fat vegetarian diet (<10% fat, 5 mg cholesterol per day) for 1 year showed a 24% decrease in total cholesterol, and a 37.4% decrease in LDL-cholesterol. Regression of atherosclerosis occurred in 82% of experimental-group subjects. Despite such positive reports among highly motivated subjects, the feasibility of such diets for most people is uncertain. Although fat consumption has been declining in North America, much of the population has difficulty in making long term major changes to their diets (Barnes and Terry, 1991;Center for Disease Control and Prevention, 1994). Such changes as elimination of most dairy products and all meat products as suggested in some aggressive diet approaches are not feasible on a regular basis for most people accustomed to typical North American eating patterns. Actual dietary intake is determined not only by what is considered nutritious, but also by psychological, emotional, social and cultural issues. Thus, severe diet modification may impact on factors that may compromise quality of life, reducing the likelihood of long term adherence. Therefore, the question arises as to whether a modified version of the very low fat vegetarian diet that incorporates fish, would be achievable and have more impact than the conventional diet on reducing cardiac risk. Fish intake, perhaps mediated by its omega-3 fatty acid and low saturated fat content has been associated with improved cardiac risk (Burr et al., 1989; Connor, 2000). Furthermore, including fish may add more variety and 2 flexibility to the vegetarian diet, thereby allowing greater feasibility of a very low fat diet program. The purpose of this study, therefore, was to compare the effects of teaching a very low fat semi-vegetarian (lacto-ovo plus fish) diet (15% fat, < 6% saturated fat, < 100 mg cholesterol per day) to the conventional modified fat diet in adults with C V D on serum lipid and lipoprotein concentrations, anthropometric measurements and nutrition-related quality of life. Feasibility of the experimental diet was also explored by analysis of food intake records, self-reported adherence, and nutrition-related quality of life measures. 3 CHAPTER II Literature Review 1. Introduction Cardiovascular disease ( C V D ) mortality has been declining in Canada since the 1960's, however, it still remains the main cause of death, accounting for 36% of all deaths in 1997 (Heart and Stroke Foundation of Canada, 1999). Although risk factors for C V D such as age, gender, and family history cannot be modified, other factors which can be altered to reduce risk include elevated plasma lipids, hypertension, smoking, diabetes, physical inactivity and obesity (Forrester et al., 1996). Nutrition plays a major role in the modification of many of these modifiable C V D risk factors such as elevated blood lipids, hypertension, diabetes and obesity. This review w i l l focus primarily on the role of nutrition in the modification of elevated blood lipids, and the implications for planning the optimal diet for reducing C V D risk. It w i l l include the following: 1. an overview of the relationship between dyslipidemia and C V D 2. the evidence for including both men and women in a study examining the management of dyslipidemia 3. the efficacy of conventional dietary guidelines in controlling dyslipidemia and C V D risk 4. the efficacy of very low fat diets in controlling dyslipidemia and C V D risk 5. the evidence for vegetarian diets in reducing C V D risk 6. the evidence for including fish in a diet for reducing C V D risk 7. the effect of body weight change on blood lipids 4 8. implications for planning the optimal diet for reducing C V D risk - consideration of feasibility of the diet and quality of life, as well as optimal control of blood lipids 9. summary and statement of the problem 2. Dyslipidemia and CVD The role of elevated blood cholesterol levels in contributing to the development and clinical manifestations of C V D has been studied extensively. High blood cholesterol is defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel II (1994) as: total cholesterol > 5.2 mmol/L, LDL-cholesterol > 4.1 mmol/L (with 1 risk factor), LDL-cholesterol > 3.4 mmol/L (with 2 or more risk factors), or L D L -cholesterol > 2.6 mmol/L (for those with CVD). In Canada, the Working Group on Hypercholesterolemia and Other Dyslipidemias has developed recommendations which provide guidelines for target lipid values based on one's 10-year risk of coronary artery disease (CAD) (Fodor, Frohlich, Genest, & McPherson, 2000). Target lipid values for those at very high risk of C A D or with a history of C V D have been established as L D L -cholesterol < 2.5 mmol/L, total cholesterohHDL-cholesterol ratio < 4, and triglyceride < 2.0 mmol/L. In the British Columbia Heart Health Survey conducted in 1989, the mean plasma total cholesterol concentrations in males and females ages 35 - 64 years were 5.5 mmol/L and 5.4 mmol/L respectively (Ministry of Health, Province of British Columbia and Welfare Canada, 1990). Among over 26,000 participants from nine Canadian provinces studied from 1986 to 1990, 46% had elevated total plasma cholesterol levels (> 5.2 mol/L) and 36% had elevated plasma LDL-cholesterol levels (> 3.4 mmol/L) (Connelly, MacLean, Horlick, O'Connor, Petrasovits & Little, 1992). These data 5 indicate that almost one in two adults in Canada is at increased risk for C V D due to elevated blood cholesterol (Connelly et al., 1992). It is suggested that even a modest reduction of blood cholesterol levels in Canadian adults could reduce the incidence of C V D in Canada by 10% - 30% in the next decade (Ministry of Health, Province of British Columbia and Welfare Canada, 1990). Epidemiological studies have illustrated the association between high blood cholesterol and C V D . The Framingham Heart study measured serum cholesterol levels in 1959 men and 2415 women in 1951 to 1955 and studied the relationship between cholesterol levels and mortality for 30 years (Anderson, Castelli & Levy, 1987). In those under age 50 years at time o f initial cholesterol measurement, cholesterol levels were related to 30 year all-cause and C V D mortality. Overall death rate increased 5% and C V D death rate increased 9% for each increase of 10 mg/dL in serum cholesterol level. The twenty-five year follow-up of the Seven Countries Study compared the relationship between serum total cholesterol and long-term mortality from coronary heart disease (CHD) in 5 European countries, the U .S . and Japan (Verschuren et a l , 1995). Results indicated that a 0.50 mmol/L increase in total cholesterol corresponded to a 17% increase in long term C H D mortality. Numerous intervention trials have provided support for the role of lowering serum cholesterol levels, particularly LDL-cholesterol levels to reduce C V D progression and mortality. In the L ip id Research Clinics Coronary Primary Prevention Trial that studied 3806 men at risk for, but without C V D , a combination of diet and cholestyramine reduced LDL-cholesterol by 18.9% as compared to 8.6% in the diet and placebo group (Lipid Research Clinics Program, 1984). There was a 19% reduction in nonfatal 6 myocardial infarctions and a 24% reduction in C V D mortality in the drug and diet group as compared to the placebo and diet group. The Scandinavian Simvastatin Survival Study (4S Study) treated 4444 patients with known C V D with either simvastatin or placebo (Scandinavian Simvastatin Survival Study Group, 1994). The simvastatin group showed a decrease in LDL-cholesterol of 35%, a reduction in nonfatal myocardial infarction of 37% and a reduction in overall mortality of 30% after 5 years as compared to the placebo group. The West of Scotland Coronary Prevention Study treated 6595 men with hypercholesterolemia, but with no history of myocardial infarction with either pravastatin or placebo for 5 years (Shepherd et al., 1995). LDL-cholesterol was reduced by 26% as compared to the placebo group, and the relative risk of a coronary event was reduced by 31%. These clinical trials provide evidence for the benefits of reducing total and LDL-cholesterol in both primary and secondary prevention of coronary heart disease (CHD). LDL-cholesterol is directly involved in the process of atherosclerosis (Berliner et al., 1995; Fuster, Gotto, Libby, Loscalzo & McGil l , 1996). The development of the fatty streak is initiated by the transport of L D L into the artery wall through injured or dysfunctional endothelium. The L D L is trapped in the extracellular matrix of the subendothelial space where it is then modified by oxidation. H D L may help to reduce the accumulation of L D L in the vessel wall by inhibiting the oxidation of L D L , and by contributing to active L D L removal from the vessel wall. The oxidation of L D L results in an inflammatory response which induces monocytes to the lesion. Monocytes then differentiate into macrophages which may cause further oxidation of L D L and accumulation of more cholesterol in the cell, resulting in the development of foam cells. 7 As foam cells become saturated with cholesterol and rupture, they can release these lipids causing further endothelial damage, inflammation, proliferation of monocyte macrophages and smooth muscle foam cells, and progression of the atherosclerotic lesion or plaque. An ischemic event occurs when there is plaque disruption in the advanced lesion with subsequent thrombus formation and lumen occlusion. Low HDL-cholesterol is classified as a major risk factor for CHD while high HDL-cholesterol (> 1.6 mmol/L) is considered to be a "negative" risk factor (National Cholesterol Education Program, 1994). The Helsinki Heart Study was a five year trial which studied the efficacy of increasing serum HDL-cholesterol and lowering other lipoproteins by using gemfibrozil (Frick et al., 1987). Mean reductions in total and L D L -cholesterol of 8%, reduction in triglycerides of 35%, and increase in HDL-cholesterol of 10% were seen in the gemfibrozil treated group, whereas there was little change seen in the placebo group. These changes in the gemfibrozil treated group were accompanied by a 26% reduction in coronary deaths and 34% reduction in the incidence of CHD. The beneficial effects seen in the study was attributed largely to the increase in HDL-cholesterol. The direct atherogenecity of triglycerides has not definitively been shown, however, various conditions are associated with elevated triglycerides which are thought to contribute to atherosclerosis (Berliner et al., 1995; Gotto A M , 1998). These conditions include: small dense L D L particles, decreased HDL, postprandial lipidemia, increased V L D L remnants, abdominal obesity, and increased insulin resistance. Thus reduction in elevated triglyceride levels are thought to be beneficial, although perhaps indirectly, in the prevention of atherosclerosis. 8 Studies show that the modification of blood lipids is a major goal for reducing the risk for C V D . Interventions that have had impact on modifying blood lipids include medication, exercise, and diet. The extent to which each of these interventions can modify blood lipids appears variable (Cox, Mann, Sutherland & Ball, 1995; Denke, 1995; McNamara, 1995). Much research has been done on the role of individual fatty acids and other dietary components in altering blood lipids, and their results have been summarized in major reviews (Caggiula & Mustad, 1997; Fraser, 1994; Grundy, 1996; Illingworth, Hatcher, Pappu, Newcomb & Connor, 1995; Katan, Zock & Mensink, 1994; Kris-Etherton et al., 1988; Kris-Etherton & Yu, 1997; Mann, 1997; Stone, Nicolose, Kris-Etherton, Ernst, Krauss & Winston, 1996). The challenge ultimately, though, is to incorporate these pertinent research results into an overall feasible diet that can most favourably affect blood lipids. 3. Dyslipidemia in Women vs Men Most studies which examine the effectiveness of various treatments for C V D or dyslipidemia have been done with men, however, according to epidemiological studies, C V D is the leading cause of death in women as it is in men (Castelli, 1988; Kannel & Wilson, 1995). The actual number of myocardial infarctions in men and women is similar, however, women develop C V D an average of 10 years later than men with the rate of C V D accelerating rapidly after menopause. In Canada during 1997, 39,838 men and 39,619 women died from C V D (Heart and Stroke Foundation of Canada, 1999). Although C V D occurs later in women than in men, there are reports of increased mortality after myocardial infarction in women. It is suggested that the older age and 9 higher prevalence of unfavourable risk characteristics in women account for the increased mortality after myocardial infarction (Vaccarino, Krumholz, Berkman & Horwitz, 1995). Most of the risk factors for C V D are common to both men and women including elevated blood lipids, smoking, hypertension, diabetes, obesity and stress (Barret-Connor, 1997; Castelli, 1988; Kannel &Wilson, 1995). However, there are reports of some differences between men and women in relation to the effects of dyslipidemia on cardiovascular risk. In the Framingham Heart Study, high serum triglyceride concentration was positively correlated with C V D risk in both genders, but was an independent risk factor only in women (Castelli, 1988). It is also suggested that low HDL-cholesterol is a stronger predictor of C V D in women than in men since very low levels are relatively infrequent in women (Houlden, 1991). Treatment guidelines and goals are the same for both men and women (Houlden, 1991). Apart from the use of hormone replacement therapy, studies so far have indicated that women's lipid levels respond to diet and medication treatment similarly to men. For example, in one study, when serum lipid response to the American Heart Association Step 1 diet was examined in 76 women and 108 men with hypercholesterolemia, both men and women showed similar results (Geil, Anderson &Gustafson, 1995). Thus it is appropriate and essential that intervention studies for reducing the development and progression of C V D include both men and women. 10 4. The Efficacy of Conventional Dietary Guidelines in Controlling Dyslipidemia Dietary modification is the first line of treatment recommended for controlling high blood cholesterol (Fodor et al., 2000; National Cholesterol Education Program, 1994). To achieve optimal cholesterol levels, the diet recommended by most national and provincial organizations including the American Heart Association (AHA) (1996), the National Cholesterol Education Program (1994), and the Working Group on Hypercholesterolemia and Other Dyslipidemias (2000) is one consisting of 30% or less of energy from fat, 8% - 10% of energy from saturated fat, and less than 300 mg of cholesterol per day (NCEP Step I Diet). Further reductions of saturated fat intake to < 7% of energy and cholesterol to less than 200 mg per day (Step II Diet) are recommended i f the serum cholesterol goals are not achieved. By following the Step I diet, the expected plasma total and LDL-cholesterol reduction is about 10% and 12% respectively, while the Step II diet is expected to lower total and LDL-cholesterol by 13% and 16% respectively (Yu-Poth, Zhao, Etherton, Naglak, Jonnalagadda & Kris-Etherton, 1999). The degree of reduction in serum cholesterol levels by dietary modification, however, appears to be variable depending on baseline cholesterol levels, dietary intake before starting the modified diet, the degree of compliance, and individual biological response (Cox et al., 1995; Denke, 1995; McNamara, 1995). Denke and Grundy (1994) have suggested that among free-living moderate risk men, implementation of the Step I guidelines will avoid the necessity of medication in 50% of the population. They suggest that 25% are biologically resistant to 11 diet modification, and that a further 25% are too noncompliant to induce cholesterol lowering. Studies have been done to examine the efficacy of the conventional modified fat diet in modifying lipid levels and other measures of cardiac risk in various populations. In one study using free-living subjects, following an A H A Step 1 diet for 8 weeks resulted in reductions in serum total cholesterol levels of 7.2% in men and 9.2% in women with hypercholesterolemia (Geil et al., 1995). In patients with hypercholesterolemia referred to the Lipid Clinic at the Montreal Clinical Research Institute, 8 weeks of following the Step 1 or 2 diets resulted in reduction in plasma cholesterol of 5.7%, LDL-cholesterol reduction of 7.3%, and weight loss of 2.4% (Dallongeville, Leboeuf, Blais, Touchette, Gervais & Davignon, 1994). In the same study, patients with hypertriglyceridema following the Step 1 diet experienced reductions in plasma cholesterol of 4.8%, plasma triglycerides of 20.7%, and weight loss of 2.8%. The St. Thomas' Atheroma Regression Study (STARS) assessed the effects of a moderate lipid lowering diet (27% total fat, 8-10% saturated fat, cholesterol 100 mg/lOOOkcal, increased soluble fibre) on plasma lipid levels and coronary arteries of subjects with C V D by analyzing coronary angiograms (Watts et al, 1992). Ninety men with C V D were randomized into usual care, modified diet or modified diet and cholestyramine for a period of 39 months. Lipid levels remained stable in the usual care group, while cholesterol levels were reduced by 14.2% in the diet group, and by 25.3% in the diet and medication group. Angiographic results showed progression of coronary narrowing in 46% of the control group, but in only 15% of the diet group, and 12% of the diet and medication group. 12 Other studies have used subjects who are not free-living, but who were provided with foods in a metabolic research unit. Normolipidemic subjects given a NCEP Step II diet with weight kept constant, had reductions in plasma total cholesterol of 20%, L D L -cholesterol of 21% and HDL-cholesterol of 16% while provided meals for 24 weeks in a metabolic research unit at Tufts University (Schaefer et al., 1995). Hyperlipidemic subjects at the research unit on the same diet for 6 weeks under isocaloric conditions reduced plasma total cholesterol by 16%, LDL-cholesterol by 18% and HDL-cholesterol by 15%. Lopez-Miranda et al (1994) studied the response of participants to a Step II diet as compared to the typical American diet (39% fat) at three different research centers in the U.S. LDL-cholesterol was reduced an average of 15% in males and 8% in post-menopausal women following the Step II diet as compared to the high fat diet. Other studies have suggested that there may be no effect of conventional diet guidelines on lipid levels. Forty-one healthy obese (body mass index 29-30 kg/m2) postmenopausal women with borderline cholesterol levels were matched into one of three treatment groups for 24 weeks in a study examining the effects of diet and exercise on C V D risk factors (Fox, Thompson, Butterfield, Gylfadottir, Moynihan & Spiller, 1996). Groups consisted of diet (500 calorie deficit) and exercise (200 calories expenditure), diet (500 calorie deficit), or diet (700 calorie deficit). A l l diets were based on the A H A guidelines with 30% of calories as fat. Although significant weight loss was achieved in all three groups, no significant change in blood lipid concentrations or other C V D risk factor reduction was achieved as compared to baseline measurements. It is suggested that possibly differences in lipid results may have been more significant i f initial lipid levels had been more abnormal, or i f the women had dieted more stringently. In a cross-over 13 study comparing a low fat diet (22% fat) to a high fat diet (39% fat), but with similar fatty acid composition and calorie content, 11 healthy men (20-35 years) with normal cholesterol levels were given each diet for 50 days (Nelson, Schmidt & Kelley, 1995). There was no difference found in plasma total, L D L or HDL-cholesterol levels between the low fat and high fat diets. However, this study involved only eleven normolipidemic healthy male subjects, and it is possible that results may differ for those with C V D or with dyslipidemia. It is possible that dietary manipulation may also modify cardiovascular risk by mechanisms other than its effect on blood lipid levels. In the Lipid Research Clinics Prevalence Follow-up Study which followed North American men and women for 12 years, coronary heart disease mortality was found to be positively related to increased total fat, saturated fat and monounsaturated fat intake, and negatively related to carbohydrate intake in 30 - 59 years old subjects (Esrey, Joseph & Grover, 1996). However, the relative risks for the dietary variables did not change when serum lipids and other known cardiac risk factors were added to the regression model, suggesting that the relationship between diet and C V D mortality was mediated by the influence of diet on factors other than that on serum lipid levels. The NCEP Adult Treatment Panel II (1994) suggests that i f the desired goal for blood cholesterol has not been attained, and weight loss is needed in patients with no C V D , further reduction of total and saturated fat beyond the Step II diet can be attempted before drug therapy is considered. It does not state, however, how much further reduction is considered optimal. The Scientific Conference on the Efficacy of Hypocholesterolemic Dietary Interventions discusses the issue of recommending a 14 reduction of fat intake to 20% or less, but at the present time, makes no further recommendation beyond the Step II diet until further studies are done (Stone et al., 1996). 5. The Efficacy of Very Low Fat Diets in Controlling Dyslipidemia and CVD Risk Epidemiological studies have shown that the incidence of C V D is lower in populations who consume very low fat diets. In 1983-1984 a nationwide dietary survey done in the People's Republic of China showed that a total fat intake of 14.5% of energy in the rural population corresponded to a mean cholesterol concentration of 3.23 - 3.49 mmol/L (Campbell & Junshi, 1994). Plasma cholesterol concentration was associated with meat and total fat intake, and inversely related to the intake of legumes and fibre. Increasing fat intake in such populations normally accustomed to very low fat intakes can be associated with subsequent increase in C V D risk as shown by a migration study of the Japanese to Hawaii and North America (Robertson et al., 1977). In an intervention study, Tarahumara Indians whose usual diet was very low in fat and cholesterol (20% of energy as fat, trace amounts of cholesterol) were given an "affluent" diet of 43% fat and 1020 mg cholesterol per day for 5 weeks (McMurry, Cerqueira, S.L. Connor & W.E. Connor, 1991). Plasma total cholesterol and L D L -cholesterol increased 31% and 39% respectively suggesting that long term consumption of such a diet could increase their risk of C V D . Various intervention studies have been done using very low fat diets in an attempt to reduce cardiovascular risk beyond what is achievable using the conventional dietary recommendations. Some studies done in metabolic research units or in residential 15 programs have shown very positive results in improving cardiac risk factors on a short term basis (Barnard, Ugianskis, Martin & Inkeles, 1992; Czernin et al., 1995; Schaefer et al., 1995). In one study, when 27 healthy subjects with moderate hypercholesterolemia were provided a weight maintaining very low fat diet (15.1% fat, 5% saturated fat, 17 mg cholesterol/1000 kcal) for 5 to 6 weeks after consuming a baseline diet for 5-6 weeks (35.4% fat, 13.8-14.1% saturated fat, 30-35 mg cholesterol/1000 kcal), there were significant decreases in total cholesterol (-12.5%), LDL-cholesterol (-17.1%), and HDL-cholesterol (-22.8%) (Schaefer et al., 1995). Triglyceride levels were increased by 47.3%; however, when the diet was changed to an ad-libitum energy very low fat diet (15.1% fat), energy intake was reduced, weight loss occurred (-3.63 kg), L D L -cholesterol decreased by 24.3% and triglycerides did not change significantly. In these studies, however, food was provided for the subjects so that they do not represent outcome of subjects coping with choosing and preparing their own foods. There have been varying results in longer studies in which patients provided their own meals (Brown et al., 1984; Thuesen, Henriksen & Engby, 1986, Kasim et al., 1993). When subjects with moderately elevated cholesterol levels who were given instruction for a 5 - 10% fat diet (Pritikin maintenance diet) were compared to those given instruction for a 25% - 30% fat diet (AHA diet), both diets showed tendencies toward improvements in weight and lipid profiles; however, only the lower fat group showed a significant drop in LDL-cholesterol from 0 to 12 months (Brown et al., 1984). In another study using free-living subjects who provided their own meals after being instructed on a 10% fat diet, total cholesterol was reduced by 14% and LDL-cholesterol by 18% after one year, however, there was no control group in this study (Thuesen et al., 1986). 16 Many of these trials involve not only diet modification, but also exercise and other lifestyle counseling to improve cardiac risk. Barnard (1991) describes the results of 4587 adults participating in a 3 week live-in program of lifestyle modification which included a high complex carbohydrate, high fibre, low fat, low cholesterol diet with 10% of energy as fat. Both total and LDL-cholesterol levels were reduced by an average of 23% during the program with greater reductions in those with higher baseline lipid levels. The Stanford Coronary Risk Intervention Project (SCRIP) was a long term trial which studied the effect of modifying both lifestyle (modified fat diet, exercise, weight control, smoking cessation) and medication as compared to usual care on the rate of progression of atherosclerosis over 4 years in 300 men and women (Haskell et al., 1994). The diet for the intervention group had a maximum goal of <20% of energy intake from fat and <6% from saturated fat, and <75 mg of cholesterol per day; however, the diet achieved consisted of 23.8% of energy from fat, 6.8% from saturated fat and 143 mg cholesterol per day. The intervention group had a 47% reduction in rate of diseased coronary artery narrowing as compared to the usual care group, as-well as a reduction in LDL-cholesterol (22%), triglyceride (20%), and body weight (4%). However, these improvements were attributed to changes not only in lifestyle measures, but also in medication. In the Heidelberg study, 113 subjects with stable angina pectoris and taking no lipid lowering agents, were randomly assigned to usual care (AHA Step 1 diet) or a exercise and intensive diet group (<20% fat, 200 mg cholesterol/day) (Schuler et al., 1992). After 12 months, patients in the intervention group achieved improvements in body weight (5%), total cholesterol (10%), triglycerides (24%), and H D L (up 3%) while the usual care group showed no changes in body weight or lipoprotein levels other than triglycerides which 17 decreased by 17%. In the Lifestyle Heart Trial, 28 motivated patients consumed a very restricted lacto-ovovegetarian diet (<10% fat, 5 mg cholesterol/day) for 12 months (Ornish et al., 1990). Total cholesterol decreased by 24.3%, L D L by 37.4%, and H D L by 3% while triglycerides increased by 22%. Angiographic analysis showed that the average percentage diameter stenosis decreased from 40.0% to 37.8% in the experimental group, but progressed from 42.7% to 46.1% in the control group. A 5-year follow up of this study indicated that further regression was observed in the experimental group while the control group experienced progression of coronary atherosclerosis (Ornish et al., 1998). However, it would be difficult for most people to adhere to such strict dietary measures on a long term basis. Despite the possible benefits attributed to very low fat diets, there have also been some concerns. Low fat high carbohydrate diets lower blood LDL-cholesterol levels, but also tend to lower HDL-cholesterol (W.E. Connor, S.L. Connor, Katan, Grundy & Willett, 1997; Knuiman, West, Katan & Hautvast, 1987). Although long term implication of such H D L lowering is not certain, it seems that H D L lowering in this way is not necessarily atherogenic (W.E. Connor et al., 1997). In a review of epidemiological studies on the relationship between diet and HDL-cholesterol, it is suggested that HDL-cholesterol concentrations in men and boys from countries with low CHD mortality is lower than, or equal to that in countries with high CHD mortality rates (Knuiman et al., 1987). Some research suggests that low fat high carbohydrate diets result in an increase in triglyceride levels, while others report that high carbohydrate diets, especially when subjects are allowed to consume calories ad libitum, result in weight loss and unchanged 18 or decreased triglyceride concentrations (Connor et al., 1997; Purnell & Brunzell, 1997; Retzlaff, Walden, Dowdy, McCann, Anderson & Knopp, 1995). It is suggested that the increase in triglycerides seen in some individuals results in increased large buoyant V L D L particles which are different from those in the dyslipidemia seen in insulin resistance syndrome (Purnell & Brunzell, 1997). Thus the implications of a very low fat diet with calories taken ad libitum may not be detrimental in terms of its effect on triglyceride levels. Diets which include more restrictive measures than conventional recommendations regarding fat content may be of benefit in further improving cardiac risk factors, however, these diets would only be useful if they are achievable and attainable on a long term basis in free-living subjects. 6. The Evidence for Vegetarian Diets in Reducing Cardiovascular Risk Vegetarian diets on the whole have been associated with reduced risk for C V D . Studies looking at C V D in Seventh Day Adventists (SDA) in the U.S. and other countries and a study of vegetarians in Britain have shown that plasma lipid levels are usually more favourable, and mortality from C V D is lower in vegetarians than in non-vegetarians (Burr & Butland, 1988; Fonnebo, 1994; Fraser, 1988; Resnicow et al., 1991). In a study of 7,285 Norwegian SDA, it was found that serum cholesterol was 15% lower in SDA men and 10% lower in women compared with matched control subjects (Fonnebo, 1994). In a study of 10 vegans, 15 lacto-ovovegetarians, and 25 omnivorous controls in the U.S., mean total cholesterol was highest in the omnivores (173 mg/dl), lower in the lacto-ovovegetarians (150 mg/dl), and lowest in the vegans (135 mg/dl) (Fisher et al, 1986). In 19 the Lifestyle Heart Trial, subjects in a lifestyle modification program followed a very low fat vegetarian diet with the only animal proteins being egg whites and one cup per day of nonfat milk or yogurt (Ornish et al, 1990, 1999). The outcome was a substantial decrease in blood lipids as well as a reduction in the progression of C V D as indicated by angiography. It is not certain, however, whether it is the abstinence from meat, better living habits (e.g. fewer smokers, less coffee consumption), or the increased intake of fruits and vegetables which provided this reduced incidence of C V D . In the Atherosclerosis Risk in Communities (ARIC) Study done between 1987 - 1989 in four U.S. communities, the consumption of vegetable fat was inversely related to carotid artery thickness, whereas animal fat was positively related (Tell, Evans, Folsom, Shimakawa, Carpenter & Heiss, 1994). A study of 65 rural counties in China showed that the proportion of total protein consumption as animal protein in China is 10.8% as compared to 69% in the U.S. (Campbell & Junshi, 1994). In this population, plasma cholesterol concentration was associated with meat intake and inversely related to legume consumption. In an intervention study, 26 men were randomly assigned to two of three diets: a high fat diet, a 30% fat lacto-ovo-vegetarian diet, and a 30% fat diet that contained some meat (Kestin, Rouse, Correll & Nestel, 1989). As compared to the high fat diet, the meat diet reduced total cholesterol levels by 5% and LDL-cholesterol by 7%, whereas the lacto-ovo-vegetarian diet reduced total cholesterol by 10% and LDL-cholesterol by 9%. Although the mechanism by which vegetarian diets appear to provide protection from C V D is not clear, it appears that the restriction of animal products, especially animal fat, would be an asset to a diet optimizing cardiovascular risk. Fish, however, has 20 a different fatty acid composition as well as other possibly valuable properties when compared to other meats, and should be considered in the optimal diet. 7. The Evidence for Including Fish in a Diet for Reducing CVD Risk The benefits of eating fish and the n-3 fatty acids it contains have been widely studied (Harris, 1997). The beneficial actions attributed to n-3 fatty acids from fish and fish oils on C V D include: prevention of ventricular arrhythmias and cardiac arrest, inhibition of thromboxane A2 synthesis with resulting antithrombotic effects, reduced atherosclerotic plaque growth, inhibition of interleukin-a and cytokines, and promotion of nitric oxide induced endothelial relaxation as well as modification of plasma lipid levels (Connor, 1997; Leaf & Kang, 1997). Various epidemiological studies have illustrated the beneficial effects of eating fish on C V D . A 20 year study in 852 men in Zutphen, the Netherlands, showed that mortality from C V D was reduced by one-half in those who ate at least 30g of fish per day as compared to those who ate no fish (Kromhout, 1985). A comparison of lipid profiles in fish-consuming coastal populations in India to that of inland populations who consumed no fish, indicated lower mean serum cholesterol and triglycerides and higher HDL-levels in the fish-eating group (Bulliyya, K . K . Reddy, G.P.R. Reddy, P.C. Reddy, Reddanna & Kumari, 1990). In the Lugalawa study, the plasma lipid concentrations of Bantu villagers living in Tanzania who ate 300-600g of fish per day were compared to that of vegetarians living nearby (Pauletto et al., 1996). Plasma levels of cholesterol and triglycerides were lower in the fish-consuming group than in the vegetarian group. 21 Studies have examined the effect of fish and fish oils on plasma lipid levels. Incorporating fish daily into a weight-loss program (energy-restricted diet, 30% of energy as fat) resulted in more significant improvements in dyslipidemia than with a weight loss diet alone (Mori, Bao, Burke, Puddey, Watts & Beilin, 1999). Having fish eight times per week was as effective as having it twice per week in reducing total and LDL-cholesterol without changing the ratio of total cholesterol to HDL-cholesterol in subjects following the NCEP Step II diet (Schaefer et al., 1996.) However, when fish or fish oils were given as a supplement rather than as a substitution for saturated fats, there appeared to be a reduction in plasma triglyceride concentrations, but no effect or a slight increase in L D L -cholesterol levels (Harris, 1997; Harris et al., 1990; Katan, 1995; Van Haouwelingen, Zevenbergen, Groot, Kester & Hornstra, 1990). The effect on HDL-cholesterol levels have been variable (Harris, 1997). The effect of n-3 fatty acids on serum lipids may be modified by the quantity of fat in the diet (Mori, Vandongen, Beilin, Burke, Morris & Ritchie, 1994). Men with elevated serum cholesterol who were randomly allocated to eating a 40% fat diet with fish or fish oil (2.6 g n-3 fatty acids per day) showed an increase in total, L D L and HDL-cholesterol, and reduced triglycerides. Men eating a 30% fat diet with no fish showed reduced total, L D L and HDL-cholesterol and unchanged triglyceride levels, while those eating a 30% fat diet with fish or fish oil daily experienced reduced total and L D L -cholesterol as well as reduced triglycerides and increased HDL2. It was not studied whether a further reduction in total fat along with regular fish intake could result in an even more favourable lipid profile. 22 There may be benefits to eating fish even when lipid profiles are not significantly altered. In the D A R T trial, 2033 men who had survived myocardial infarctions (MI) were randomly allocated to receive or not to receive dietary advice on one of the following: modification of dietary fat, increase in fibre intake, or increase in fish intake to at least two portions of fatty fish per week (Burr et al., 1989). After 2 years of follow up, those who received advice to increase fish intake had a relative risk of 0.71 (95% CI, 0.54 - 0.93) or a 29% reduction in all cause mortality as compared to those who were not given advice to increase fatty fish intake. These studies suggest that it would be prudent to include fish in the optimal diet for reducing cardiovascular risk, however, not all studies have found an inverse relationship between fish consumption and C V D . In the Health Professionals Follow-up Study involving 44,895 men from 1988 to 1992, there was no significant association found between dietary intake of n-3 fatty acids or fish intake and the risk of C V D (Ascherio, Rimm, Stampfer, Giovannucci & Willett, 1995). The multivariate relative risk of CHD for men with the highest quintile of n-3 fatty acid intake as compared with those with the lowest was 1.12 (95% CI, 0.96 - 1.31). The multivariate relative risk of coronary disease for men who consumed the most fish as compared with those who consumed the least was 1.14 (95% CI, 0.86 -1.51). However, it is suggested that although fish intake may not reduce incidence of C V D , it may reduce mortality due to C V D . The relative risk of death from C V D among men who ate any amount offish as compared to those who ate no fish was 0.74 (95% CI, 0.44 - 1.23). The relative risk, though, did not decrease with increasing fish intake beyond one to two servings per week, 23 suggesting that there is no benefit in increasing fish intake beyond one to two servings per week in reducing risk of C V D mortality. One may also consider whether a vegetarian diet without the addition of fish may be of greater benefit in optimizing cardiovascular risk. An epidemiological study compared the lipid and lipoprotein levels of controls to vegetarians of whom 40% ate fish once per week or more, 28% ate dairy products and 11% ate eggs (Sacks, Castelli, Donner & Kass, 1975). When multiple regression analysis of various dietary variables was done, the results suggested that dairy products and eggs were positively associated with lipid levels in these vegetarians whereas fish was not. Thus the addition of fish to a vegetarian diet did not appear to compromise the benefits of a vegetarian diet in optimizing cardiovascular risk. It could be suggested that n-3 fatty acids from plant sources in the form of a-linolenic acid could provide similar beneficial effects as that of eicosapentaenoic (EPA) or docosahexaenoic (DHA) acids found in fish, however, the results have not been entirely consistent. The Lyon Study found that teaching a Mediterranean diet with increased a-linolenic acid (about 2 g/day) in post-MI subjects was associated with a risk ratio of 0.30 for total mortality and 0.27 for incidence of ischaemic events after 27 months and maintained after 4 years, as compared to those provided no dietary advice other than that in hospital or by the physician (a-linolenic acid intake about 0.6g/day) (DeLorgeril et al, 1994,1999). However, other studies have found that a-linolenic acid may not be as effective as fish oil in changing cardiac risk factors. In a double-blind cross-over study of 11 subjects with well-controlled diabetes, taking linseed oil (54% a-linolenic acid) for 3 months did not reduce plasma triglyceride concentrations, while 24 taking the equivalent amount of n-3 fatty acids in fish oil resulted in significantly reduced plasma triglyceride levels (McManus, Jumpson, Finegood, Clandinin & Ryan, 1996). It is suggested that an intake of 3-4 g/day of ot-linolenic acid could be equal to an intake of 0.3 g/day of EPA in its effect on the EPA content of plasma phospholipids (McKeigue, 1994). Because of the uncertainty of the degree of effect of a-linolenic acid on cardiac risk factors, encouraging the use of fish in addition to a vegetarian diet may be prudent in an optimal diet for reducing C V D risk. An intervention trial which studies the effect of a very low fat semi-vegetarian (lacto-ovo plus fish) diet on lipid levels has not been documented as yet. 8. Low Fat Diets and Body Weight Change - Their Effect on Blood Lipids Obesity, especially abdominal obesity is associated with hyperlipidemia, hypertension, diabetes mellitus, and an increased risk for C V D (Pi-Sunyer, 1991; Reeder, Angel, Ledoux, Rabkin, Young & Sweet, 1992). The Canadian Heart Health Surveys showed that the prevalence of obesity (BMI > 27) in the Canadian population was 35% in men and 27% in women (Reeder et al., 1992). The importance of controlling obesity in optimizing serum lipid levels and reducing C V D risk is well documented (National Cholesterol Education Program Adult Treatment Panel II, 1994; Rabkin, Chen, Leiter, Liu & Reeder, 1997; Reeder et al., 1992). In the Canadian Heart Health Survey, L D L -cholesterol, triglycerides and the ratio of total cholesterol to HDL-cholesterol increased with increasing BMI, whereas HDL-cholesterol decreased (Reeder et al., 1997). When correlation analysis was conducted between anthropometric measurements (BMI, waist circumference, hip circumference, and waist-hip ratio) and cardiovascular risk variables 25 (blood pressure, LDL-cholesterol, HDL-cholesterol, and triglycerides), abdominal obesity showed the greatest association with plasma lipid levels. It was concluded that waist circumference was the measure of abdominal obesity most highly correlated with lipid levels and other C V D risk factors. The combination of waist circumference and fasting triglyceride levels together is suggested to be a possible tool for identifying men with an atherogenic metabolic profile of hyperinsulinemia, elevated apo B, and small dense L D L particles (Lemieux et al., 2000). There is yet, however, little report of waist circumference being used as an outcome measure in intervention trials studying the effect of diet on C V D risk. Intervention studies have supported the value of weight loss in controlling blood lipid concentrations (Dengel, Katzel & Goldberg, 1995; Katzel, Coon, Dengel & Goldberg, 1995; Lichtenstein, Ausman, Carrasaco, Jenner, Ordovas & Schaefer, 1994). Weight loss appeared to have an additional effect in lowering lipid levels in men with B M I > 30 and lipid levels at < 90th percentile who consumed an A H A weight maintenance diet for 3 months followed by a weight loss program for 9 months, as compared to those who remained on the weight maintenance A H A diet (Dengel et al., 1995). The A H A diet after 3 months resulted in a reduction of 16% in plasma total cholesterol, 14% in LDL-cholesterol, 17% in HDL-cholesterol and 11% in triglycerides. Subsequent weight loss during the 9 month weight loss period resulted in further reductions of 4% in cholesterol, 7% in LDL-cholesterol, 17% in triglycerides and a 15% increase in HDL-cholesterol as compared to lipid levels at the end of the 3 months on the A H A diet. Those on the 9 month weight maintenance program experienced no further improvement of lipid levels. In a study comparing the effects of 15% fat diets to those 26 with 29% and 36% fat on plasma lipid concentrations, it is suggested that very low fat diets in the short term (10 weeks), have a beneficial effect on plasma lipid profiles only when accompanied by weight loss due to the large increase in triglyceride and large decrease in HDL-cholesterol concentrations observed in the very low fat diet without weight loss (Lichtenstein et al., 1994). Thus weight loss in overweight persons appears to be an important aspect of the benefits of a very low fat diet. 9. Implications for Planning the Optimal Diet in Controlling Blood Lipids and CVD Risk The data above suggest that further reductions in C V D risk could be achieved possibly by stricter modifications to the conventional dietary guidelines (NCEP Step I and Step II diets). However, the effectiveness of any dietary intervention in free-living persons is not determined solely by the possible metabolic effects of any dietary component alone. Instead consideration must be given to various factors. Firstly, any recommendation must be based on whole foods within a balanced diet suitable for overall good health. Recommendations cannot be made based only on the value of any one specific nutrient since one's diet choices consist of whole foods which are combinations of many nutrients. Those recommendations must be appropriate not only for heart health, but also for overall well being. Secondly, the diet must be feasible. Consideration must be given to cost, taste and availability of foods as well as to difficulties people may face with motivation, and changing long ingrained eating habits and attitudes (Lloyd, Paisley & Mela, 1995; McAllister, Baghurst & Record, 1994; Naylor & Paterson, 1996). Social 27 and cultural factors must also be considered. Thirdly, the optimal diet for minimizing C V D risk must not compromise one's perception of his/her quality of life. The Women's Health Trial Vanguard Study examined the feasibility of a < 25% fat diet as compared to the control diet which contained 37% fat in 303 women who were at high risk for breast cancer over a 2 year period (Hendersen, Kushi, Thompson, Gorbach, Clifford & Insull, 1990). Ability to comply to dietary recommendations was measured by changes in nutrient consumption according to food groups and their relationship to overall fat intake, and by assessment of the expected effect of recorded diets on blood cholesterol concentrations. At each follow-up, dietary fat intake was approximately 21%, and the differences in plasma cholesterol at 12 and 24 months agreed closely with the expected differences as calculated from Keys equation, suggesting that dietary intervention to reduce fat intake to less than 25% of energy can be achieved and maintained for 2 years by motivated women. Feasibility of low fat diets can be enhanced by such measures as intensive nutrition counseling, providing flexibility in fat-reduction strategies, including significant members of the patient's household and enhancing self-efficacy (McCann, Retzlaff, Dowdy, Walden & Knopp, 1990; Rhodes, Bookstein, Aaronson, Mercer & Orringer, 1996; Smith-Schneider, Sigman-Grant & Kris-Etherton, 1992). The feasibility of a 15% fat lacto-ovo-vegetarian plus fish diet has not been documented. Quality of life as it relates to nutrition can be described as "a balance between:....food intake as a tool for prevention as primarily determined by exogenous considerations based on scientific calculations and experiments...and food as a means of enjoyment and self-concept as chosen by endogenous psychological mechanisms" 28 (Schlettwein-Gsell, 1992) A low fat diet did not appear to reduce perception of quality of life in some studies. A study examined the effect of a low fat (achieved 21% fat) ad-libitum diet as compared to a low energy (achieved 30% fat) diet on quality of life in overweight women over 6 months (Shah, McGovern, French and Baxter, 1994). Although weight loss and satiety were not statistically different between the two groups, quality of life and palatability were enhanced in the low fat group, but not in the low energy group. Changes in negative emotions were examined in 305 young men and women who participated in the Family Heart Study which was a dietary intervention program aimed at reducing fat intake in families during a 5 year period (Weidner, S.L. Connor, Hollis & W.E. Connor, 1992). Improvement in diet was associated with improved plasma cholesterol concentrations, as well as reductions in measures of depression and aggressive hostility. In another study, patients' acceptance (as defined by measures of quality of life) of a commercially pre-packaged, C VD-risk reducing diet was compared to a similar diet that was self-selected (Hatton, Haynes, Oparil, Kris-Etherton, Pi-Sunyer & Resnick, 1996). Both groups achieved significant improvements in weight and cardiovascular risk factors, however, the pre-packaged diet group showed greater improvements in the various measures of quality of life. In applying the findings of this study, though, one must consider whether such pre-packaged meals would be practical from the standpoint of both cost and overall health on a long-term basis. 10. Summary The optimal diet for controlling cardiac risk factors has not yet been defined. While some researchers have shown that a very low fat vegetarian diet can reduce cardiac 29 r i s k f a c t o r s b e y o n d w h a t i s a c h i e v e d b y t h e c o n v e n t i o n a l d i e t i n h i g h l y m o t i v a t e d i n d i v i d u a l s , s u c h s t r i c t d i e t s m a y n o t b e f e a s i b l e f o r t h e a v e r a g e N o r t h A m e r i c a n p e r s o n w i t h C V D . A c o m p r o m i s e b e t w e e n t h e l i m i t a t i o n s o f t h e v e r y s t r i c t 1 0 % f a t v e g e t a r i a n d i e t d e s c r i b e d i n s u c h t r i a l s a s t h e L i f e s t y l e H e a r t S t u d y , a n d t h e c o n v e n t i o n a l m o d i f i e d f a t d i e t c o u l d b e a 1 5 % f a t s e m i - v e g e t a r i a n ( l a c t o - o v o p l u s f i s h ) d i e t . S u c h a d i e t i n c o r p o r a t e s n u t r i t i o n a l p r i n c i p l e s w h i c h h a v e b e e n s h o w n t o m a x i m i z e c a r d i o v a s c u l a r r i s k r e d u c t i o n , y e t m a y b e l e s s r i g i d a n d t h u s m o r e f e a s i b l e t h a n a v e r y l o w f a t v e g e t a r i a n d i e t . S o f a r , t h e r e a r e n o r e p o r t s o f a n y s t u d i e s t h a t h a v e e x a m i n e d t h e f e a s i b i l i t y o f a 1 5 % f a t s e m i v e g e t a r i a n ( l a c t o - o v o p l u s fish) d i e t , a n d i t s e f f e c t o n b o d y w e i g h t , w a i s t c i r c u m f e r e n c e , p l a s m a l i p i d c o n c e n t r a t i o n s a n d q u a l i t y o f l i f e . T h e f i n d i n g s f r o m s u c h a s t u d y m a y a s s i s t d i e t i t i a n s i n d e v e l o p i n g o p t i m a l d i e t a r y g u i d e l i n e s f o r r e d u c i n g c a r d i a c r i s k f o r p a t i e n t s w i t h C V D . 11. Statement of the Problem T h e f o l l o w i n g q u e s t i o n s w e r e e x p l o r e d i n t h i s s t u d y : 1 . I s t h e r e a d i f f e r e n c e b e t w e e n t e a c h i n g a v e r y l o w f a t s e m i - v e g e t a r i a n ( l a c t o -o v o p l u s fish) d i e t a n d t h e c o n v e n t i o n a l m o d i f i e d f a t d i e t t o a d u l t s w i t h C V D o n c a r d i a c r i s k f a c t o r s ( s e r u m l i p i d c o n c e n t r a t i o n s a n d a n t h r o p o m e t r i c m e a s u r e m e n t s ) ? 2 . I s t h e r e a d i f f e r e n c e b e t w e e n t h e t w o d i e t s o n t h e i r e f f e c t s o n n u t r i t i o n - r e l a t e d q u a l i t y o f l i f e ? T h e r e f o r e , t h e f o l l o w i n g n u l l h y p o t h e s e s w e r e s e t : 30 1. There is no difference between teaching a very low fat semivegetarian diet and the conventional modified fat diet to adults with C V D on cardiac risk factors (serum lipid concentrations and anthropometric measurements). 2. There is no difference between teaching a very low fat semivegetarian diet and the conventional modified fat diet on nutrition-related quality of life. 31 CHAPTER III Methodology 1. Overview of Design This was a 12 week randomized clinical trial comparing the effect of teaching a very low fat semi-vegetarian diet vs the conventional modified fat in adults with cardiovascular disease (CVD) or at high risk for C V D . Outcome variables were anthropometric measures (body weight, BMI, waist circumference), serum lipid measurements (total cholesterol, LDL-cholesterol, HDL-cholesterol, total cholesterol/HDL-cholesterol ratio, and triglycerides), and nutrition-related quality of life measurements. 2. Setting Subjects for this study were recruited from the Cardiac Rehabilitation Program (CRP) at St. Paul's Hospital. St. Paul's is a teaching hospital located in downtown Vancouver, but serves patients from the Greater Vancouver area. The CRP of the Healthy Heart Program at the hospital is a multidisciplinary cardiac rehabilitation program for patients with atherosclerosis, post myocardial infarction, and/or post cardiac surgery. Patients, who are referred to the program by local cardiologists and family practitioners, are introduced to the program in the Intake Clinic before actually starting exercise classes, usually about one to two months after the Intake Clinic. Patients participate in the program for 16 weeks during which time they attend one hour exercise classes twice per week and an optional half day education class once per week. Education classes consist of general lectures on cardiac risk factors with topics such as 32 stress management, nutrition, lipids, hypertension, smoking cessation and pharmacological therapy. Individual counseling on risk factor reduction is also provided as necessary. Nutrition therapy is a major component of the program with individual counseling and follow up throughout the duration of the program. Participants are also provided with opportunities to attend cooking classes or supermarket tours. The nutritional guidelines used are the principles of the modified fat diet, which are similar to the American Heart Association (AHA) diet or National Cholesterol Education Program (NCEP) Step I and II diets. 3. Sample Size The proposed study sample of 58 subjects was estimated as follows: Although there are several outcome measures, the primary endpoint was considered to be total cholesterol. Thus the proposed sample size was based on the numbers required to detect a meaningful difference in total cholesterol levels. Calculated on the basis of power = 80 % (p= 0.8), p < .05 (a= .05, two-tailed) Meaningful difference = total cholesterol of 0.55 mmol/L Expected variability in the difference = .732 mmol/L Variability was determined by calculating the standard deviations of the difference in the pretest and posttest total cholesterol levels of a random sample of 76 patients who completed the CRP. Cholesterol tests were done prior to beginning, and 33 after completion of the program. Patients followed a modified fat diet (similar to N C E P Step I and II diets) during the program. Although the difference in cholesterol measurements over time is a within subjects factor, the difference in those cholesterol measurements between groups is a "between groups" factor. Thus the formula used was based on the estimated number required to detect a significant difference between two independent groups. n = ( S D , 2 + SD 2 2 ) x ( Z i . B + Z , . ^ ) 2 ( x 2 - x , ) 2 n = (.7322 + .7322) x (.84 + 1.96)2 0.552 n = r.54 + .54) x (7.84) = 8.47 0.30 0.30 n = 28.2 per group Total number of subjects required: 58 4. Recruitment Subjects for the study were recruited from the C R P during the Intake Cl inic of the program between March 1998 and September 1999. The study was approved by the University of British Columbia Research Services (Appendix A ) and the St. Paul's Hospital Ethics Committee for Human Experimentation (Appendix B) . Patients' charts were screened for eligibility by the dietitian during the Intake clinic. 34 Inclusion criteria were as follows: referral to the CRP (acceptance to program indicating the presence of C V D or very high risk for CVD); at least two months post myocardial infarction or cardiac surgery at time of baseline lipid measurements (Rosenson, 1993); 35 years or older; total cholesterol > 4.5 mmol/L; triglyceride < 4 mmol/L; nonsmoker or ex-smoker; ability to understand necessary dietary modifications; stable medications throughout the study period including hormone replacements and any other medication or vitamins which may affect lipid levels (statin drugs to be stable for at least 2 weeks, and niacin and fibrate drugs to be stable for at least 4 weeks prior to initial blood test and throughout the study period) (Moghadasian M H , Mancini GB & Frohlich JJ, 2000; verbal communication, Frohlich J); alcohol intake < 14 drinks per week; agreement to include at least 2 servings of fish per week, if randomized to the experimental group. Exclusion criteria were as follows: inability to meet any of the inclusion criterion; insulin dependent diabetes mellitus; renal disease; allergies or any other medical condition in which study diet modifications would not be suitable; any unstable medical conditions such as untreated hypothyroidism; participation in any other program or medication regimen which may induce rapid weight change. Eligible patients were approached and the study protocol was explained to prospective subjects by the Intake Clinic dietitian. An information sheet summarizing the diet study was also shown to interested patients (Appendix C). Written consent forms were signed by all patients who agreed to participate in the study (Appendix D). Subjects were withdrawn from the study if they were unable to meet study conditions. Subjects who consented to the study were randomized before starting the 35 CRP, into either the control or experimental group by means of a draw after 2 or more subjects were recruited. 5. Diets 5a. Description of Diets Used The experimental diet instructed was a very low fat lactoovovegetarian plus fish diet that was nutritionally balanced according to Canada's Food Guide to Healthy Eating (Appendix E). The diet consisted of total fat <15% of energy, saturated fat < 6%, and cholesterol < 100 mg per day. Cholesterol and saturated fat content were reduced by limiting animal fats to fish and whatever minimal fat is found in skim milk products. Vegetarian meals using legumes and skim milk products as major protein sources were encouraged. Fruits and vegetables, and whole grains were encouraged as according to Canada's Food Guide to Healthy Eating. Added fats were limited to minimal use of appropriate oils and spreads within a given fat budget. The control diet instructed was the modified diet that is usually used in the Cardiac Rehabilitation Program (Appendix F). It follows the principles of the A H A and NCEP guidelines of up to 30% total fat, 7 -10% saturated fat, and 200 - 300 mg cholesterol daily. It includes lean meats, fish, and poultry and low fat dairy products. Added fats are limited to 3 - 6 teaspoons per day within a given fat budget. Fruits and vegetables, and whole grains are encouraged according to Canada's Food Guide to Healthy Eating. 36 5b. Diet Instruction Appropriate diet instruction (experimental or control) was provided during the first two weeks of beginning the CRP by one of three dietitians who usually work in the CRP. One of the dietitians was the investigator for this study, and explained the details of the experimental diet to the other dietitians until all were familiar with the principles before beginning the study. The control diet was the usual diet used in the CRP and all dietitians were accustomed to teaching its principles. Subjects who were already following a lower fat intake than the diet assigned to them were not necessarily encouraged to increase their fat intake, but were given appropriate instructions for their assigned diets using a fat budget that provided a maximum of 30% of energy as fat for the control, and 15% of energy for the experimental diet. As part of usual participation in the CRP, subjects completed a diet history form at the Intake Clinic, prior to seeing the dietitian (Appendix G). The information on this form provided primarily information on which to base diet instruction. It also provided data on the frequency of fish intake prior to starting the study. Follow up was provided throughout the course of the study as needed to help subjects adhere to the diet program. Written guidelines appropriate for the specific diet were given along with other brochures as necessary to help with compliance to the diet. All subjects attended exercise and education classes as usual. No difference in treatment was given to either group other than the different diets. 5c. Diet Monitoring To monitor progress, collect diet intake data, and assess adherence to the appropriate diet, subjects completed the following records: 37 • Subjects were given food record forms to be completed prior to being given diet instruction (week 0) and instructed on how to keep accurate diet records (Appendix H). Three day food records (one weekend day and two weekdays) were kept at the beginning (prior to diet instruction), after four weeks, and at the end of the study (week 12). On submission, food records were reviewed by the dietitian with subjects to clarify quantities and ambiguous record items. A l l data from food records were entered into the computer by the investigating dietitian. • A diet adherence chart to indicate diet adherence days and frequency of fish intake was completed by the subjects throughout the course of the study (Appendix I ) . Subjects were asked to check off each day that they were able to adhere to the diet, and to indicate which days they consumed fish. 6. Anthropometric Measurements 6a. Body Weight and Body Mass Index Height was measured to the nearest centimetre at the beginning of the study (week 0), using the standard measurement tool for measuring height on the balance scale. Measurement was taken with the subject at full inspiration, standing erect, looking straight ahead, knees straight, arms at sides, and feet flat with no shoes (Gibson, 1990). Weight was measured to the nearest 0.1 kilogram at weeks 0,4, 8 and 12 during the exercise class in indoor clothing and no shoes using a calibrated balance beam scale. B M I was calculated using the formula of weight in kilograms divided by the square of height in meters. One measurement was recorded for each parameter at weeks 0, 4, 8 and 12. 38 6b. Waist Circumference Waist circumference was measured at weeks 0 and 12 using the procedure described in the Canadian Heart Health Surveys (Ledoux, Lambert, Reeder & Despres, 1997). Measurements were taken at the end of a normal expiration at the level of noticeable waist narrowing with the subject standing erect. If the narrowing could not be determined, then the measurement was taken at the lateral level of the 12th rib. One measurement was recorded to the nearest 0.5 centimetre at weeks 0 and 12. 7. Lipid Measurements Lipid measurements were taken within 2 weeks prior to week 0 and at week 12. Lipid measurements were taken after a 12 hour fast with no alcohol for 72 hours prior to the test. Serum total cholesterol, HDL-cholesterol, LDL-cholesterol and triglyceride levels were measured by the St. Paul's Hospital laboratory using standardized procedures. A l l laboratory measures for lipids at St. Paul's are standardized to the Center for Disease Control in Atlanta, Georgia, and to the Canadian Reference Foundation Laboratory in Vancouver, B.C. Total cholesterol was determined by using an enzymatic assay that uses cholesterol esterase and cholesterol oxidase, measured in a colorimetric procedure. (Cholesterol CHOD-PAP method for BM/Hitachi 911, Boehringer Mannheim). The measurement of triglyceride was based on the enzymatic assay of glycerol with glycerol 3 phosphate-oxidase after hydrolysis of triglycerides with lipoprotein 39 lipase, measured in a photometric procedure. (Technicon R A Systems Method No. SM4-0173G90, Technicon Instruments Corporation) HDL-cholesterol was determined using an enzymatic assay and measured colorimetrically (see cholesterol measurement above) after the removal of V L D L and LDL-lipoproteins by the addition of sodium phosphotungstic acid and magnesium chloride. (Warnick GR et al. Laboratory Measurement of Lipids, Lipoproteins and Apolipoproteins, American Association of Clinical Chemistry Press, Wash. D.C. 1994.) LDL-cholesterol was calculated using the formula: LDL-cholesterol = total cholesterol - HDL-cholesterol - triglycerides/2.2 The cholesterol to HDL-cholesterol ratio was obtained by dividing total cholesterol by HDL-cholesterol. One subject in the experimental group obtained his final measurements from Richmond Health Services. The Richmond Hospital laboratory also participates in the Canadian Reference Foundation Cholesterol Certification Program that standardizes measurements used by laboratories throughout Canada, including St. Paul's. Accordingly, his measurements were included in the study. 8. Nutrition-Related Quality of Life Measurements Quality of life was measured using nutrition-specific instruments developed by Hatton et al. (1996) (Appendix J). The questionnaire addressed four areas: 1) hassles or stress associated with nutritional concerns such as shopping, food preparation, monitoring nutrient intake and cravings, 2) perception of health in relation to the diet, 3) effects of diet on social function, and 4) effect of diet restriction on mood such as frustration and 40 impatience. The last section of the questionnaire consisted of 3 questions to assess global nutrition-related quality of life. This self-administered questionnaire was completed at weeks 0 and 12. 9. Other Records Used Anthropometric and laboratory records were maintained on a time-line record form by the dietitian following the subject throughout the study (Appendix K) . Food records and adherence charts were given to the investigator as they were collected from the subjects. A l l other records were given to the investigator after each subject completed the study. A l l documents on each subject on completion of the study were maintained by the investigator. 10. Data Ana lyses A l l data analyses were performed by the investigator. 10a. Food Intake Data Macronutrients, cholesterol, fibre, vitamin and mineral content were determined by analysis of 3-day food records using nutrition analysis software Nutritionist IV ™ for Windows Version 4.1, 1995 (First DataBank Division, The Hearst Corporation, San Bruno, CA). The Canadian Nutrient File data was used when possible. Initial diet was determined by analysis of the food records given before diet instruction (Week 0). The diet during the study was determined by the average of nutrient intake from diet records at Weeks 4 and 12. 41 The exception to this procedure was the analysis of fish intake, which was done as follows: Fish intake at baseline was self-reported on the diet questionnaire given prior to beginning the study, and reported as seldom; once, twice or three times per week; once or twice per day; or more often. When reported as two to three times per week, the intake was recorded as three times per week for purposes of the analysis. Fish intake during the study was analyzed using a daily record of fish consumption on the calendar, but analyzed as servings per week. 10b. Nutrition-related Quality of Life Each of the 5 sections of the nutrition-related quality of life questionnaire consisted of a number of questions, each with a 7-point Likert summated scale for responses. The scoring system used was that according to Hatton et al. (1996). Scores were assigned to each of the 7 possible responses with 1 being most negative and 7 most positive, thus the higher the score, the greater the nutrition-related quality of life. Where there was no response given for a question, the average score of the section was calculated and added to the total score for the section. The highest possible score for each section was as follows: hassles 343, health 56, social life 49, mood 49, global 21. 10c. Analysis of Adherence Adherence was analyzed by calculating the number of days on the calendar for which participants checked that they had followed the diet, divided by the total number of days recorded, and expressed as a percentage. 42 10c. Statistical Analysis Statistical analyses were performed using SPSS 9.0 for Windows (SPSS Inc., Chicago, IL 1998). Data were entered and checked for accuracy. Any errors were corrected before statistical analyses were done. Differences in diet intake were calculated by subtracting the data at week 0 from that of the average of weeks 4 and 12. Differences in outcome measures were calculated by subtracting the data at week 0 from that of week 12. Percent weight difference was calculated by dividing the weight difference by the original weight and multiplying by 100%. The following analyses were then performed: • Summary statistics for each group were calculated to obtain frequency and distribution of demographic variables. • The independent samples t-test was done to compare the diets of the control and experimental groups at the beginning of the study. • The General Linear Model (GLM) repeated measures procedure was used to compare the effects of the intervention on the two groups. The G L M repeated measures procedure performs analysis of variance (ANOVA) to analyze the effect of within subjects factors (e.g. time) and between subjects factors (e.g. group) on outcome measures. Thus this procedure was used to test the null hypothesis: that there is no statistical difference between teaching the conventional modified fat diet and the very low fat semi-vegetarian diet on dependent variables (BMI, waist circumference, serum lipid and lipoprotein concentrations, and nutrition-related quality of life). The G L M repeated measures procedure was also used to examine the mean difference of diet variables before and after the intervention in the two groups. 43 • The Pearson correlation coefficient was used to examine the relationships among the anthropometric, lipid, quality of life and diet variables. The relationship between adherence and these variables was also examined using the Pearson correlation coefficient. • Stepwise entry multiple linear regression analysis was used to find variables that could best predict the outcome measures which showed significant changes during the study. Variables that showed significant relationships using the Pearson correlation coefficient were entered as possible predictors of the dependent variables. A l l results other than correlation analyses, were considered significant at p< .05. Due to the large numbers of correlation analyses performed, a more conservative p value (p<.01) was selected for these analyses. 1 1 . Miscel laneous A l l subjects who completed the study were given a copy of the cookbook, "Eating Light and Loving Lt" (Johnson and Ratner, Macmillan Canada, Toronto, 1998). This cookbook is a collection of low fat recipes that were submitted by patients of the Healthy Heart Program (Appendix L). 44 CHAPTER IV Results 1. Recruitment Between March 1998 through September 1999, 625 patients were seen by a dietitian in the Intake Clinic, and of those, 450 subjects who fit the inclusion were invited to participate in the study. Of those who were invited, 82 subjects consented to participation and were randomized into either the experimental or control groups. Of those who consented, 39 subjects were eliminated before starting the study for the following reasons: 17 had total cholesterol levels which were too low for the inclusion criteria at week 0; 12 did not come into the CRP as planned due to various reasons such as illness, joining another program, and other unknown reasons; 2 had thyroid disease; 1 had very high cholesterol levels at week 0 which required immediate medication; 1 had uncontrolled diabetes; 2 changed their minds; 1 had a spouse who did not wish the patient to participate; and 3 had medication changes just prior to starting the study. The remaining 43 subjects started the study, completed the CRP program, and completed all laboratory analysis and dietary food records. Subsequently 3 further subjects (1 experimental, 2 control) were eliminated because of medication changes during the study period, and 1 subject (experimental) was eliminated due to final blood tests being performed well after the experimental dietary period. Thus, the data from the remaining 39 subjects were used for all analyses involving laboratory blood results and any comparisons between the two groups. Of the 39 subjects, 17 (43.6%) had been randomized into the control group, and 22 (56.4%) into the experimental group. Of the eligible subjects, not all subjects complied with completing questionnaires, such that 4 5 quality of life data were completed by 33 subjects. Complete anthropometric data were obtained on 38 subjects and adherence data on 33 subjects. The available data from all 43 subjects were used in correlation and regression analysis of the variables not involving laboratory blood results. 2. Subject Characterist ics There were no significant differences between the control and experimental groups prior to the study (Table 1). Average age was 60.5 ± 10.6 years, and gender was evenly distributed. As a group, subjects were overweight and had slightly elevated cholesterol levels. Twenty-three percent of the subjects were taking lipid-lowering medication, and remained so with no changes throughout the study. Table 1: Subject characteristics Group 1 (control) n=17 Group 2 (experimental) n=22 males " 8(47.1%) 10 (45.5%) females 9 (52.9%) 12 (54.5%) age (yr) 60.0 ± 9.7 60.9 ±11.5 BMI (kg/m2 ) 28.4 ±5 .0 27.3 ±4 .8 serum cholesterol (mmol/L) 5.79 ± .83 5.57 ± .80 on lipid-lowering medication 4 (23.5%) 5 (22.7%) Subjects in the two groups did not differ in their diets prior to commencing the study (Table 2). As recorded in 3-day diet records at baseline, energy, fat, cholesterol, alcohol, 46 fibre and fish intakes were similar in both groups. Energy intake was 1616 ± 358 kcal per day with protein 18.2 ± 4.6%, fat 19.8 ± 5.7%, carbohydrate 59.3 ± 7.8 % and alcohol 2.5 ± 4.1% of energy. Saturated fat intake was 5.2 ± 2.5% of energy, and cholesterol 133 ± 75 mg per day. Subjects had been eating fish 2.4 ±1 .7 times per week. Table 2: Comparison of initial diet of subjects in the control and experimental groups Diet variable Group 1 (control) n =17 mean (± SD) Group 2 (experimental) n=22 mean (± SD) t(p) energy (kcal/d) 1546(189) 1671 (444) -1.083 (.286) %fat 17.9 (5.5) 21.2 (5.6) -1.863 (.070) %saturated fat 4.9 (2.1) 5.5 (2.7) -.754 (.456) %monounsaturated fat 7.1 (2.8) 7.9 (2.9) -.846 (.403) %polyunsaturated fat 3.8(1.5) 4.6(1.5) -1.645 (.108) %protein 18.4 (5.4) 18.0 (4.1) .233 (.817) %carbohydrate 60.6 (7.8) 58.3 (7.7) .923 (.362) % alcohol 2.7 (4.1) 2.3 (4.1) .306 (.762) cholesterol (mg/d) 121 (58) 143 (85) -.928 (.360) E P A + D H A 1 (g/d) 0.47 (0.57) 0.44 (0.51) .183 (.856) a-linolenic acid (g/d) 0.40 (0.21) 0.61 (0.42) -1.884 .(067) fibre (g/d) 24.9(10.5) 22.6 (8.0) .789 (.435) fish servings/wk 2.1(1.1) 2.7 (2.1) -.970 (.339) eicosapentaenoic acid and docosahexaenoic acid 47 3. Intervention - Diet During Study Diet instruction and follow-up counseling were provided by the 3 dietitians in the CRP with each dietitian counseling the following proportions of subjects: 53.8%, 35.9% and 10.3%. Three-day food records were used to assess nutrient intake at the beginning of the study. For the analysis of diet throughout the study, the average of the nutrient analysis of 3-day food records taken at weeks 4 and 12 were used, except for in 4 subjects who did not keep food records at week 4, and 1 subject who did not keep records at week 12. In those subjects, analysis for the diet throughout the study was recorded as that for the 3-day food records either at week 4 or at week 12, whichever was available. Thus for most subjects in the study, the diet followed throughout the study is that based on the analysis of 6 days of food records. Analysis did not include vitamin or mineral supplements consumed by the subjects, however, all supplements reportedly remained unchanged throughout the study. Repeated-measures A N O V A with time as the within-subject factor and group (control or experimental diet group) as the between-subject factor showed that, for the most part, both groups followed similar diets during the study despite the different diets being taught to them (Table 3). Analysis indicated that subjects overall reduced their energy, total fat, and monounsaturated fat intake, and increased their fish intake throughout the study. Both groups did so similarly except in total fat intake, in which the subjects in the experimental group reduced their fat intake more so than those in the control group. Although the two groups did not differ significantly initially in fat intake, the initial difference was somewhat close to significance (p = .07), with the control group having a slightly lower fat intake than the experimental group. Thus the percent fat 48 intake between the two groups during the study did not differ significantly. The other dietary variables, for the most part, remained unchanged. L N A intake was significantly lower in the control group as compared to the experimental group, and remained unchanged in both groups throughout the study. Table 3: Comparison of initial diet to diet followed during study by the two groups, analyzed by repeated-measures A N O V A (time = within-subject factor, group = between-subject factor) Variable Group 1 (control) n=17 Group 2 (experimental) n=22 F T i m e l mean ( ± S D ) Time 2 mean (±SD) Time 1 mean (+SD) Time 2 mean ( ± S D ) Group F (P) TimeF (P) Time/ group F(p) energy (kcal/d) 1546 1441 1671 1493 .834 9.876 .661 (189) (232) (444) (345) (.367) (.003)* (.422) %fat 17.9 17.8 21.2 17.0 .777 4.854 4.340 (5.5) (5.9) (5.6) (5.1) (.384) (.034)* (.044)* %saturated fat 4.9 4.7 5.5 4.2 .009 2.987 1.697 (2.1) (2.2) (2.7) (1.8) (.925) (.092) (.201) %monounsaturated 7.1 6.7 7.9 5.9 .000 4.836 2.151 fat (2.8) (2.7) (2.9) (2.1) (.986) (.034)* (.151) %polyunsaturated 3.8 3.9 4.6 4.0 1.764 .990 1.699 fat (1.5) (1.3) (1.5) (1.1) (.192) (.326) (.200) %protein 18.4 20.2 18.0 18.1 .877 2.023 1.492 (5.4) (4.5) (4.1) (3.9) (.355) (.163) (.230) 49 %carbohydrate 60.6 60.2 58.3 62.5 .000 2.368 3.493 (7.8) (7.8) (7.7) (7.7) (.994) (.132) (.070) %alcohol 2.7 1.3 2.3 2.1 .023 4.036 2.102 (4.1) (2.1) (4.1) (3.8) (.879) (.052) (.156) cholesterol (mg/d) 121 146 143 127 .008 .092 1.841 (58) (84) (85) (93) (.931) (.763) (.183) E P A + D H A 1 (g/d) 0.47 0.44 0.44 0.47 .001 .000 .126 (0.57) (.37) (0.51) (0.28) (.982) (.986) (.724) a-linolenic acid (g/d) 0.40 0.34 0.61 0.48 4.637 3.349 .423 (0.21) (0.20) (0.42) (0.28) (.038)* (.075) (.519) fibre (g/d) 24.9 23.4 22.6 24.2 .072 .000 1.588 (10.5) (9.8) (8.0) (8.8) (.790) (.984) (.215) fish servings/wk 2.1 3.3 2.7 4.0 .753 18.262 .548 (1.1) (1.7) (2.1) (1.2) (.393) (<.001)* (.465) *significant at p<.05 'eicosapentaenoic acid and docosahexaenoic acid 50 Thus, the overall diet followed during the study by the two groups consisted of 1470 ± 298 kcal, 19.0 ± 4.2% energy as protein, 17.4 ± 5.4% as total fat, and 61.5 ± 7.8% as carbohydrate. Saturated fat intake was 4.4 ± 2.0% of calories, cholesterol 135 ± 88 mg and fibre 24 ± 9 g per day. There was no difference between the two groups in self-reported adherence scores, with the control group reporting a mean adherence score of 79.7 ± 22.2% (n=15) and the experimental group reporting a score of 79.3 ± 16.8% (n=16). Thus subjects in the experimental group did not see themselves to be any less adherent to the more restricted diet than those in the control group. In comparison to the diets that were taught to the subjects in each of the groups, the actual diet followed represents a diet closer to the experimental diet (Table 4). Changes made to fat intake by the experimental group brought their diet variables closer to that of the experimental diet, however, the goal of 15 % fat was not achieved. The goal of 100 mg of cholesterol per day of the experimental diet was also not achieved. Table 4: Comparison of diets instructed and actual diet followed Diet variable Actual diet during study1 Control diet plan Experimental diet plan %total fat 17.4 (5.4) <30 15 %saturated fat 4.4 (2.0) 7-10 <6 cholesterol (mg/day) 135 (88) 200 < 100 Values are Mean (SD) 51 4. Outcome Measurements There were no significant differences in outcome measures between the groups as a result of teaching either the experimental or control diets (Table 5). It is interesting to note, though, that health perceptions in relation to diet approached significance in group and time factors compared to the other variables. The health perception scores of the subjects in the experimental group appeared to increase somewhat more so than those of the control group, although the control group did initially score somewhat higher. There were similar changes by both groups in some of the outcome measurements. Both groups improved significantly in all anthropometric measurements performed. Body weight decreased by an average of 1.8 ± 2.6 kg or 2.1% (F =16.318, p<. 001), B M I by 0.6 ±0 .9 kg/m 2 or 2.1% (F=15.384, p<.001), and waist circumference by 1.7 ± 3.0 cm or 1.7% (F=l 1.069, p=.002). Serum total cholesterol and LDL-cholesterol improved significantly and similarly in both groups. Total cholesterol improved by 0.24 ± .65 mmol/L or 3.7% (F=5.317, p=.027) and LDL-cholesterol by .21 ± .46 mmol/L or 5.3% (F=8.591, p=.006). Triglyceride and HDL-cholesterol concentrations remained unchanged. The change in cholesterol/HDL ratio bordered on significance (F=3.997, p=.057) due to the significant change in total cholesterol and the unchanged HDL-cholesterol. Health perceptions in nutrition-related quality of life improved significantly during the 12 weeks by 21% ± 35% (F=l 1.534, p=.002) in both groups. There were no significant changes in relation to effects of diet on hassles, mood, social function, and global concerns in relation to quality of life. 52 Teaching either of the diets was not associated with any negative changes in anthropometric measures, lipids or nutrition-related quality of life. 53 I e a » \ $ o z «< <s> <u u 3 <n 03 0> a X J a a* u C .2 *E « a> ©X) <u > 4> (A ha O 03 C _© e e La © O O 6X3 U C •-^ achi -sub en «H CU o £ cu la-s CU £3 © II u II a s s O o u ©X) ITS #s ha ©3 u 03 .« H (M W 0> s CU ha s c/5 03 CU cu a © a o ha JS e < c a *c cu Q. O f f N & 3 © ha o f N © ha • « e o u a s © ha a s .2 03 Q. cu § J fa CU a H D a s o ha o f N CU a 3 53 a +j 1 I 8 f N a « 9 CU CZ3 a +i 03 3 8 a +i CO oo o 0 0 3 8 2 V ro CN CO CN ^f iri VO CN 0 0 CN 0 0 OX) WO oo CN CN ro *0 oo ^ 8 0 0 m CO ir> OS SO CN r-CN 0 0 os CN OS oo CN © iri ~5i CO oo o OS o CN o o SO ^O CO "1 CN —; od 0 0 —« 0 0 OS oo *-a a=t OS sO CN OS <*o 93 1*0 o V a 03 a 03 u s *S * I N Q . 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Correlation Between Diet and Outcome Measures 5a. Correlation Between Diet Changes and Changes in Outcome Variables Further analyses were performed to explore the relationship between the intervention (diet changes made as a result of diet instruction) and changes in outcome measures (anthropometric, serum lipids, and nutrition-related quality of life). Change in diet was calculated as the difference between the average of diet measurements at weeks 4 and 12, and those at week 0. Changes in outcome measures were calculated as the difference between measurements made at week 12 and those at week 0. Weight difference was calculated as a percent change from that at Week 0 to account for variations in body weight. When the changes in dietary variables were correlated with changes in anthropometric data, no significant relationships were seen at p<.01. Only energy intake difference approached a significant relationship to % weight change at p=.046 (Table 6). 57 Table 6: Correlation between changes in diet and changes in anthropometric measures Changes in anthropometric measures changes in diet r(p) kcal total fat sat fat protein carbohydrate % weight .310 .227 .077 -.108 -.123 (.046) (.148) (.627) (.494) (.436) BMI .248 .216 .059 -.115 -.126 (.113) (.169) (.710) (.467) (.426) waist circumference .009 (.954) .012 (.940) .002 (.989) -.004 (.980) .013 (.934) When changes in diet were correlated with changes in lipids, changes in energy intake approached significant relationships to changes in serum total cholesterol (p=.010) and LDL-cholesterol (p=.035) (Table 7). Although protein intake did not change significantly during the study, changes in protein intake approached a significant relationship to changes in HDL-cholesterol (p=.010). Change in fish intake was not related to any changes in lipid variables. 58 Table 7: Correlation between changes in diet and changes in lipid measurements Changes in lipids changes in diet r(p) kcal total fat sat fat protein carbohydrate total cholesterol .405 -.017 .047 .040 -.015 (.010) (.916) (.777) (.810) (.926) LDL-cholesterol .338 -.088 .015 .011 .062 (.035) (.595) (.927) (.948) (.707) HDL-cholesterol .113 .125 .200 .406 -.314 (.493) (.449) (.223) (.010) (.052) ratio chol/HDL .141 -.126 -.164 -.247 .264 (.393) (.446) (.318) (.130) (.105) triglycerides .294 .024 -.046 -.189 .063 (.069) (.883) (.782) (.250) (.702) Changes in diet were not correlated to any changes in nutrition-related quality of life (Table 8). Thus there were no negative changes in quality of life measurement associated with further reduction in calorie and total fat intake. 59 Table 8: Correlation between changes in diet and changes in quality of life measurements Changes in quality of life measurements changes in diet r(p) kcal total fat sat fat protein carbohydrate Hassles .074 -.127 .007 .132 .052 (.667) (.459) (.966) (.444) (.765) Mood -.032 .066 .124 .278 -.202 (.854) (.706) (.478) (.106) (.243) Social life -.169 -.060 .121 .168 -.052 (.332) (.732) (.490) (.335) (.765) Health -.172 -.269 -.159 -.024 .190 (.323) (.118) (.363) (.891) (.274) Global -.234 -.190 -.017 .014 .051 (.177) (.273) (.922) (.938) (.771) 5b. Correlation Between Diet Followed During the Study and Outcome Measures Since the diet followed during the study did not differ greatly from the initial diet coming into the study, the relationship between the dietary variables during the study period and the outcome measures at the end of the study were also examined. Overall, saturated fat and cholesterol intakes were significantly related to anthropometric measurements (Table 9). Saturated fat and cholesterol intakes were both 60 significantly related to body weight and BMI, while cholesterol intake was also related to waist circumference. B M I also showed a significant relationship to total fat intake. Table 9: Correlation between diet followed during study and anthropometric outcome measurements anthropometric measures diet during study r(p) kcal total fat sat fat protein carbohydrate cholesterol weight .120 .343 .411 .144 -.284 .564 (.447) (.026) (.007)* (.364) (.069) (<.001)* BMI -.063 .416 .489 .157 -.349 .449 (.692) (.006)* (.001)* (.320) (.039) (.003)* waist .054 .282 .312 .216 -.240 .469 circumference (.733) (.070) (.045) (.170) (.127) (.002)* * significant at p<.01 Diet variables during the study did not show a strong relationship to lipid measurements made at the end of the study (Table 10). Only serum triglyceride showed a significant relationship to dietary cholesterol. Fish intake during the study approached an inverse relationship to serum LDL-cholesterol (r=-.358, p=.044) and to the total cholesterol/HDL ratio (r=-.389, p=.028). 61 Table 10: Correlation between diet followed during study and lipid measurement outcome lipid measurements diet during study r(p) kcal total fat sat fat protein carbohydrate cholesterol total cholesterol -.313 .315 .277 .114 -.322 .208 (.052) (.051) (.088) (.489) (.045) (.203) LDL-cholesterol -.158 .198 .244 .080 -.130 .054 (.336) (.228) (.135) (.630) (.430) (.742) HDL-cholesterol -.314 .150 .028 -.067 -.288 -.013 (.052) (.361) (.865) (.686) (.075) (.939) ratio chol/HDL .165 .049 .175 .148 .069 .177 (.315) (.768) (.288) (.369) (.675) (.282) triglycerides -.081 .211 .183 .207 -.188 .413 (.622) (.198) (.265) (.206) (.251) (.009)* * significant at p<.01 62 Both total fat and saturated fat intake during the study showed significant relationships to some components of nutrition-related quality of life measurements made at the end of the study, whereas energy, protein and carbohydrate intakes showed no significant correlations with quality of life measurements (Table 11). Overall, lower total fat intake was associated with higher scores for mood, health and global nutrition-related quality of life measurements. Saturated fat intake, too, showed an inverse relationship to health scores, and approached a significant inverse correlation with scores for mood and global quality of life. Table 11: Correlation between quality of life measurement outcome and diet followed during study quality of life measurements diet during study r(p) kcal total fat sat fat protein carbohydrate Hassles -.078 -.234 -.221 .176 .109 (.622) (.136) (.159) (.266) (.494) Mood -.042 -.440 -.351 .094 .235 (.796) (.004)* (.024) (.559) (.139) Social life .037 -.094 -.084 .131 -.060 (.820) (.561) (.600) (.415) (.710) Health .261 -.502 -.488 .176 .285 (.099) (.001)* (.001)* (.271) (.071) Global .021 -.407 -.314 .158 .308 (.898) (.008)* (.046) (.325) (.050) * significant at p<.01 63 6. Correlation Among Outcome Measures Since outcome measures may impact on each other, the relationships between the various outcome measures were examined to help explain the results obtained. 6a. Correlation Among Changes in Outcome Measures The relationship between changes in anthropometric measurements and changes in l ipid measurements was first examined (Table 12). Overall, improvements in anthropometric measurements were associated with improvements in total cholesterol, LDL-cholesterol and triglycerides. Percent differences in weight were significantly related to changes in total cholesterol and triglycerides, and approached significance with LDL-cholesterol concentrations. Changes in B M I showed a significant relationship to triglyceride levels, and approached significant relationships to total cholesterol and L D L -cholesterol. Changes in waist measurements approached significant relationships with changes in total cholesterol and triglycerides. Changes in anthropometric measurements showed no significant correlations with changes in HDL-cholesterol or cholesterol/HDL-cholesterol ratio. 64 Table 12: Correlation between changes in anthropometric measures and changes in lipid measurements Changes in anthropometric measures changes in lipid measurements r(p) cholesterol triglycerides HDL-chol LDL-chol ratio % weight .432 .436 -0.40 .351 .276 (.007)* (.006)* (.810) (.031) (.094) BMI .410 .421 -.044 .331 .279 (.011) (.008)* (.795) (.042) (.089) waist circumference .328 • .377 -.035 .240 .258 (.045) (.019) (.835) (.147) (.118) *significant at p<.01 65 Changes in anthropometric measurements and their relationship to changes in quality of life measurements were next explored (Table 13). In general, improvements in anthropometric measurements (reductions in measurements) were associated with positive changes in quality of life in relation to perceptions of nutrition-related hassles and somewhat also with health. A more positive score in relation to nutrition-related hassles was associated with reductions in weight, BMI, and waist measurements. More positive scores for nutrition-related health approached significant association with greater reductions in B M I and waist measurements. There were no significant correlations between changes in anthropometric measurements and changes in mood, social life, or global nutrition-related quality of life. 66 Table 13: Correlation between changes in quality of life measurements and changes in anthropometric measures Changes in quality of life measurements changes in anthropometric measures r(p) % wt BMI waist circumference Hassles - . 4 3 3 - . 4 6 5 - . 4 9 3 ( . 0 0 9 ) * ( . 0 0 5 ) * ( . 0 0 3 ) * Mood - . 0 2 1 - . 0 5 7 - . 0 5 4 ( . 9 0 4 ) ( . 7 4 9 ) ( . 7 6 2 ) Social life - . 2 8 5 - . 2 6 4 - . 2 8 5 ( . 1 0 2 ) ( . 1 3 1 ) ( . 1 0 2 ) Health - . 3 2 1 - . 3 4 6 - . 3 7 2 ( . 0 6 4 ) ( . 0 4 5 ) ( . 0 3 0 ) Global - . 2 6 1 - . 2 1 7 - . 2 9 9 ( . 1 3 6 ) ( . 2 1 8 ) ( . 0 8 6 ) *significant at p<.01 Changes in quality of life measurements were not related to changes in lipid measurements (data not shown). 67 6b. Correlation Between Quality of Life Measurements and Changes in Outcome Measures Since subjects' perceived nutrition-related quality of life throughout the study may impact on outcome measures, its relationship to other outcome measures were examined. Higher scores for nutrition-related health perceptions were associated with improvements in all anthropometric measures performed (Table 14). Global quality of life scores were inversely related to changes in waist circumference, and approached significant inverse relationships with % weight and BMI changes. Waist measurements also approached a significant inverse relationship with social life scores. Hassles and mood were not related to any changes in anthropometric measures. 68 Table 14: Correlation between quality of life during the study and changes in anthropometric measurements quality of life measurements during study changes in anthropometric measures r(p) % weight BMI waist circumference Hassles -.283 -.256 -.233 (.073) (.106) (.142) Mood -.188 -.153 -.302 (.246) (.345) (.059) Social life -.310 -.296 -.398 (.051) (.064) (.011) Health -.531 -.521 -.593 (<.001)* (.001)* (<.001)* Global -.357 -.335 -.575 (.024) (.035) (<.001)* *significant at p<.01 When quality of life and its relationship to changes in lipid measurements were studied, only health perceptions showed significant relationships, although other quality of life variables approached significance (Table 15). Higher scores for nutrition-related health perceptions throughout the study were associated with reductions in L D L -cholesterol concentrations and cholesterol/HDL-cholesterol ratios. Health perceptions 69 approached significant inverse relationships with changes in total cholesterol and triglyceride concentrations. Changes in total cholesterol levels also approached significant inverse relationships with hassles, social life and global quality of life scores. Table 15: Correlation between quality of life measurements during the study and changes in lipid outcome quality of life measurements during study changes in outcome lipid measures r(p) total chol LDL-chol HDL-chol ratio triglycerides Hassles -.364 -.283 .050 -.257 -.400 (.025) (.085) (.767) (.120) (.013) Mood -.096 -.070 .061 -.051 -.144 (.572) (.680) (.722) (.765) (.395) Social life -.364 -.343 -.037 -.252 -.248 (.027) (.038) (.826) (.132) ,( .138) Health -.400 -.425 .189 -.450 -.342 (.014) (.009)* (.262) (.005)* (.038) Global -.340 -.261 -.023 -.170 -.324 (.039) (.119) (.895) (-314) (.050) *significant at p<.01 70 7. Adherence in Relation to Diet and Outcome Measurements Since subjects' adherence to the dietary intervention may influence outcome measures, the role of adherence was explored. The adherence score, calculated as the percentage of days that subjects followed their diet during the study, was used to examine the subjects' assessment of adherence in relation to both the intervention (diet followed), and the outcome (anthropometric, lipid, and quality of life measures). 7a. Correlation Between Adherence and Diet When the correlation between adherence and diet followed during the study was examined, adherence was inversely related to total fat and saturated fat intake (Table 16). When other dietary components were also examined in their relationship to what subjects viewed as adherence to diet principles, correlation with calcium, vitamin A , P-carotene and fibre intake approached significance. 71 Table 16: Correlation between adherence and diet variables during study Diet variable Correlation with adherence r(p) total fat -.526 (.002)* saturated fat -.532 (.001)* energy .041 (.823) protein .248 (.163) carbohydrate .272 (.126) dietary cholesterol -.311 (.078) calcium .347 (.048) vitamin A .383 (.028) P-carotene .362 (.038) fibre .441 (.010) * significant at p<.01 72 The question of whether adherence to diet was translated to any changes in diet during the study was examined. Although no changes in dietary variables showed a significant relationship to adherence, an inverse relationship with total fat intake change approached significance (Table 17). Table 17: Correlation between adherence and changes in diet variables Diet variables Correlation with adherence r(p) total fat change -.376 (.031) saturated fat change -.201 (.262) energy change -.150 (.404) protein change .334 (.058) carbohydrate change .175 (.330) 7b. Correlation Between Adherence and Outcome Measures The relationships between adherence to diet and changes in outcome measures were examined (Table 18). Although no significant relationships were found between adherence and changes in anthropometric and blood lipid measurements, inverse relationships to changes in weight, BMI, and LDL-cholesterol approached significance, No relationship was found between adherence and changes in quality of life measures. 73 Table 18: Correlation between adherence and changes in outcome measures Correlation with Adherence Changes in Changes in lipids Changes in quality of life anthropmetric measures r(p) r(p) r(p) % weight -.442 total chol -.333 hassles -.085 (.011) (.067) (.666) BMI -.381 LDL-chol -.355 mood -.305 (.031) (.050) (.122) waist -.182 HDL-chol .255 social .038 (.319) (.167) (.851) chol/HDL -.284 health -.003 ratio (.122) (.987) - triglycerides -.299 global -.133 (.102) (.509) However, when the correlation between adherence and absolute values for outcome measures at the end of the study was examined, a higher adherence score was related to a more positive perception of nutrition-related health (Table 19). The relationship between adherence and more positive hassles scores also neared significance. There was no relationship found between adherence and anthropometric outcome measurements. When the relationship between adherence and lipid measurements were examined, total cholesterol approached a significant inverse relationship to adherence. 74 Table 19: Correlation of adherence with outcome measures Correlation with adherence Anthropometric measurements r(p) Lipids r(p) Quality of life r(p) weight -.039 (.834) total chol -.458 (.010) hassles .441 (.010) BMI -.281 (.119) LDL-chol -.308 (.092) mood .342 (.055) waist -.146 (.426) HDL-chol -.229 (.216) social .310 (.084) chol/HDL ratio .035 (.853) health .550 (.001)* triglycerides -.238 (.197) global .310 (.084) *significant at p<.01 8. Multiple Linear Regression Since several variables were found to correlate significantly with outcome measures, multiple linear regression analysis was done to determine which variables could best predict the changes in the outcome measures. Thus multiple linear regression analysis was performed on all the outcome measures that exhibited change during the study period i.e. changes that occurred in weight, B M I , waist, blood total cholesterol, and LDL-cholesterol. Independent variables entered in a stepwise fashion were those 75 variables that showed or approached a significant correlation with changes in the outcome measures, and would be of logical clinical consequence (Table 20). When changes in anthropometric measurements were used as the dependent variable, health perceptions in nutrition-related quality of life was identified as the strongest predictor for improvements in all three anthropometric measurements. When percent change in weight was the dependent variable, and overall total fat intake, changes in energy intake, health perceptions, hassles and global quality of life were available for entry, health perceptions together with changes in energy intake entered the equation and accounted for 45% of the change in weight. Total fat intake approached significance. When similar variables were entered with change in B M I as the dependent variable, understandably, a similar pattern of predictors resulted with health together with changes in energy and total fat intake accounting for 46% of the change in BMI . Only health perceptions emerged as the predictor for changes in waist measurements accounting for 36% of its changes when health, energy changes, fat intake changes, and social and global quality of life variables were entered. Changes in lipid outcome measurements exhibited a more diverse pattern of predictors. Only percent change in weight was shown to be a predictor for the change in serum total cholesterol levels, accounting for 23% of the change when it was entered along with dietary cholesterol, changes in energy intake, hassles, social life, health, and global quality of life as dependent variables. Health perceptions and changes in energy intake emerged as predictors for changes in LDL-cholesterol, accounting for 26% of the change when they were entered along with percent change in weight and social life. Thus it appears that weight loss, mediated in part by reduced energy intake and accompanied 76 by positive perceptions of diet-related health, may be a predictor for some improvement in blood cholesterol levels. Since adherence to diet showed possible correlation with change in some outcome variables, multiple linear regression analysis was performed with the adherence score as the dependent variable. When those variables were entered stepwise into the model, only health perceptions emerged as the predictor for adherence to diet accounting for 28% of the adherence score, suggesting the importance of subjects' perceptions of the effect of nutrition on their health, in influencing their adherence to a dietary regimen. 77 CO cu U 3 « cu E cu £ o s o c/5 CU two e cs •S c#5 CU s .2 "E cs X ) cu .3 "o3 I* c 03 w e ©X) C#5 C/l CU i . DX) CU •a S-03 CU a "3 E >> s cu CU C/5 CU C/3 fN CU s 03 H Other variables entered total fat (p=.05), global, hassles global, hassles kcal change, fat change, social life, global t (P) -5.093 (<.001) 3.450 (.001) -5.570 (<.001) 3.078 (.004) -2.563 (.015) -4.687 (<.001) Beta CN ^_ CN fsi -.787 .373 -.357 -.610 Variable health kcal change health kcal change total tat Adjusted R2 o\ ro ai OU' O sO Model health, kcal change health, kcal change, total fat health Dependent variable % weight change BMI change waist circumference change 00 JS 60 O -ST 60 fi o l-H (D O -fi o JS c/T CU ctT 6 0 fi o O o o <u 60 '•S 60 '5 <4-H o o CO -4-> O co CD -fi T3 O O CD 60 '53 to O -fi o h-l Q i - l of 60 c -fi o <u 60 e c3 o f--I O CD O X! o OS C N CO C N o o o CO •"Cj-o o C N O o\ CO C N © © © i n m i n C O C O C N i n i n cd -fi <D 60 c .fi o 13 o ON Os C N C N ON i n CN Os o C N © i n Os i n C N m i n -fi _60 '33 CD 6 0 fi fS • f i o -fi CU 60 u JS o CU VJ •5 w W (3D •2 g •S CJ cu 6X) s J3 o -J Q o e CU CU 4= CHAPTER V Discussion 1. Overview The purpose of this study was to examine whether teaching a modified, less strict version of a very low fat lacto-ovo-vegetarian diet with the addition of fish, to patients enrolled in a cardiac rehabilitation program (CRP) would be of any further benefit than teaching the standard modified fat diet. Outcome measures examined included blood lipids, anthropometric measurements, and nutrition-related quality of life. Results showed that there was no difference in short-term outcome measures between the two interventions, although both groups benefited similarly from either intervention with no detrimental effects on nutrition-related quality of life. Subjects, regardless of group assignment, reduced their energy and fat intake, lost weight, reduced waist circumference, and improved blood total and LDL-cholesterol concentrations. The results thus suggest that teaching a more restricted diet is not necessary in a CRP to improve cardiac risk factors in subjects already following a low fat diet, at least in the short term. Although not part of the original hypotheses, further analyses were done to examine the relationships among the outcome variables and changes that occurred in both groups to help explain the results obtained. When the outcome measures that showed positive changes were more closely examined by multiple linear regression analysis, it emerged that health perceptions in relation to diet were significantly associated with factors which affect energy and fat intake, adherence to diet, and subsequent weight and blood lipid changes. 8 0 In this chapter, study findings are discussed in relation to other reports in the literature on the effect of diet on cardiac risk outcomes and quality of life. The correlation data and multiple linear regression analyses results are discussed to help explain the results obtained. Study limitations are addressed, implications for dietetic practice are discussed, and conclusions are outlined. 2. Effect of Experimental Diet vs Control Diet on Outcome Measures The results from our study suggest that there is no further benefit in teaching a more restricted diet than the standard modified fat diet to patients attending our CRP. Although studies by researchers such as Ornish et al. (1990, 1998) and Barnard (1991) have found greater benefits in blood lipid outcomes between teaching a conventional diet or a more restricted fat diet, other studies in free-living subjects have found no further benefit. Brown et al. (1984) found that subjects taught Pritikin's 5-10% fat diet achieved 14% fat in their diets, but after one year, plasma lipids did not differ from those following a 25-30% fat A H A diet. In the Dietary Alternatives Study, hypercholesterolemic men taught diets with 30%, 26%, 22% and 18% fat achieved fat intakes of 27%, 26%, 25% and 22% respectively for 1 year (Knopp et al., 1997). Mean total-cholesterol level decreased 3.3%, 10.2%, 6.5%, and 8.3%, and LDL-cholesterol decreased 5.3%, 13.4%, 8.4% and 13.0% respectively. Weight losses of 2 -3 kg were achieved, but greater fat restriction was not associated with greater weight reduction. Thus in this study, further benefits in blood lipids and body weight were not achieved with a fat restriction beyond 26% fat per day. Aquilani et al. (1999) also found that male ex-smokers after following either a NCEP Step II diet or a < 20% fat diet had no significant difference between the 81 groups in total and LDL-cholesterol concentrations. Noakes and Clifton (2000) studied the effects of 3 diets all 6500 kJ: a 10% total fat, 3% saturated fat diet vs a 32% fat, 17% saturated fat diet vs 32% fat 6% saturated fat for 12 weeks on plasma lipids. The results indicated similar reduction in LDL-cholesterol levels with both the 3% and 6% saturated fat diets as compared to the high saturated fat diet, regardless of the total fat content. Thus, other studies support our findings that there may be no further benefit from teaching a more restricted diet to reduce cardiac risk outcome. In our study, although no benefits were observed by teaching a very low fat diet, no deleterious effects were seen either. Triglycerides, HDL-cholesterol, and total cholesterol/HDL-cholesterol ratios did not change significantly in this study. Other studies have suggested that very low fat diets may in fact increase triglycerides, decrease HDL-cholesterol and increase total cholesterol/HDL-cholesterol ratios resulting in a worse lipid profile, although the impact on atherosclerosis of lowering HDL-cholesterol levels by the consumption of a low fat diet is still debated. (S.L. Connor, W.E. Connor, Katan, Grundy, & Willett, 1997; Katan, 1998; Lichtenstein and Van Horn, 1998). In the Dietary Alternatives Study, greater decreases in HDL-cholesterol and increases in triglycerides were seen in those given the 18% and 22% fat diets as compared to the 26% and 30% fat diets (Knopp et al., 1997). It is possible that the reduction in H D L was not seen in our study because subjects did not remarkably further reduce their fat intake. Had the initial fat intake been higher, a lowering of HDL-cholesterol may have been seen, especially in the experimental group. Although the weight loss observed in our study was small, it also may have helped to prevent the decrease in HDL-cholesterol and increase in triglycerides, as 82 suggested by the significant correlation seen in our study between the change in triglycerides and changes in body weight and BMI. Lichtenstein, Ausman, Carrasco, Jenner, Ordovas and Schaefer (1994) found that subjects following a weight maintenance 15% or 29% fat diet showed significant reductions in total, L D L , and HDL-cholesterol as well as a 75% increase in triglyceride levels above baseline while they were on the 15% fat diet. When subjects lost weight after calorie intake was reduced, the increase in triglycerides was reduced to 22%. In a similar study, Schaefer et al. (1995) too, found that under weight maintenance conditions, hypercholesterolemic men and women following a 15% fat diet experienced significant reductions in total and LDL-cholesterol (12.5% and 17.1% respectively), but also a 22.8% reduction in HDL-cholesterol and 47.3% increase in triglycerides. However, when these subjects lost a mean of 3.63 kg in body weight while following a 15% fat ad libitum energy intake diet, a 24.3% reduction in LDL-cholesterol, and normalization of total cholesterol/HDL-cholesterol ratios and triglyceride levels were seen. In a study by Kasim-Karakas, Almario, Mueller and Peerson (2000), postmenopausal women followed a euenergetic diet that was reduced in fat stepwise from 35% to 15% over 4 months, then an ad libitum energy 15% fat diet for the next 8 months. While total, L D L and HDL-cholesterol decreased and triglyceride levels increased during the eucaloric intake phase, triglycerides normalized during the ad libitum energy phase along with a weight loss of 4.6 kg. In this study, however, HDL-cholesterol did not normalize with weight loss. In conjunction with the possible impact of weight loss, the exercise component of the CRP may have also prevented HDL-lowering in our subjects. Subjects in our program attended 1-hour cardiac exercise classes twice per week throughout the study. 83 They were also encouraged by the exercise staff to participate in exercise activities appropriate for their needs at home. Subjects in the Heidelberg Study followed a 20% fat, 200 mg cholesterol per day diet plus a daily exercise program for 12 months (Schuler et al., 1992). Body weight decreased by 5% along with a 10% reduction in serum cholesterol levels, 24% reduction in triglycerides and 3% increase in HDL-cholesterol. In the Lifestyle Heart Trial which included regular exercise, HDL-cholesterol levels did not change significantly in the experimental group despite a reduction in fat intake from 31.5% of energy to 6.8% (Ornish et al., 1990). Subjects in our study increased their fish intake during the study. Fish intake also approached an inverse relationship to the total cholesterol/HDL ratio. S.L. Connor and W.E. Connor (1997) suggest that the ideal nutrition program to optimize plasma lipid concentrations is a diet that is low in cholesterol and saturated fat to reduce L D L plasma concentrations, and that contains some fish oil to suppress V L D L production and lower triglyceride concentrations. Other researchers have suggested similar findings of the triglyceride-lowering capacity of fish oils (Nestel, 2000; Simopoulos, 1999). However, in our study, fish intake did not show a significant relationship to triglyceride or H D L concentrations perhaps because the amount of omega-3 fatty acids consumed was low and did not change throughout the study. It is suggested that slightly more than 1 g per day of omega-3 fatty acids are required to reduce V L D L triglyceride production (Nestel, 2000). In our study, subjects consumed a mean of 0.46 ± .32 g/d of eicosapentaenoic (EPA) and docosahexaenoic (DHA) and 0.42 ± .25 g/d of a-linolenic acid. Thus it is likely that fish intake in our study had little impact on reducing triglyceride concentrations. 84 Studies suggest that the HDL-lowering seen with weight loss is transient, and that HDL-cholesterol changes beneficially again once weight loss is stabilized (Hecker, Kris-Etherton, Zhao, Coval & St. Jeor, 1999). It is possible that in our study, weight loss had stabilized by 12 weeks, and thus HDL-cholesterol levels appear unchanged. Furthermore, subjects in our study were following a low fat diet upon entering the study, yet their triglyceride and HDL-cholesterol levels were not abnormal, suggesting perhaps long term adherence to a low fat diet. It is possible that there is no further improvement in blood lipids by following a diet that is more restricted than the conventional diets, unless it is as severely restricted as those of Ornish et al. (1990) or Barnard (1991). Individual fatty acids, especially individual saturated fatty acids have differing, yet marked effects on LDL-cholesterol concentrations (Kris-Etherton & Yu, 1997). The diets used by Ornish and Barnard are particularly restricted in saturated fatty acids with minimal dietary cholesterol, such that their impact on lowering plasma lipids may be more apparent than with less restricted diets. By including fish in the experimental diet, the saturated fat content of our diet (4.4%) was higher than that for the very low fat vegetarian (<3%) diets (Lichtenstein, 1998). Cholesterol intake mainly from fish sources was also higher at 135 mg per day as compared to 5-25 mg of the very low fat vegetarian diets. Although there are individual variations in responsiveness to dietary cholesterol, a meta-analysis of the effects of dietary cholesterol on serum cholesterol suggests that the greatest response to dietary cholesterol is expected when dietary cholesterol is near zero (Hopkins, 1992). This suggests that a greater difference in serum cholesterol may be seen when comparing intakes of near zero to those that are above 100 - 150 mg per day. Thus it is possible that 85 a diet that is further restricted in cholesterol and saturated fat than our experimental diet is necessary to achieve greater reductions in blood lipids. 3. Diet and Outcome of Both Groups as a Whole Although there were no differences between groups in the actual diet followed, subjects overall reduced their calorie and fat intake and experienced improvements in anthropometric measurements and blood lipids. The improvements in blood lipids appear small (total cholesterol improved by 0.24 mmol/L or 3.7% and LDL-cholesterol by .21 mmol/L or 5.3%). As suggested earlier, changes in blood lipids and anthropometric measurements may have been larger if subjects in this study had been eating a more conventional diet at baseline. In a study by Davidson, Hunninghake, Maki, Kwiterovich and Kafonek (1999) that compared the effects of eating different types of meat on lipids in free-living subjects, subjects who were more compliant with the NCEP Step I diet at baseline, had significantly smaller reductions of blood lipids during the intervention than did those who were noncompliant at baseline. The degree of response to diet intervention may also vary depending on baseline lipid levels. Boyd, Cousins, Beaton, Kriukov, Lockwood and Tritchler (1990) observed changes in serum cholesterol in women who reduced their fat intake from 37% to 21% for 12 months. Those subjects whose initial serum cholesterol was in the upper tortile showed the greatest change with a reduction in serum cholesterol of 10% while the middle and lowest tertile showed a 4% reduction and 3% increase respectively in serum cholesterol concentrations. In a study by Nicklas, Katzel, Bunyard, Dennis and Goldberg 86 (1997), hypercholesterolemic women experienced 13% and 14% reductions in total and LDL-cholesterol levels respectively, in response to the A H A diet and weight loss interventions. However, no significant lipid changes resulted in normocholesterolemic or mildly hypercholesterolemic women. In Canada, the average total blood cholesterol level in men 55- 64 years is reported to be 5.56 mmol/L while that of women in the same age group is 5.95 mmol/L (Connelly et al., 1992). Our subjects had a mean blood cholesterol concentration of 5.67 ± .81 mmol/L and LDL-cholesterol of 3.51 ± .68 mmol/L at the beginning of the study, suggesting that a large decrease in blood cholesterol levels may not be expected. Even a small change in blood cholesterol, though, may have some impact on C V D outcome. The results of the Lipid Clinics Coronary Primary Prevention Trial suggests that a 1% decrease in total cholesterol is associated with a 2 % reduction in incidence of coronary heart disease (CHD) (Lipid Research Clinics Program, 1984). Law, Wald and Thompson (1994) in an analysis of 10 cohort studies and 28 randomized trials calculated that a 10% reduction in serum cholesterol concentration reduces ischemic heart disease by 50% at age 40,40% at age 50, 30% at age 60, and 20% at age 70. Predictive equations for changes in blood cholesterol in relation to changes in dietary fats have been developed by various researchers (Kris-Etherton & Y u , 1997). The equation by Mensink and Katan (1992) suggests that the change in total cholesterol (mmol/L) = .039 AS - .003 A M - .015 AP, with AS, A M , and AP being changes in percentage of daily energy from saturated, mononunsaturated, and polyunsaturated fatty acids, respectively. Since there was just a small change in monounsaturated fatty acid 87 intake, only a trend towards decreased saturated fatty acid intake and no significant changes in polyunsaturated fatty acids, the calculated expected change in blood cholesterol of 0.021 mmol/L was less than what was observed in our study. The meta-analysis by Yu-Poth et al. (1999) suggests that for every 1% decrease in energy from dietary total fat, total blood cholesterol is reduced by .06 mmol/L and LDL-cholesterol by .042 mmol/L. This would account for .14 mmol/L of the change in total cholesterol, and .10 mmol/L of the LDL-cholesterol. Thus the change in blood cholesterol could be attributed possibly to variables other than changes in the amount and type of dietary fat consumption, such as weight loss as a result of reduced energy intake observed in our study. Multiple regression analysis in our study suggests that the small change in lipids is accounted for in part, by changes in body weight and calorie intake. The decrease in energy intake during the study (1616 kcal to 1470 kcal per day) is consistent with a 1.5 kg decrease in body weight during the 12 weeks of the study. When changes in diet were correlated with changes in lipids, changes in energy intake approached significant relationships with changes in serum total cholesterol and LDL-cholesterol. Improvements in anthropometric measurements were also generally associated with improvements in total cholesterol, LDL-cholesterol and triglycerides. Although B M I also showed a significant relationship to total fat intake, it appears that the decrease in energy intake and improvement in anthropometric measurements and their association to improvements in serum lipid levels may be the most significant relationship. Other studies have had similar findings. Kasim et al. (1993) found that reduction in dietary fat intake from 36% to 17% per day was related to decreases in total energy 88 intake and body weight. Changes in percent body fat and weight, but not changes in nutrient intake, were correlated to changes in total and LDL-cholesterol. In a study by Dengel, Katzel and Goldberg (1995), subjects after following the A H A diet for 3 months were randomized into an A H A plus weight maintenance diet or an A H A plus weight loss diet for 9 months. The weight loss group reduced total cholesterol by 4%, L D L -cholesterol by 7%, and triglycerides by 17% beyond what was achieved during the A H A diet alone, while the weight maintenance group had no further changes in blood lipids. When Noakes and Clifton (2000) compared the effect of 3 energy restricted diets with differing amounts of saturated fats on plasma lipids, after 12 weeks, only weight loss correlated with the change in LDL-cholesterol and accounted for 17% of the variance. However, results of some studies do not suggest a primary role for weight loss in some populations. For example, in a study by Nicklas et al. (1997), normocholesterolemic and mildly hypercholesterolemic subjects following the A H A diet for 2 months, followed by a weight loss diet, had no further significant changes in total or LDL-cholesterol on the weight loss diet. Hypercholesterolemic subjects (LDL-cholesterol 4.57 ±.11) , however, showed a significant reduction in LDL-cholesterol with weight loss suggesting that weight loss is beneficial in improving blood lipids primarily in this population. Fox, Thompson, Butterfield, Gylfadottir, Moynihan and Spiller (1996) found that obese postmenopausal women following the A H A diet for 24 weeks achieved an average weight loss of 6.5 kg, but had no significant changes in mean blood lipid or measures of body fat distribution. The subjects in this study, however, were older obese women (65.6 ± 3.3 years, 120-140% of ideal body weight), and the authors suggest that weight loss may not significantly affect the classic C V D risk factors such as blood lipids 89 in this population. Further study on the effects of weight loss on blood lipids in specific population groups is warranted. Percent weight change accounted for 23% of the variance in total cholesterol change in our study. A meta-analysis of 70 studies that examined effects of weight reduction on blood lipids found that weight reduction was associated with 10% and 8% of the variance in change in total cholesterol and LDL-cholesterol respectively (Dattilo and Kris-Etherton, 1992). The meta-analysis also found that for every kilogram decrease in body weight there was a .05 mmol/L decrease in total cholesterol, and .02 mmol/L decrease in LDL-cholesterol. Using this calculation, .08 mmol/L change in total cholesterol, and .03 mmol/L change in LDL-cholesterol can be predicted by effect of weight loss in our study. Although the actual effect seems small since both weight loss and blood lipid changes were small in our study, weight loss may partially explain the observed improvements in total and LDL-cholesterol levels. Suggested mechanisms for the effect of reduced energy intake on lipid levels include the inhibition of H M G CoA reductase by energy restriction resulting in reduced hepatic cholesterol synthesis, and enhanced cholesterol excretion in bile as a result of weight loss (Hecker et al., 1999). 4. Effect of Fish in the Experimental Diet Our experimental diet included fish in addition to the very low fat vegetarian diet. Fish was included in the study to allow further variety in food choices while enhancing the very low fat vegetarian diet with its omega-3 fatty acid content. Since both groups increased fish intake similarly, a conclusion cannot be made regarding the effectiveness 90 of including fish in the experimental diet. D H A and EPA intake did not change throughout the study and remained less than 0.5 grams per day suggesting that our subjects ate lean fish rather than fatty fish most of the time. No apparent benefits were seen in our study by adding fish to the vegetarian diet, although fish intake approached an inverse relationship to serum LDL-cholesterol and to the total cholesterol/HDL ratio. L N A intake, another source of omega-3 fatty acids, although lower in the control group, was consistent in both groups throughout the study, and did not impact on study results. However, the effects of including fish in the diet cannot be measured by the effect on blood lipids alone since benefits of eating fish on other cardiac outcome measures have also been suggested in some studies. A review of prospective cohort studies suggests that 40 - 60 g mixed fish per day in high risk populations is associated with 40 -60% reduced risk of CHD death (Marckmann and Gronbaek, 1999). In the Diet and Reinfarction Trial, 2.4 g EPA per week, or approximately 0.3 grams per day was associated with a 29% reduction in 2 year mortality (Burr et al., 1989). Some research suggests that reduced risk for cardiac mortality is mediated in part through the omega-3 fatty acid content of fish by such mechanisms as prevention of ventricular tachycardia and fibrillation, its antithrombotic properties, and stimulation of endothelial-derived nitric oxide, all of which act independently of blood lipid concentrations (Connor, 2000; Simopoulos, 1999). There are also suggestions that it may be components of fish other than omega-3 fatty acids that may contribute to the decreased risk of mortality observed in epidemiological studies (Marckmann and Gronbaek, 1999). Thus although a conclusion regarding the effects of fish cannot be made on the basis of the outcome measures used in this study, other unmeasured benefits of eating fish may have occurred. 91 5. Feasibil ity of Experimental Diet Although it seems unlikely, we cannot exclude the possibility that had patients in the experimental group actually reduced their fat intake to 15% and cholesterol intake to 100 mg per day, a difference may have been seen between the two groups. However, the effectiveness of a very restrictive diet is not meaningful to clinical practice i f the diet is not feasible for patients to follow. Given instructions and support to reduce fat intake to 15% and cholesterol to 100 mg per day, participants in the experimental group, although very close to the desired goals for our study, were unable to achieve this restriction. This suggests that even though very restricted diets may achieve more optimal cardiac risk factors, they may not be feasible for most patients with C V D . A review of studies on adherence to cholesterol-lowering diets in free-living subjects who prepared their own meals, suggested that maintaining adherence to very restricted low-fat, low-cholesterol diets may be difficult (McCann, Retzlaff, Dowdy, Walden and Knopp, 1990). A study which explored the effects of attitudes of post myocardial infarction patients on adherence to cardiac diets suggested that changes such as eating fish, and limiting cheese, fried foods and meat portion sizes were difficult to make (Barnes and Terry, 1991). Difficulty in making such changes may reduce one's ability to adhere to diets that are very restricted in total and saturated fat. In our study, though, the self-reported adherence scores with either the 15% fat experimental diet or <30% fat control diet did not differ, and subjects reported adhering to the diets approximately 79% of the time. 92 In ward studies or in those studies in which food was provided to subjects, compliance to more restricted diet guidelines has been more feasible and physiologic responses have been maximized (Wing, 1997). Dietary compliance and cardiovascular risk reduction in a 15-20% fat diet consisting of prepared meals that were delivered to subjects' homes as compared to a self-selected diet were examined in a 10-week study (Metz et al., 1997). In this study, 78% of those subjects with prepared meals were able to adhere to a <20% fat diet, while only 23% of self-selected diet participants were able to do so. Other studies have found that free-living patients taught a more restrictive diet of < 20% fat have been unable to achieve that goal. Buzzard et al.i?(1990) used a two step low fat intervention program designed to reduce fat intake to 15% of energy intake in free-living postmenopausal women with breast cancer. After 3 months of the program, subjects achieved a 25% reduction in energy intake along with a reduction in fat intake from 38% to 23%. Although the reduction in fat intake was significant and useful for their purposes, the intended 15% fat intake was not achieved. In another study, Kasim et al. (1993) taught a 15% fat diet to healthy women who were able to achieve 17% fat after 3 months and maintained that for 1 year. In the Stanford Coronary Risk Intervention Project (SCRIP), subjects taught a < 20% fat diet with < 75 mg cholesterol per day achieved 24% fat and 143 mg cholesterol intake (Haskell et al., 1994). Subjects in the Dietary Alternative Study taught a diet with 18% fat and 100 mg cholesterol per day achieved 22% fat and 136 mg cholesterol per day (Knopp et al., 1997). Thus in free living subjects, it is possible that a very low fat diet is not feasible on a long term basis. 93 6. Relationship Between Diet and Quality of Life A reason for the inability of subjects to follow a more restricted diet may be the detrimental effects of a lower fat intake on quality of life. However, subjects in this study reduced their fat intake further without detrimental effects on nutrition-related quality of life measures. In fact, overall, lower total fat intake was associated with higher scores for mood, health and global nutrition-related quality of life measurements. Saturated fat intake, too, showed an inverse relationship to health scores, and approached a significant inverse correlation with scores for mood and global quality of life. There was no correlation found between fat intake and nutrition-related hassles or social functions. Other studies have also shown that low fat diets are not necessarily associated with reduced quality of life. Moderately obese women following a low-fat ad-libitum complex-carbohydrate diet for 6 months showed improvements in satiety and quality of life, while those on a low-energy diet had reductions in those effects (Shah, McGovern, French, & Baxter, 1994). In the Family Heart Study, there was improvement in overall emotional state in all groups after 5 years of a dietary intervention program, with those on a low-fat high complex-carbohydrate diet showing greater improvements in depression and hostility as compared to those eating a typical American diet (Weidner, S.L.Connor, Hollis & W.E. Connor, 1992). Hypercholesterolemic subjects assigned to a < 20% fat diet, a Mediterranean diet with fat 30% of energy, or the control group for 12 weeks, showed no group differences in psychological well-being, including that of mood (Wardle et al., 2000). Subjects with stable angina pectoris following a 20% fat diet for 12 months in the Heidelberg study showed no difference in the degree of depression as compared to subjects in the control group (Schuler et al., 1992). Subjects provided a low 94 fat diet emphasizing fruits, vegetables, low-fat dairy products, and whole grains for 8 weeks in the Dietary Approaches to Stop Hypertension (DASH) trial showed greater improvements in overall quality of life scores as compared to those on the control diet (Plaisted, Lin, Ard, McClure & Svetkey, 1999). However, when free-living subjects with strong risk factors for C V D following a self-selected 17% fat diet for 10 weeks, were compared to those given prepackaged foods, only those with the prepackaged meals understandably showed reductions in nutrition hassles (Hatton et al., 1996). Both groups, though, had significant improvements in nutritional health perceptions and mood. In one study, healthy volunteers who were provided firstly with a 41% fat diet for one month, and then a 25% fat diet for another month, showed negative changes in mood as compared to those who continued to eat a high fat diet (Wells, Read, Laugharne & Ahluwalia, 1998). However, these subjects were healthy volunteers who may not necessarily be as motivated to change their diets as compared to those who may have medical reasons to do so. Also, the effects were measured after only one month on the lower fat diet, and it is possible that effects may be different with a longer term intervention. Thus, the results from our study, which indicate that reducing fat intake did not compromise nutrition-related quality of life for subjects with or at risk for C V D , are generally supported by other studies. 7. Nutrition-related Health Perceptions and Adherence to Diet The ultimate outcome of any dietary intervention is dependent not only on the metabolic effects of the diet in an individual, but also on his/her motivation to make those 95 dietary changes and adhere to them (Rhodes, Bookstein, Aaronson, Mercer & Orringer, 1996). In our study/using multiple linear regression analysis, nutrition-related health perceptions emerged as a predictor of positive cardiovascular risk changes. Not only did subjects show improved scores at the end of the study as compared to baseline, improved health perceptions scores were associated with overall improved measurements (i.e. greater reductions) for most outcome measures. It is important to note, however, that the design of the study does not permit causation to be inferred - it is also possible that improvement in outcome measures (e.g. a loss of weight) led to improved perceptions of the nutritional quality of the diet. Linear regression analysis in our study, showed that self-reported adherence to dietary recommendations was also predicted by perceptions of health. This, too, suggests the significance of subjects' perceptions of the healthiness of their diet and its effect on their health, in determining their diet-related actions. The importance of health perceptions in determining dietary actions has been assessed in other studies. For example, in a European study with over 14,000 subjects, staying healthy and preventing disease were perceived as the main benefits associated with healthy eating (Zunft et al., 1997). This relationship was stronger with increasing age in both men and women. Another paper describing the same study suggests that of the factors influencing food choices, "trying to eat healthy" was among the five most important factors identified by subjects, preceded by quality and freshness of food, price, and taste, and followed by family preferences (Lennernas et al., 1997). Females, older persons, and more educated subjects tended to choose "trying to eat healthy" as being a major factor in their food choices. In another study, 38 patients with cardiovascular metabolic disease who followed a self-selected 17% fat diet for 10 weeks had significant 96 improvements in nutritional health perceptions and affect and showed improvements in weight, lipids and blood pressure (Hatton et al., 1996). Analysis of the relationship between diet and adherence scores in our study provides some insight into subjects' perceptions of adherence to diet. Subjects in our study generally reported good adherence to their diet (i.e. followed their diet approximately 79% of days recorded). More positive adherence scores were inversely related to total fat and saturated fat intake during the study, suggesting that subjects viewed adherence to diet as a lower total and saturated fat intake. Adherence scores also approached significant relationships with calcium, fibre, and P-carotene intake. In translating these into food items, these nutrients are those found especially in dairy products, fruits and vegetables. Thus subjects who felt they were adhering more closely to their diets were most likely to have eaten less total and saturated fat, more fruits and vegetables, and possibly more skim milk products. Similar perceptions for healthy eating are described by Margetts, Martinez, Saba, Holm and Kearney (1997), who in a survey of subjects in Europe, found that subjects who believed that healthy eating was beneficial for weight control, described healthy eating as low in fat and high in fruits and vegetables. Therefore, although subjects in the experimental group showed no difference in cardiac risk outcome measures as compared to those in the control group, both groups overall tried to eat a low fat diet that they felt was beneficial to their health. In doing so, they achieved some improvement in blood lipids and anthropometric measures, without compromising quality of life. 97 8. Limitations It is necessary to recognize the limitations in interpreting the findings in this study including such issues as subjects and methods used. Subjects entering our study were not eating a typical North American diet of 34% fat, 12% saturated fat, 291 mg cholesterol/day (Ernst, Sempos, Briefel & Clark, 1997). Instead, both groups entered the study already following a diet lower in fat and cholesterol than the conventional diet, and then followed generally similar diets throughout the study. Subjects in the experimental group, despite being taught a more restricted diet, did not reduce total fat and cholesterol levels to that desired for the experimental diet. Changes made to fat intake by the experimental group brought their diet variables closer to those of the experimental diet (from 21.2% to 17.0% of energy as fat), however, the goal of 15 % fat and 100 mg cholesterol per day was not achieved. Cholesterol intake did not change significantly at 127 mg per day. Subjects in the control group on the other hand, too, were already following a diet lower in fat (17.9% of energy) than the diet allocated, and did not increase their fat intake to that permitted in the control diet. Saturated fat intake did not change significantly in either group, remaining at generally <5% of energy intake throughout the study. Thus, no difference was found in outcome between the two groups in this study. Although it can be concluded that teaching a more restricted diet as compared to the standard diet showed no further improvements in cardiac risk outcomes, the physiological effectiveness of a more restricted diet as compared to the conventional diet on cardiac risk outcomes, could not be determined on the basis of this study. 98 The findings from this study can be generalized only for participants already on a low fat diet, who have C V D or are at high risk for C V D , and participate in a cardiovascular risk reduction program. Such subjects are more likely to believe in the health benefits of lifestyle modification and have the motivation to try improving their cardiac risk status, simply by the fact that they have made the effort to participate in the CRP. Furthermore, it is possible that due to the nature of the study, it attracted cardiac patients who had preconceived ideas of the benefits of very low fat diets and were already following more restrictive diets. Thus our subjects' baseline diets, motivation to adhere to diet modifications, and their perception of nutrition-related quality of life may not be the same as others who are less convinced of the impact of lifestyle measures on their well-being. Teaching the different diets to less motivated subjects may have had different results. Another possible reason for the very low fat baseline diets of our subjects was the approximate 2 weeks to 2 months delay between recruitment and baseline diet assessment. It is possible that subjects may have changed their diets in the interim, especially after study details had been explained to them at recruitment. Thus baseline data may not have reflected usual diet prior to participation in the study. Only 39 eligible subjects fully completed the study rather than the original goal of 56 subjects. If our goal of 58 subjects had been attained, there may have been slightly different results in the correlation data in that some of those results that approached significance may have had clearer findings with a larger subject number. However, it is unlikely that the overall outcome regarding our hypothesis would have changed since most of our subjects came into our study following diets more restricted than the 99 conventional diets. In fact, the standard deviation for % fat intake at baseline indicates that 84 % of our subjects ate less than 25.5% of energy as fat coming into the study. Thus teaching a more restricted diet to a larger group would not have changed our results from teaching a conventional diet or a more restricted one. Another possibility for variations in our results is the variability among subjects in response to diet. Both noncompliance and biological resistance have been suggested as reasons why one third of patients in a study by Denke and Grundy (1994) did not respond to a standard cholesterol lowering diet. The degree of response to dietary modifications in a study population may depend on the number of responders and non-responders to dietary modifications in the study group (Denke, 1995). The relatively small response observed in our study could have resulted due to the subject recruitment process. Twenty percent of subjects who were recruited and consented for the study were eliminated because their blood cholesterol levels were too low to comply with the inclusion criteria. These subjects may have been those who could be considered more responsive to dietary modifications, while those remaining in the study could have included a greater proportion of those who are nonresponders to diet modification. Food intake data and adherence scores were based on self-report, and such data may not necessarily reflect actual intake. A major bias of food record is a tendency to underreport food intake (Lichtman et al., 1992; Schoeller, 1990). Furthermore, use of one 3 day food record for the initial diet data, and 6 days for the diet during the study may not reflect actual intakes during that time since there may be a tendency toward greater adherence to an expected diet during the record keeping period (Schoeller, 1990). However, food records were reviewed with subjects and every effort was made to 100 encourage accurate reporting. Multiple day food records are considered to be a valid tool for assessing food intake during the recording period (Thompson & Byers, 1994). Also, the same tool was used in examining the difference in diet between the two groups at two different time periods, thus reducing the variability caused by the tool itself. There may be been some limitation associated in interpretation of the quality of life questionnaires. Some patients found a few questions to be confusing, especially in the "hassles" portion of the questionnaire and may not have answered them with the accuracy desired. However, the hassles section of the questionnaire consists of 49 questions and the effect of an inappropriate response to the occasional question would likely have minimal impact on the overall score for the section. Also, the same questionnaire was used for pre- and post-intervention such that the variability caused by the questionnaire itself should be minimized. The Pearson's correlation coefficient calculations involved the analyses of many variables. Therefore, in interpreting the correlation data, the increased possibility of making a type I error must be considered. To reduce the probability of a type I error, a more conservative level of significance was chosen, and p was set at <. 01 for correlation analyses. Three dietitians were involved in counseling subjects and it is possible that various dietary aspects may have been given different emphasis depending on the dietitian. Counseling techniques that may have influenced how subjects were able to follow the assigned diets may have varied among the dietitians. However, all dietitians were familiar with both diets and counseled all subjects as usual. The distribution of subjects in experimental versus control group did not differ among the three dietitians 101 (data not shown). Standardized diet instruction sheets and other handouts were also provided such that variations among dietitians were minimized as much as possible. No difference in outcomes were observed when the data were analyzed according to which dietitian provided the diet counseling (data not shown). Fish intake data as described in the "methods" portion of this paper, was obtained by 2 different methods. Fish intake at baseline was self-reported on the diet questionnaire given prior to beginning the study and reported as frequency of servings in a day or week. Fish intake during the study, however, was analyzed using a daily record of fish consumption on the calendar, but analyzed as servings per week. This difference in data collection may account for some inaccuracy in comparing fish intake before and during the study. Frequency of fish servings were indicated by both methods, but quantities of a serving were not specified such that actual quantities of fish consumed are not available except on the 3 day food records. However, in comparing the change in number of servings of fish from one time to another within-subjects, the variability in interpretation of fish serving size is reduced. In interpreting the frequency of fish servings during the study, suggested portion sizes for fish and other protein sources were given during diet counseling. Fish intake data indicated that both groups increased their fish intake although this was not encouraged in the control group beyond what is usually recommended. There are two possible reasons why this may have occurred. Firstly, there was the possibility of "group contamination" in that both control and experimental groups participated in the same CRP classes allowing opportunities for discussion among study participants. Secondly, all subjects were asked to complete the adherence calendars indicating not only 102 adherence to diet, but also frequency of eating fish. Noting fish consumption on the calendars may have contributed to increased fish intake in both groups. Body weight and waist measurements were performed by the dietitian assigned to the particular patient. There may be variations in measurement as a result of the different dietitians, however, all dietitians used standard procedures and performed the measurements as accurately as possible. Another limitation in the interpretation of this study is the short term length of the intervention considering that long term eating behaviour change is not necessarily measured in 12 weeks. The act of eating is a complex issue that combines psychological, emotional, physiological, cultural, and social needs in a given environmental setting. If the environment should change such as the availability of appealing very low fat foods and adoption of fat substitutes, the issue of feasibility may also change. Thus this study needs to be interpreted as a stepping stone that may provide guidance as to what directions dietitians might take in terms of helping patients to optimize their cardiac risk through diet. Cardiac outcome measures after 12 weeks does not necessarily reflect what processes may occur over the years it might take for cardiac events to happen. Lipids are not the only markers for severity or progression of disease. The development of CVD involves many other factors besides lipids and weight, these being intermediary measurements of CVD development. There may be other unmeasured positive outcomes as a result of changes in the diet in areas such as endothelial health, thrombogenesis and oxidation of the LDL particle. In the Lifestyle Heart Study, angiographic studies showed that further regression in coronary atherosclerosis had occurred after 5 years in those who 103 continued to follow a very low fat diet (Ornish et al., 1998). For those in the control group, although LDL-cholesterol levels did not differ between the two groups after 5 years, atherosclerosis continued to progress. Thus the outcome observed must be interpreted in the context of the short duration of the study. Lastly, patients during the study participated in a CRP that includes regular supervised exercise and stress management classes. It is possible that some improvements in outcome may be attributed to the effects of other components of the program. Exercise may have an effect on lipoprotein concentrations, however, since both groups participated in the exercise program, exercise should not be a confounder in examining the difference in outcome between the two groups. While keeping in mind the limitations noted, relevant implications for dietetic practice can be inferred based on the results obtained from our study. 9. Implications for Dietetic Practice There is much speculation and discussion as to what is the optimal diet for controlling heart disease. However, despite what is thought to be physiologically optimal, the ability of subjects to implement and adhere to diet principles determines the ultimate outcome of teaching a diet. Our results suggest that even in this motivated population, it may be difficult for patients to adhere to a 15% fat semi-vegetarian, <100 mg cholesterol per day diet. Eating occurs in an environment of culture, food availability, and other circumstances, and if that environment changes, it is possible that such a diet may be more feasible in the future. However, at the present time, it appears that teaching the standard modified fat diet to patients in a CRP appears to have similar 104 results in blood lipid and anthropometric changes as teaching a more restricted diet. Therefore, the results of this study suggest that it is unnecessary to teach a more restricted diet than the conventional diet to patients enrolled in a CRP. Such motivated patients appear to be already following a diet more restricted than the conventional diet, and in response to dietary counseling, make changes to reduce energy and fat intake with similar positive cardiac risk outcomes, regardless of the difference in specific details provided. It appears that patients' perception of the effect of dietary changes on their health has more impact on their adherence to diet principles and ultimate change in cardiac risk measures, rather than the strictness of the diet that is taught to them. Even in the area of weight management for cardiac patients, helping people to change their thinking towards optimal weight and waist circumference as mediators for better health, may help them to change their eating habits. Since weight loss appears to have a significant relationship to improvements in blood lipids, dietitians need to develop such useful strategies that will enable them to assist patients in making behaviour changes for long term weight loss. How important patients see their diet as affecting their health appears to be a predictor for weight loss. Therefore, to maximize the impact of diet counseling sessions for cardiac patients, dietitians could emphasize the nutrition-related health benefits of dietary modifications to encourage greater adherence to diet principles. 10. Directions for Further Research The search for the optimal diet for controlling heart disease continues. The question of whether a 15% fat semi-vegetarian diet is physiologically more beneficial than the conventional modified fat diet remains unanswered since our subjects did not 105 follow their assigned diets. Another trial with subjects following a NCEP Step II diet as the control diet as compared to the experimental needs to be done to answer this question. Results from such a trial may be beneficial to some very motivated individuals who may want to maximize the effect of lifestyle modification. Small changes in outcome measures were achieved after 12 weeks in this study. A longer-term study is necessary to determine whether subjects continue to maintain the dietary changes made with subsequent improvements in cardiac risk. Furthermore, outcome measures that include lipids and anthropometric measurements as well as other indicators of C V D could be done to obtain a more complete picture of the effect on atherosclerosis. The outcome of dietary counseling is determined by patients' adherence to dietary recommendations. Since nutrition-related health perceptions emerged as the strongest predictor for diet adherence in this study, further research to determine whether such health perceptions can be changed, what factors can influence those changes, and whether those changes translate into improved cardiac risk outcome, is needed. A better understanding of the effects of nutrition-related health perceptions and other motivation issues will enable dietitians to develop more effective counseling sessions to help patients achieve optimal dietary management of C V D . 1 1 . Conc lus ions There is no difference in short-term outcome by teaching a <15% fat lacto-ovo-vegetarian plus fish diet as compared to the conventional modified fat diet to adults with C V D who are already following a low fat diet, and enrolled in a CRP. Subjects benefit 106 equally from either diet intervention with no negative effects on nutrition-related quality of life. Further diet modifications and subsequent improvements in blood lipid and anthropometric measurements occur even when subjects at baseline are following a diet more restricted than the conventional modified fat diets. 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Br J Nutr 1998;79:23-30. Wing RR. Food provision in dietary intervention studies. Am J Clin Nutr 1997;66:421-422. Yu-Poth S, Zhao G, Etherton T, Naglak M , Jonnalagadda S, Kris-Etherton P M . Effects of the National Cholesterol Education Program's Step I and Step II dietary intervention programs on cardiovascular disease risk factors: a meta-analysis. Am J Clin Nutr 1999;69:632-646. Zunft HJF, Friebe D, Seppelt B, de Graaf C, Margetts B, Schmitt A et al. Perceived benefits of healthy eating among a nationally-representative sample of adults in the European Union. Eur J Clin Nutr 1997;51 (Suppl 2):S41-S46. 118 Appendix C. Information Sheet for Interested Subjects Would you be interested in participating in a diet research study? A dietitian in our program who is also studying at U.B.C. is looking into whether there is a better diet for controlling heart disease. Why look for a better diet? We really are not sure what kind of diet might be the most effective in controlling heart disease. The usual diet is a low fat low cholesterol diet which includes lean meat, poultry, fish, and low fat dairy products, and that has been shown to reduce cholesterol levels for most people. But, some studies have suggested that a much stricter diet might be even more effective in reducing cholesterol levels and weight. Therefore, we would like to see if a diet that is semi-vegetarian and very low in fat would be more effective than the usual diet that we recommend. What does the study involve? Half of the people involved in the study will follow the usual diet and the other half will follow the study diet during the cardiac rehabilitation program. This means that if you are assigned the study diet, you will be asked to eat about 1/2 of the fat usually recommended. Fish, egg whites, skim milk dairy products, and legumes will be your main protein sources. You will be asked to eat no meat or poultry for the duration of the study if you are assigned this study diet. Your program will not be different in any way from the usual program, except that you will be taught a different diet. If you are unable to follow the diet once you start the study, it is okay. We want to know that too. You can ask to drop out of the study at any time if you wish to do so. We would just like to ask you to give it a try. 121 Study procedures About 60 patients in the Healthy Heart Program are expected to participate in this study. You are not eligible for the study if: • you are a smoker • you are unable to eat fish twice per week • you are involved in any other program which might cause rapid changes in weight • you have insulin dependent diabetes, renal disease, or any unstable medical condition such as hypothyroidism which is not yet treated, or • you have allergies or any other medical condition in which study diet modifications would not be suitable. The study will take place during the first 12 weeks of your participation in the exercise classes. If you choose to participate in this study, you will be randomly assigned (by equal chance) to one of two groups. • One group will follow the usual diet. The usual diet is a low fat low cholesterol diet (less than 3 0 % fat, 200-300 mg cholesterol) with lean meat, poultry and fish, low fat dairy products, plenty of whole grain products and fruits and vegetables. It also includes limited amounts of eggs, margarine, and oil. • The other group will follow the very low fat semi-vegetarian diet (about 1 5 % fat, 100 mg cholesterol). The diet will not include any meat or poultry, but will include egg whites, fish, skim milk dairy products, and legumes as main protein sources. You will be asked to eat fish at least twice per week. The diet includes only minimal amounts of margarine and oil. It includes plenty of fruits and vegetables and whole grain products as in the usual diet. Your program will not differ in any way to the usual Cardiac Rehabilitation Program except in the type of diet that you will follow if you are assigned to the very low fat diet group. Every one will attend exercise sessions and education classes and receive dietary instruction as usual. You will be given appropriate diet instruction by the dietitian sometime during the first two weeks of starting the exercise sessions. Further help with the diet will be given as you need it throughout the program. As part of the study we need to keep track of how you are eating. You will be asked to keep a record of what you eat for 3 days. You will keep these records three times during the study - at the beginning, in one month and at the end of the study. You will also keep a record of the number of times you ate fish each week, and the days that you were unable to follow the appropriate diet. As usually done during the program, you will have a blood test for cholesterol, other blood fats, and other tests that are routinely done as part of the program before starting the program and again, after 12 weeks of being in the program. Your weight will be monitored throughout the program, and recorded at the 123 beginning and once per month thereafter. Your height will be taken once in the beginning of the study. Your waist will be measured in the beginning and at the end of the study. You will complete a questionnaire which will look at how diet affects your quality of life. This will be completed at the beginning of the study, and again at the end. Extra time required beyond what is normally required during the program as a result of this study, is the time it will take you to complete the 3 sets of 3 day food records, the record of how you were able to adhere to your diet, and the quality of life questionnaire. This will likely require a total of about 90 minutes over the course of the study. Potential Discomforts, Side Effects and Risks There is likely neglible risk in following the usual diet or the very low fat semivegetarian diet. There should also be no uncomfortable physical changes or significant side effects as a result of following these diets. Potential Benefits Both diets may lower cholesterol and other fats in the blood, and may also help you to control your weight, but we do not know if the very low fat semivegetarian diet will be any more effective than the usual diet. We also do not know if the very low fat diet will affect your quality of life any more or less than the usual diet. In addition, the results of this study could help dietitians to make diet guidelines that may best help other patients to reduce the progression of heart disease. We will discuss with you your progress in weight control and changes in cholesterol and other blood fats. Confidentiality Any information resulting from this research study will be kept strictly confidential. The findings will be recorded on documents which will be identified by a code number, and not by name. All documents will be kept in a filing cabinet accessible only to the investigator and coinvestigators. The results of this study may be published in scientific journals or presented at medical meetings, but no one's identity will be disclosed. Participation Your participation in this study is entirely voluntary. You may refuse to participate or even withdraw once the study has started without affecting your normal treatment in the program. Your decision to withdraw or not to participate will in no way affect your medical care. 124 Your participation may also be terminated by the investigator. This could happen if there is an unforeseen change in your medical condition or a change in your medication which might affect the results of the study. If this happens, this will not affect your normal treatment in the program or your medical care. If you have any questions or concerns at any time during the study, you may contact Dr. Frohlich, Dr. Barr or Frances Johnson at the above listed numbers. If you have any concerns about your treatment or rights as a research subject, you may contact the Director of Research Services at the University of British Columbia, Dr. Richard Spratley, Director, Office of Research Services and Administration, at 822-8598. Subject Signature and Consent I have read and understand this consent form. My questions have been answered and I voluntarily consent to participate. A copy of this consent has been provided to me. Signature of Patient Date Printed Name of Patient Signature of Witness Date Printed Name of Witness Signature of Investigator Date Printed Name of Investigator 125 Appendix E. Experimental Diet MAKING HEALTHY CHOICES ON A SEMI-VEGETARIAN DIET Choose to eat..... But be careful to Protein foods • eat fish (4 ounces, 120 grams) at least 2 times per week (this includes all fish, clams, mussels, and scallops) • for other protein sources, eat legumes, tofu products, and egg whites as you like • avoid all meat, organ meats, and poultry • avoid egg yolks, except for what might be present in small amounts in prepared foods • limit shrimp and prawns to very small amounts on special occasions only • include two protein foods each day Skim milk dairy products • use skim milk, yogurt and 1% cottage cheese • eat only low fat cheese that is 7% m.f. or less • avoid cream, sour cream, whipping cream and regular cheese • avoid dairy fats as much as possible Whole grain breads, cereals, grains and pasta • eat enough each day to suit your energy needs • watch the spread on the bread and the sauces on the pasta • use tomato based sauces rather than cream based types • use as little fat as possible to prepare your meals Fresh fruits and vegetables • eat plenty each day, choosing a wide variety • watch the sauces or cooking fats • drink less juice and eat fruit instead Vegetable oils, soft margarine, peanut butter, and salad dressings in very small amounts • use fat-free salad dressings and ultra-light mayonnaise whenever possible • choose low fat condiments such as mustard, relish, ketchup, light jam, cranberry sauce, and salsa • use oils, margarine and other high fat spreads only when necessary. Remember - "if you don't need it, don't use it." • eat nuts and seeds only when you know you can stop after having just a couple. Low fat desserts in moderation, such as angel food cake, fat-free frozen yogurt, sorbet, and low fat cookies • make homemade loaves and muffins using no more than 1/4 cup (50 mL) oil or margarine per loaf or dozen muffins (equal to about 5 grams of fat per muffin or slice) • remember that the best choice for dessert is fruit • avoid high fat baked goods, ice cream and chocolates • try Dare Simple Pleasures ™low fat cookies • keep in mind that half of a portion is also half the fat Low fat snacks such as pretzels, plain popcorn, cereals, and fresh fruit • limit potato chips, corn chips, nuts and other high fat snack foods 126 FACTS ABOUT FAT • Do I need to eat any fat? Yes - fat is a component of most foods including plant and animal products and is an important part of your diet. It acts as a carrier for the fat soluble vitamins A, D, E, and K, and can be a major source of energy. It also provides essential fatty acids that are necessary for good health. However, eating too much fat has been linked to health problems such as heart disease, cancer, and obesity. • What kind of fat should I eat? Not all fats are created equal. Dietary fats are made up of a mixture of saturated, monounsaturated and polyunsaturated fatty acids, and some are better for you than others. Saturated fats raise blood cholesterol. They are found in largest amounts in meat and dairy products, as well as in coconut and palm oils. Choose foods low in saturated fats. Monounsaturated and polyunsaturated fats lower cholesterol levels when substituted for saturated fats. Monounsaturated fats are especially high in such oils as olive, canola, and peanut oils. Polyunsaturated fats are found mainly in plant products such as safflower, sunflower, corn, and soybean oils. Choose unsaturated fats, but be careful not to have too much. Omega 3 fatty acids are polyunsaturated fats found in fish and some vegetables. Studies have shown that these fats may help to reduce your risk for heart disease. Include fish regularly in your diet. Trans fatty acids are fats formed by a process called hydrogenation when liquid oils are converted to solid fats. These trans fatty acids behave like saturated fats and can increase blood cholesterol. Choose foods low in trans fatty acids. 127 HOW MUCH FAT SHOULD I EAT? Conventional recommendations suggest that no more than 3 0 % of the calories you eat should come from fat. However, some researchers report that reducing the fat you eat to 1 5 % of calories may be even more beneficial in lowering blood cholesterol and of all the fats you eat, saturated fat, especially can raise your blood cholesterol and should be limited. What this means is that a person eating 2000 calories per day should eat no more than 33 grams of total fat and 11 grams of saturated fat each day. Use the following chart as a guide for estimating your daily fat budget: Estimated daily energy intake (calories) Total fat budget (grams) Saturated fat budget (grams) 1200 20 7 1500 25 8 1800 30 10 2000 33 11 2400 40 13 HOW MUCH CHOLESTEROL SHOULD I EAT? Cholesterol is a fat-like substance found in foods of animal origin, mainly meat, poultry, fish, and dairy products. It is especially high in foods such as egg yolks and organ meats. It is not found in any food that comes from plants. It is recommended that you eat no more than 150 mg of cholesterol per day. 128 My daily fat budget is: Total fat Saturated fat_ Cholesterol .grams per day grams per day .milligrams per day Use the following chart to help you stay within your fat budget Milk and Milk Products Food item Portion Total fat Saturated Cholesterol per portion (fl) fat per portion (g) per portion (mg) Skim milk 1 cup (227ml) <1 <1 4 1% milk 1 cup (227ml) 3 2 10 2% milk 1 cup (227ml) 5 3 18 Whole milk 1 cup (227ml) 8 5 33 Evaporated skim milk 1 cup (227ml) 1 <1 9 Evaporated 2% milk 1 cup (227ml) 5 3 20 Cheese (30%m.f.) 1 oz(30g) 9 6 30 Part-skim cheese (15%m.f.) 1 oz(30g) 5 3 8 Skim cheese (7% m.f.) 1 oz (30g) 2 1 6 Feta cheese (22% m.f.) 1 oz(30g) 6 4 6 Parmesan cheese 1 Tbsp(15ml) 2 1 4 Cream cheese 1 Tbsp(15ml) 5 3 16 Light cream cheese 1 Tbsp(15ml) 3 2 8 1 % cottage cheese 1 cup (227ml) 2 1 10 Half and half cream 1 cup (227ml) 28 17 89 Whipping cream 1 cup (227ml) 77 48 276 129 Meat and alternates Food item Portion Total fat Saturated Cholesterol fat per portion per portion per portion (9) (g) (mg) Beef, rib 3 oz(90g) 17 7 57 Beef, round 3 oz (90g) 6 2 57 Ground beef, extra lean 3 oz (90g) 12 5 68 Ground beef, regular 3 oz(90g) 18 7 75 Pork tenderloin 3 oz (90g) 4 2 57 Pork shoulder 3 oz (90g) 11 4 63 Pork spareribs 3 oz (90g) 21 8 66 Veal chops 3 oz (90g) 8 2 107 Lamb chops 3 oz (90g) 12 4 103 Ham 3 oz(90g) 5 2 47 Sausage 1 oz(30g) 4 2 11 Bacon 1 slice 3 1 6 Weiner 1 (57g) 17 6 29 Turkey weiner 1 (57g) 10 4 64 Chicken breast, no skin 3 oz(90g) 3 1 72 Chicken wing 3 oz (90g) 17 5 72 Chicken leg, no skin 3 oz(90g) 8 2 90 Turkey breast 3 oz (90g) 1 <1 71 Turkey, dark meat 3 oz(90g) 6 2 72 Scallops 1 cup 1 <1 45 Oysters 3 oz (90g) 1 <1 21 Red snapper 3 oz(90g) 1 <1 31 Clams 3 oz(90g) 3 1 68 Crab 3 oz (90g) 1 <1 84 Halibut 3 oz(90g) 2 <1 27 Salmon 3 oz(90g) 10 2 74 Simulated crab 3 oz(90g) 1 <1 26 Trout 3 oz (90g) 5 1 59 Tuna, canned in water 3 oz(90g) 1 <1 26 Tuna, canned in oil 3 oz (90g) 7 1 15 Cod 3 oz(90g) 1 <1 31 Mackerel 3 oz 9 2 51 Shrimp 1/2 cup 1 <1 125 Egg 1 6 1 242 Egg white 1 0 0 0 130 Vegetarian Products Food item Portion Total fat per portion (g) Saturated fat per portion (g) Cholesterol per portion (mg) Money's Gardenburger 1 patty 2 <1 Vegetarian chili 1 cup (227 ml) 1 <1 0 Beans - kidney, navy, pinto 1 cup (227 ml) 1 <1 0 Lentils 1 cup (227 ml) 1 <1 0 Green soybeans 1/2 cup (114ml) 6 1 0 Mature soybeans 1/2 cup (114ml) 8 1 0 Retried beans, pork & 1 cup (227ml) 6 3 0 beans Yves Veggie Just Like 55g <1 0 0 Ground Yves Veggie Deli slices 31g <1 0 0 Soy cheese 1 oz (30g) 5 1 0 Tofu, firm 3 oz(90g) 7 1 0 Tofu, medium firm 3 oz (90g) 4 1 0 Tofu, soft 3 oz(90g) 3 1 0 Nuts e.g. peanuts 1/2 cup (114ml) 36 5 0 Sunflower seeds 1/2 cup (114ml) 32 3 0 Coconut, dried 1/2 cup (114ml) 12 11 0 i f in in Grain Products Food item Portion Total fat per portion (g) Saturated fat per portion fa) Cholesterol per portion (122} Rice - brown, white, basmati Bread - white, whole grain Pasta, cooked - macaroni, spaghetti Most cereals Granola - Harvest Crunch Granola - Kellogg's low fat Crackers - graham wafers Crackers - saltines 1 cup (227ml) 1 1 slice 1 1 cup (227ml) 1 1 cup (227ml) 1 1 cup (227ml) 22 1 cup (227ml) 6 4 3 4 1 <1 <1 <1 <1 16 1 1 <1 0 0 0 0 0 0 0 0 131 Fruits and Vegetables Food item Portion Total fat per portion (g) Saturated fat per portion (g) Cholesterol per portion (mg) Most fruits and vegetables 1 cup (227 ml) <1 <1 0 Potato 1 <1 <1 0 Avocado 1 30 5 0 Olives, black 4 2 <1 0 U Fats and Oils Food item Portion Total fat per portion Saturated fat per portion Cholesterol per portion (g) (g) (mg) Butter 1 Tbsp (15ml) 12 8 33 Margarine, soft 1 Tbsp (15ml) 11 2 0 Oil, canola 1 Tbsp (15 ml) 14 1 0 Oil, olive 1 Tbsp (15 ml) 14 2 0 Oil, corn 1 Tbsp (15 ml) 14 2 0 Mayonnaise 1 Tbsp (15 ml) 11 2 10 Light mayonnaise 1 Tbsp (15 ml) 5 1 0 Italian dressing 1 Tbsp (15 ml) 7 1 0 Peanut butter 1 Tbsp (15 ml) 8 2 0 132 © h Miscellaneous Foods Food item Portion Total fat Saturated Cholesterol fat per portion p e r portion per portion (9) (gj (mg) Cookies, Simple Pleasures 1 <1 <1 0 by Dare Cookies, arrowroots 2 1 <1 0 Chocolate 1 oz (30g) 9 6 6 Potato chips 1 oz (30g) 10 2 0 Pretzels 1 oz (30g) 1 <1 0 Popcorn, plain 1 oz (30g) 1 <1 0 Licorice 3 sticks <1 <1 0 133 Appendix F. The Control Diet GUIDELINES FOR MAKING HEALTHY FOOD CHOICES Choose to eat..... But be careful to L e a n meat, pou l t ry o r f ish up to 6 ounces (180 grams) per day • eat fish 2- 3 times per week • replace meat, poultry or fish with a vegetarian entree such as legumes or tofu at least once per week • eat egg whites as you like • cut off all fat and remove poultry skin • limit high fat processed meats such as salami and sausages • avoid organ meats • limit egg yolks to a maximum of 1-3 per week S k i m m i l k da i r y products • use 1% m.f. or skim milk, yogurt and cottage cheese • eat low fat cheese that is 15% m.f. or less • limit cream, sour cream, whipping cream and regular cheese Who le gra in breads, cereals, grains and pasta • eat enough each day to suit your energy needs • watch the spread on the bread and the sauces on the pasta Fresh frui ts and vegetables • eat plenty each day, choosing a wide variety • watch the sauces or cooking fats • drink less juice and eat fruit instead Vegetable oils, soft margar ine , peanut butter , and salad dressings in very smal l amounts • use light salad dressings and light mayonnaise whenever possible • choose low fat condiments such as mustard, relish, ketchup, and salsa • use tomato based sauces • use oils, margarine and other high fat spreads sparingly. Remember - "if you don't need it, don't use it. " • avoid high fat creamy sauces • eat nuts and seeds only when you know you can stop after having just a few L o w fat desserts in moderat ion , such as angel food cake, low fat f rozen yogurt , and low fat cookies • make homemade loaves and muffins using no more than 1/4 cup (50 mL) oil or margarine per loaf or dozen muffins • remember that the best choice for dessert is fruit • limit high fat baked goods, ice cream and chocolates • keep in mind that half of a portion is also half the fat L o w fat snacks such as pretzels, p la in popcorn , baked chips, cereals, and fresh f ru i t • limit potato chips, corn chips, nuts and other high fat snack foods • remember that too many low fat snack foods can add up to too many calories! 134 FACTS ABOUT FAT • Do I need to eat any fat? Yes - fat is a component of most foods including plant and animal products and is an important part of your diet. It acts as a carrier for the fat soluble vitamins A, D, E, and K, and can be a major source of energy. It also provides essential fatty acids that are necessary for good health. However, eating too much fat has been linked to health problems such as heart disease, cancer, and obesity. • What kind of fat should I eat? Not all fats are created equal. Dietary fats are made up of a mixture of saturated, monounsaturated and polyunsaturated fatty acids, and some are better for you than others. Saturated fats raise blood cholesterol. They are found in largest amounts in meat and dairy products, as well as in coconut and palm oils. Choose foods low in saturated fats. Monounsaturated and polyunsaturated fats lower cholesterol levels when substituted for saturated fats. Monounsaturated fats are especially high in such oils as olive, canola, and peanut oils. Polyunsaturated fats are found mainly in plant products such as safflower, sunflower, corn, and soybean oils. Choose unsaturated fats, but be careful not to have too much. Omega 3 fatty acids are polyunsaturated fats found in fish and some vegetables. Studies have shown that these fats may help to reduce your risk for heart disease. Include fish regularly in your diet. Trans fatty acids are fats formed by a process called hydrogenation when liquid oils are converted to solid fats. These trans fatty acids behave like saturated fats and can increase blood cholesterol. Choose foods low in trans fatty acids. 135 HOW MUCH CHOLESTEROL SHOULD I EAT? Cholesterol is a fat-like substance found in foods of animal origin, mainly meat, poultry, fish, and dairy products. It is especially high in foods such as egg yolks and organ meats. It is not found in any food that comes from plants. It is recommended that you eat no more than 200 - 300 mg of cholesterol per day. My daily fat budget is: Total fat grams per day Saturated fat grams per day Cholesterol milligrams per day 136 Food Item Portion Fat(g) Cholesterol (mg) per portion per portion Beef, ground, extra lean 3 oz (90 g) 14 70 Beef, rib roast 3 oz (90 g) 18 61 Beef, rump roast, lean only 3 oz (90 g) 7 66 Veal, loin chop 3 oz (90 g) 12 90 Ham, lean and fat 3 oz (90 g) 15 56 Ham, lean only 3 oz (90 g) 5 47 Pork, spareribs 3 oz (90 g) 27 109 Pork, tenderloin 3 oz (90 g) 4 67 Lamb, shoulder, lean and fat 3 oz (90 g) 25 88 Lamb, leg, lean only 3 oz (90 g) 6 90 Chicken, drumsticks, no skin 2(90g) 5 84 Chicken, breast, no skin 'A (90 g) 3 76 Chicken breast, fried, skin/batter ft (140 g) 18 119 Turkey, dark meat, no skin 3 oz (90 g) 6 76 Turkey, white meat, no skin 3 oz (90 g) 3 62 Sausages, pepperoni, bologna 3 oz (90 g) 30 70 Wieners, beef/pork 1 11 19 Wieners, chicken 1 7 37 Bacon, crisp 2 slices (13 g) 6 11 Back bacon 1 slice (23 g) 2 13 Liver 3 oz (90 g) 7 434 Whole egg 1 6 214 Egg white 1 0 0 Fish, cod 3 oz (90 g) 5 73 Fish, sole 3 oz (90 g) 1 62 Fish, tuna, canned in water 3 oz (90 g) 1 50 Fish, salmon 3 oz (90 g) 12 35 Scallops 3 oz (90 g) 1 48 Shrimp 3 oz (90 g) < 1 176 Lobster 3 oz (90 g) 2 77 Crab 3 oz (90 g) 1 65 Clams 3 oz (90 g) 2 60 Milk, whole 1 cup (250 mL) 9 35 Milk or yogurt, 2% MF 1 cup (250 mL) 5 19 Milk or yogurt, 1%MF 1 cup (250 mL) 3 10 Milk or yogurt, skim 1 cup (250 mL) < 1 5 Milk, soy, regular 1 cup (250 mL) 5 0 Cream, 10% MF 1 cup (250 mL) 31 99 Whipping cream, 35% MF 1 cup (250 mL) 88 322 Frozen yogurt, 2 - 4% MF '/2Cup(125mL) 4 • 13 Ice cream, 16% MF !/2cup(125mL) 12 46 Sherbet !/2cup(125mL) 2 7 Cheese, 32% MF eg Cheddar 1 oz (30 g) 10 31 Cheese, skim, 15% MF 1 oz (30 g) 5 18 Cheese, skim, 7% MF 1 oz (30 g) 2 --Cheese, feta, 22 % MF 1 oz (30 g) 7 27 Cheese, parmesan 2 Tbsp 3 8 Cheese, soy 1 oz (30 g) 5 0 Cream cheese, 32% MF 1 oz (30 g) 10' 31 Light cream cheese, 16% MF 1 oz (30 g) 5 13 Cottage cheese, 1% MF Vi cup (125 mL) 1 5 137 Food Portion Fat(g) Cholesterol (mg) per portion per portion Butter 1 T b s p ( 1 5 m L ) 11 31 Margarine, soft 1 Tbsp(15 m L ) 11 0 Oil eg: canola, olive 1 T b s p ( 1 5 m L ) 14 0 Mayonnaise 1 T b s p ( 1 5 m L ) 11 8 Light mayonnaise 1 T b s p ( 1 5 m L ) 5 0 Salad dressing eg: French, Italian 1 T b s p ( 1 5 m L ) 6 - 1 2 0 Ketchup, mustard, relish, salsa 1 Tbsp(15 m L ) < 1 0 Legumes eg: lentils, split peas 1 cup (250 m L ) 1 0 Nuts eg: peanuts, walnuts l / 2 cup(125 m L ) 37 0 Seeds eg: sunflower seeds M> cup (76 g) 38 0 Chestnuts Vi cup (75 g) < 1 0 Peanut butter 1 Tbsp(15 m L ) 8 0 Tofu, medium firm 3 oz (90 g) 4 0 Most fruits and vegetables 1 cup (250 m L ) < 1 0 Avocado 1 (173 g) 30 0 Olives, black 5 ( 2 0 g ) 3 0 Coconut, dried Vi cup (49 g) 17 0 Most breads, bagels, pita 1 slice (30 g) <1 <1 Tortilla, roti, English muffin 1 <1 <1 Most Cereal 1 cup (250 m L ) <1 <1 Granola 1 cup (250 m L ) 34 0 Pasta/rice, cooked 1 cup (250 m L ) <1 0 Instant noodles 2 cups (500 m L ) 18 72 Potato chips 10(20 g) 7 0 Pretzels, sticks 5 < 1 0 Popcorn, air popped, plain 1 cup (250 m L ) < 1 0 Crackers, saltines 4 1 0 Crackers, graham 4 3 0 Cookies, social tea/arrowroot 2 2 <1 Cookies, shortbread 2 8 11 Doughnut, plain, glazed 1 10 14 Chocolate 1 oz (30 g) 10 6 Licorice, sticks 3 (33 g) <1 0 Hamburger, 4 oz patty 1 21 70 Fish sandwich, fast food 1 27 91 French fries medium 17 0 Macaroni and cheese 1 cup (250 m L ) 23 72 Beans in tomato sauce 1 cup (250 m L ) 5 0 138 Appendix G. Diet History Healthy Heart Program, B180-1081 Burrard Street, Vancouver, BC V6Z1Y6 • Phone 604-631-559Fax 604-631-5590 ^Nutrition History Name Birthdate Healthy Heart Program' Dietitians Phone Height Has your weight changed recently? Eating Habits ^ Which meals do you eat regularly? HI Do you snack? #lf so, what do you eat for snacks? ^ Who prepares your meals? How are your meals prepared? 4" Baked 4" Boiled ^ Do you salt your food: #During preparation? #At the table? H What oils & spreads do you use? 4" Butter _ Weight_ ^ G a i n X Breakfast 4" Yes Loss X Lunch 4" No 1 No change Dinner 4" Fried • 4" Stirfried 4" DeeD fried X BBQ • X Poached X Microwaved X None • 4" Liqhtlv • X Heavily X None • X Liqhtlv • X Heavily • X Margarine X Mayonnaise T O i l Type Type Type | How many meals do you eat away from home each week (include breakfasts and lunches)? 1 Do you take vitamin supplements? ^ Yes ^ #lf so, please list. No | Do you drink alcoholic beverages? ^ Yes ^ No #How many drinks (beer, wine, liquor) do you usually consume per week? 1 What beverages do you drink each day? 4" Coffee Cups/day T Tea Cups/day 4" Juice Cups/day X Cream X Milk X Sugar X Cream X Milk 4" Sugar 139 Food Frequency # Indicate how often you have the following food groups. Number of servings Seldom 1x/wk 2-3x/wk 1x/day 2x/day more often Meat (eg: beef, pork) Poultry Fish Vegetarian meals (eg: lentils, tofu, beans) Sausages/bacon Cold cuts/Hot dogs Eggs Milk (4" whole 4" 2% 1% 4" skim) Cheese (4" regular 4" low fat) Breads/cereals/rice/pasta Vegetables Fruit Commercial muffins/cakes/pies/cookies Ice cream Snack foods (eg: chips, nuts) Food Intake Record # Describe what you ate yesterday. Record the amount and rype of foods and beverages you had, including snacks, sweets, alcoholic beverages, butter, margarine, oil, salad dressing, mayonnaise and sauces used. Breakfast Lunch Dinner Morning Snack Afternoon Snack Evening Snack For office use only IBW BMI Goal Weight A P 140 Appendix H. Food Records Healthy Heart Program, B180-1081 Burrard Street, Vancouver, BC V6Z1Y6 • Phone 604-631-5591 • Fax 604-631-5590 I 1?3-Day Food Intake Record Healthy Heart Program Dietitians Name Birthdate Height Weight Instructions Please complete the following food intake record. • Record what you have eaten for 3 consecutive days using 2 week days and 1 weekend day. • Record all food and beverages consumed each day. • Include all snacks eaten throughout the day. • Include the amount of butter, margarine, oil, mayonnaise, salad dressings, sauces, etc., you have used in preparing the food. • Estimate food portion sizes as accurately as possible. Sample descriptions Orange juice, unsweetened I cup Tuna sandwich: whole wheat bread 2 slices water Dacked tuna • CUD liaht mayonnaise 1 TbsD soft maraarine 2TSD Salad: lettuce 1 CUD tomato I cucumber 3 slices Italian dressing 1 TbsD Please list any vitamin or mineral supplements you take. 141 DAY 1 Date For Office Use Only Code Quantity Time of Day Type of Food include preparation method (ie: boiled, fried, baked) Amount of Food Consumed 142 Appendix I. Adherence chart oo D O < 7 Fish • DietQ 14 Fish • Diet • 21 Fish Q Diet Q 28 Fish a Diet Q 6 Fish • Diet • 13 Fish • DietQ 20 Fish Q DietQ 27 Fish a Diet Q Fish • Diet • 12 Fish • Diet • 19 Fish Q Diet Q 26 Fish a Diet Q 4 Fish • Diet • 11 Fish • Diet • 18 Fish Q Diet Q 25 Fish a Diet Q Fish • Diet • 10 Fish • Diet • ... 17 Fish a DietQ 24 Fisli a Diet Q 31 Fish a DietQ 2 Fish • Diet • 9 Fish • DietQ 16 Fish Q DietQ 23 Fish Q Diet Q 30 Fish Q Diet Q Fish • Diet • Fish • DietQ Fish Q Diet Q Fish Q Diet Q 29 Fish Q DietQ t 5 i J 3 -X — 1 " -143 Appendix J. Nutrition-related Quality of Life Questionnaires Nutrition-related Quality of Life Questionnaire Section 1 Hassles are irritants that can range from minor annoyance to fairly major pressures, problems, or difficulties. They can occur few or many times. Listed are a number of ways in which a person can feel hassled about nutrition and diet. Please rate the following items according to the irritability of those hassles experienced during the past month: Not Slightly Somewhat Moderately Quite Very Extremely irritating irritating irritating irritating irritating irritating irritating 1. Concerns about eating the O O O O O O O right foods 2. Cravings for foods not on O O O O o o O your diet 3. Finding the right foods o O O o o o O 4. Avoiding favourite foods o O O o o o O 5. Figuring out which foods o O O o o o O to buy 6. Preparing food o O O o o o O 7. Time spent preparing food o O O o o o O 8. Taste of food on diet o O O o o o O 9. Foods not satisfying o O O o o o O 10. Time required to shop for o O O o o o O food 11. Choosing food to eat o O O o o o O 12. Digesting food o O O o o o O 13. Going out to dinner o O o o o o O 14. Not going out to dinner o O o o o o 0 15. Eating right when not at o o o o o o o home 16. Family problems over o o o o o o o food 17. Lack of control over diet o o o o o o o 18. Learning new recipes o o o o o o o 19. Don't like what you eat o o o o o o o 20. Planning menus o o o o o o o 21. Feeling hungry o o o o o o o 22. Keeping track of o o o o o o o cholesterol 23. Keeping track of salt o o o o o o o 24. Keeping track of fat o o o o o o o 25. Keeping track of calories o o o o o o o 26. Eating junk food 0 o o o o o o 27. Reading nutrition labels o o o o o o o 28. Eating too much o o o o o o o 144 Not Slightly Somewhat Moderately Quite Very Extrerr irritating irritating irritating irritating irritating irritating irritati 29. Understanding which O O O O O O O foods you should eat 30. Finding time to eat O O O O o 0 O 31. Food portions O O O O o o o 32. Remembering what to eat O O O o o o o 33. Remembering when to eat O O O o o o o 34. Changing food habits O O O o o o o 35. Refusing food that is O O O o o o o offered 36. Telling others about diet O o O o o o o 37. Holidays and special O o O o o o o occasions 38. Avoiding sweets O o O o o o o 39. Not enjoying food O o O o o o o 40. Eating enough vegetables O o O o o o o 41. Eating enough fruit O o o o o o o 42. Getting enough fibre O o o o o o o 43. Eating when not hungry O o o o o o o 44. Cost of food O o o o o o o 45. Keeping track of sugar O o o o o o o 46. Keeping track of vitamins O o o o o o o 47. Keeping track of minerals O o o o o o o 48. Embarrassment about diet O o o o o o o 49. Boring food o o o o o o o Section 2 The next set of questions are about your diet and health. Please read each of the following statements, then answer the questions by checking the circle next to the answer that best describes your experience during the past month. Some of the questions may look or seem like others, but each question is different, and should be answered by itself. 1. During the past month, how healthy were the foods you ate? O Not healthy at all O Slightly healthy O Somewhat healthy O Moderately healthy O Quite healthy O Very healthy O As healthy as they could be 2. During the past month, did you think that you were getting all the nutrients that you need from the foods you ate? O No, not at all O No, almost none O Less than half of my needs O Only about half O More than half, but not all of my needs O Yes-, almost everything O Yes, everything that I need 145 3. During the past month, have you been worried or concerned about how your diet has been affecting your health? O Extremely so O Very much so O Quite a bit O Some but not a lot O A little bit O Practically never O Not at all 6. How balanced do you think your diet was during the past month? O Extremely well balanced O Very well balanced O Well balanced O Somewhat balanced O A little balanced O Not very balanced O Not balanced at all 4. Do you think you worried about the effect of your diet on your health more than other people did, during the past month? O Yes, all of the time O Yes, most of the time O Yes, a good bit of the time O Yes, some of the time O A little of the time O No, hardly any of the time O No, none of the time 7. Do you feel healthier now than you did one month ago? O Yes, definitely so O Yes, very much so O Yes, quite a lot O For the most part O Some, but not a lot O Not very much O Not at all 5. During the past month, did you think that your diet improved your health? O Yes, definitely so O Yes, very much so O Yes, quite a lot O For the most part O Some, but not a lot O Not very much O Not at all 8. How confident have you felt about your diet during the past month? O Not at all confident O A little confident O Somewhat confident O Moderately confident O Quite confident O Very confident O Extremely confident Section 3 The following questions are about how your diet influences your social life. Please read each of the following statements, and then answer the questions by checking the circle next to the answer that best describes your experience during the past month. Some of the questions may look or seem like others, but each question is different, and should be answered by itself. 146 1. During the past month, how satisfied were you with your social life? O Extremely satisfied O Very satisfied O Quite satisfied O Somewhat satisfied O Quite unsatisfied O Very unsatisfied O Extremely unsatisfied • 2. How much of the time during the past month would you say that your diet interfered with parties, holidays and special occasions? O All of the time O Most of the time O A lot of the time O A good bit of the time O Some of the time O A little of the time O None of the time 3. How much of the time during the past month would you say that your diet interfered with the quality of your family relationships? O All of the time O Most of the time O A lot of the time O A good bit of the time O Some of the time O A little of the time O None of the time 6 Not applicable 4. How much of the time during the past month would you say that your diet interfered with socializing at work? O All of the time O Most of the time O A lot of the time O A good bit of the time O Some of the time O A little of the time O None of the time O Not applicable 5. How much of the time during the past month would you say that your diet interfered with socializing with friends? o All of the time o Most of the time o A lot of the time o A good bit of the time o Some of the time o A little of the time o None of the time 6. Do you think that your diet had a positive effect on your social life during the past month? O No, not at al O Hardly any effect O A little effect O Somewhat O Quite a bit O Yes, very much so O Yes, definitely so . 7. Do you feel more attractive now than you did one month ago? O No, not at all O Hardly any effect O A little effect O Somewhat O Quite a bit O Yes, very much so O Yes, definitely so 147 Section 4 Please rate each of the following items according to how these things have affected your mood within the last month. 1. During the past month, how angry have you been about having an illness that demands changes in your normal eating habits? O Extremely angry O Very angry O Quite angry O Moderately angry O Somewhat angry O A little angry O Not angry at all 2. During the past month, how irritable have you been? O Extremely irritable O Very irritable O Quite irritable O Moderately irritable O Somewhat irritable O A little irritable O Not irritable 3. During the past month, how frustrated have you been? O Extremely frustrated O Very frustrated O Quite frustrated O Moderately frustrated O Somewhat frustrated O A little frustrated O Not frustrated at all 4. How impatient have you been during the past month? O Not impatient at all O A little impatient O Somewhat impatient O Moderately impatient O Quite impatient O Very impatient O Extremely impatient 5. How stressed have you felt during the past month? O Extremely stressed O Very stressed O Quite stressed O Moderately stressed O Somewhat stressed O A little stressed O Not at all 6. During the past month how much of the time have you felt in control of your diet? O All of the time O Most of the time O A good bit of the time O Some of the time O A little of the time O Hardly any of the time O None of the time 7. Do you feel younger now than you did one month ago? O Yes, definitely so O Yes, very much so O Yes, quite a lot O For the most part O Some, but not a lot O Not very much O Not at all 148 Section 5 Global Quality of Life Questions 1. During the past month, how you you rate your overall quality of life? O Excellent O Great O Good O Moderate O Not very good O Fairly poor O Very bad 2. While on this diet, did you feel you were doing the right thing? O Yes, definitely O Yes, very much so O Yes, for the most part O Yes, but I could have done more O Yes, only partially O No, not much O No, not at all 3. During the past month, did you feel relieved knowing that your diet was as healthy as it could be? O No, not at all O Only slightly O A little O Somewhat O Yes, for the most part O Yes, very much so O Yes, extremely relieved 149 Appendix K. Time Line Record Patient Time Line Intake Cl in ic WeekO Week 4 Week 8 Week 12 Date Diet history questionnaire X Quality of life questionnaire X x Height X Weight -calculation of BMI X x x x Waist circumference x X Consent form X Randomization x Lipid tests x# X Assign and collect 3 day food record * x x X Completion of diet compliance chart x x x X Teach appropriate diet x Diet follow up x x X • # lipid tests to be assigned and completed 2 weeks prior to week 0. *assign food record booklet to be completed for week 0. 150 Appendix L Cookbook Eating Light and Loving It! « v -7 Simple Recipes for Good Health Recipes from friends of the St Paul's Hospital Lipid Clinic Collected by Frances Johnson, R.D.N. and Shauna Ratner, R.D.N. 151 

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