Ischemic heart disease is the largest cause of death due to cardiovascular origins. A better understanding of the mechanisms responsible for ischemic heart disease increases the potential for therapies. This will lead to decreased mortalities in Canada and around the world. Nutritional interventions have gained increasing attention as causes or treatments for cardiovascular disease. For example, trans fats (TFAs) have both beneficial and deleterious effects on cardiovascular disease [1]. In this study, we would like to examine this phenomenon. We contrast the effects of two different TFAs on cardiomyocyte viability. We compare the industrially produced trans-fat elaidic acid (EA) and the ruminant trans-fat vaccenic acid (VA) on apoptotic and autophagic markers during non-ischemic (control), ischemic (ISCH) and ischemia/reperfusion (IR) conditions. Rat cardiomyocytes are exposed to medium containing fatty acids conjugated with bovine serum albumin for 24 hours. VA and EA have no significant effect on biomarkers of apoptosis or cell death. Interestingly, a similar effect is observed with autophagic and apoptotic markers of LDLr-/- mice whose diets were supplemented with VA or EA. Cells pre-treated with EA prior to 60 minutes of simulated ISCH and 120 minutes of IR increased cell death compared to control through augmented apoptosis. VA decreases the number of dead cells during ISCH and IR. However, the apoptotic parameters remain unchanged. We also observe that VA decreases oxidized phospholipid content in non-ischemic conditions. We conclude that not all TFAs are deleterious to the heart. EA is toxic to cardiomyocytes with or without ISCH or IR whereas VA is cardioprotective during IR and ISCH conditions. We believe VA decreases oxidized phospholipid content to produce this cardioprotective effect. For the purposes of comparison, we examined the effects of α-linolenic acid (ALA), an essential polyunsaturated fatty acid found in foods like flaxseed. Omega-3 fatty acids have been associated with improved cardiovascular outcomes. Here, isolated adult rat cardiomyocytes from male Sprague Dawley rats were exposed to medium containing ALA for 24 hours and then exposed control, ISCH or IR conditions. Cell death increases during ISCH and IR. An increase in DNA fragmentation and caspase-3 activity was observed in both the ISCH and IR conditions. Pre-treatment of the cells with ALA subsequently inhibits cell death during ISCH and IR challenge and significantly reduced both DNA fragmentation and caspase-3 cleavage during ISCH and IR. Cardiomyocyte resting Ca2+ increased and Ca2+ transients decreased during ISCH or I/R but ALA pre-treatment did not improve either parameter significantly. We hypothesize that apoptosis is initiated through phosphatidylcholine oxidation within the cardiomyocytes. Pre-treatment of cells with ALA resulted in a significant incorporation of ALA within cardiomyocyte phosphatidylcholine. Two pro-apoptotic oxidized phosphatidylcholine (OxPC) species, 1-palmitoyl-2-(5'-oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC) were significantly increased during both ISCH and IR. ALA pre-treatment significantly decreased the production of POVPC and PGPC during ISCH and I/R. It is concluded that ALA protects the cardiomyocyte from apoptotic cell death during simulated ISCH and IR by inhibiting the production of specific pro-apoptotic OxPC species. In summary, we observe a differential effect of ALA, VA and EA on parameters of cardiomyocyte viability during ISCH or IR.

It is becoming increasingly evident that the development of atherosclerotic coronary heart disease (CHD) can largely be regulated by lifestyle and dietary choices. The type of fatty acids regularly consumed may promote or prevent atherogenesis. Flaxseed, the richest plant source of the omega-3 fatty acid alpha-linolenic acid (ALA) is thought to protect against atherosclerotic disease. However, the mechanism(s) by which flaxseed exerts these anti-atherogenic effects requires further investigation. Alternatively, there are dietary fatty acids that are thought to induce significant deleterious effects upon our cardiovascular health. Epidemiological evidence associates dietary trans fatty acids (TFAs) with atherosclerotic CHD. This evidence has largely focused on the main source of TFAs in the North American diet, industrially hydrogenated vegetable shortening (iTFAs). It is assumed that TFAs stimulate atherosclerosis but the only studies to date have shown no effect of TFAs on atherosclerosis. Even less is known of the impact of naturally occurring TFAs from dairy and meat products of ruminant animals (rTFAs) on atherosclerotic disease. We investigated the effects of flaxseed supplementation on atherosclerosis and vascular function in two animal models, the hypercholesterolemic rabbit and the cholesterol fed, low density lipoprotein receptor (LDLr-/-) deficient mouse. New Zealand White rabbits and LDLr-/- mice were fed a diet containing flaxseed in the absence or presence of dietary cholesterol for a period of 6 to 24 weeks. We found that dietary flaxseed inhibits the atherogenic effects of a high cholesterol diet in both animal models. The anti-atherogenic effect was achieved in the mouse model through a capacity to lower circulating cholesterol levels and at a cellular level by inhibiting cell proliferation and inflammation. This reduction is also associated with an improved vascular relaxation response as demonstrated in the rabbit model. We also investigated the effects of consuming TFAs from two sources, industrially hydrogenated iTFAs rich in elaidic TFA (C18:1t-9) or naturally-occurring ruminant rTFAs rich in vaccenic TFA (C18:1t-11), on atherosclerotic development in the LDLr-/- mouse in the presence or absence of elevated dietary cholesterol. Our results demonstrate that consuming iTFAs dose dependently initiates atherosclerotic development but not beyond the effects of dietary cholesterol alone. However, consuming rTFAs rich in vaccenic acid protects against hyperlipidemia and atherosclerosis in the presence or absence of dietary cholesterol. The effects of combining dietary flaxseed and iTFAs in the diet were also examined in this model. Adding whole ground flaxseed or flaxseed oil (ALA) to diets containing low and high doses of iTFAs completely prevented atherosclerotic development in the absence of dietary cholesterol. Flaxseed was also able to partially prevent atherosclerosis caused by iTFAs and cholesterol. Our results suggest that the omega-3 ALA fatty acid rich content of flaxseed is mainly responsible for the anti-atherogenic effects of flaxseed. Our results highlight potential mechanisms for the beneficial effects of dietary flaxseed and the mixed effects of TFAs on cardiovascular health and underscore the need for further basic and clinical investigations.

It is becoming increasingly evident that the development of atherosclerotic coronary heart disease (CHD) can largely be regulated by lifestyle and dietary choices. The type of fatty acids regularly consumed may promote or prevent atherogenesis. Flaxseed, the richest plant source of the omega-3 fatty acid alpha-linolenic acid (ALA) is thought to protect against atherosclerotic disease. However, the mechanism(s) by which flaxseed exerts these anti-atherogenic effects requires further investigation. Alternatively, there are dietary fatty acids that are thought to induce significant deleterious effects upon our cardiovascular health. Epidemiological evidence associates dietary trans fatty acids (TFAs) with atherosclerotic CHD. This evidence has largely focused on the main source of TFAs in the North American diet, industrially hydrogenated vegetable shortening (iTFAs). It is assumed that TFAs stimulate atherosclerosis but the only studies to date have shown no effect of TFAs on atherosclerosis. Even less is known of the impact of naturally occurring TFAs from dairy and meat products of ruminant animals (rTFAs) on atherosclerotic disease. We investigated the effects of flaxseed supplementation on atherosclerosis and vascular function in two animal models, the hypercholesterolemic rabbit and the cholesterol fed, low density lipoprotein receptor (LDLr-/-) deficient mouse. New Zealand White rabbits and LDLr-/- mice were fed a diet containing flaxseed in the absence or presence of dietary cholesterol for a period of 6 to 24 weeks. We found that dietary flaxseed inhibits the atherogenic effects of a high cholesterol diet in both animal models. The anti-atherogenic effect was achieved in the mouse model through a capacity to lower circulating cholesterol levels and at a cellular level by inhibiting cell proliferation and inflammation. This reduction is also associated with an improved vascular relaxation response as demonstrated in the rabbit model. We also investigated the effects of consuming TFAs from two sources, industrially hydrogenated iTFAs rich in elaidic TFA (C18:1t-9) or naturally-occurring ruminant rTFAs rich in vaccenic TFA (C18:1t-11), on atherosclerotic development in the LDLr-/- mouse in the presence or absence of elevated dietary cholesterol. Our results demonstrate that consuming iTFAs dose dependently initiates atherosclerotic development but not beyond the effects of dietary cholesterol alone. However, consuming rTFAs rich in vaccenic acid protects against hyperlipidemia and atherosclerosis in the presence or absence of dietary cholesterol. The effects of combining dietary flaxseed and iTFAs in the diet were also examined in this model. Adding whole ground flaxseed or flaxseed oil (ALA) to diets containing low and high doses of iTFAs completely prevented atherosclerotic development in the absence of dietary cholesterol. Flaxseed was also able to partially prevent atherosclerosis caused by iTFAs and cholesterol. Our results suggest that the omega-3 ALA fatty acid rich content of flaxseed is mainly responsible for the anti-atherogenic effects of flaxseed. Our results highlight potential mechanisms for the beneficial effects of dietary flaxseed and the mixed effects of TFAs on cardiovascular health and underscore the need for further basic and clinical investigations.

No description available.

Master of Science / Department of Food Science / Delores Chambers / Research has shown that trans fat consumption increases the levels of low-density lipoprotein (LDL) and has a direct correlation to the incidence of heart disease. It is now widely believed that trans fat intake adversely affects the health of consumers. A Food and Drug Administration (FDA) ruling, effective January 1, 2006, required declaration of trans fat content on all Nutrition Facts labels of food products. Around the same time local governments, such as the city of New York, and some restaurants followed suit by eliminating trans fats from their menus. The food industry’s initial concern with trans fat elimination/reduction was the loss of some functionality such as shelf life, stability, and creaming ability with trans-free fats and oils. Researchers are working to develop new trans-free fats and oils that do not have negative sensory properties and maintain the functionality of traditionally hydrogenated oils when used in baked and fried goods. This is an overview of the chemistry, health risks, and research that has been performed to either reduce or eliminate trans fats in food products.

2 pp. / [Healthy Fats -- Guide for Improving the Quality of Fat Intake] / The fact sheet reviews healthy fats and how to incorporate a healthy amount of fat into our diet. Fats are necessary for our bodies to function properly. In fact, fats are an important part of a healthy diet and we can't live without them. Fats can be grouped into two groups: saturated and unsaturated. Unsaturated fats include polyunsaturated and monounsaturated fats. Both these fats, when eaten in moderation and used in place of saturated and trans fats, can help lower cholesterol levels and decrease the risk of heart disease. We provide a list of "Do's" and "Tips" which gives examples of how to select fats wisely and incorporate healthy changes into our diet. We also provide a guide for selecting an appropriate portion size of fat.

2 pp. / The fact sheet reviews healthy fats and how to incorporate a healthy amount of fat into our diet. Fats are necessary for our bodies to function properly. In fact, fats are an important part of a healthy diet and we can't live without them. Fats can be grouped into two groups: saturated and unsaturated. Unsaturated fats include polyunsaturated and monounsaturated fats. Both these fats, when eaten in moderation and used in place of saturated and trans fats, can help lower cholesterol levels and decrease the risk of heart disease. We provide a list of "Do's" and "Tips" which gives examples of how to select fats wisely and incorporate healthy changes into our diet. We also provide a guide for selecting an appropriate portion size of fat.

Consumption of food away from home (FAFH) is widely believed to be a contributing factor to the current obesity crisis and other diet related problems in North America. At present, in Canada, a number of issues related to FAFH consumption such as the relationship between obesity and fast foods, trans-fats, sugar and sodium content of restaurant foods, and restaurant advertising for children are being widely discussed. In these discussions, it is apparent that the interrelationships between FAFH, nutrition and diet related diseases are complex. Therefore, there are significant gaps in our knowledge. In this study, a number of important research questions related to FAFH consumption were studied in order to provide a detailed understanding of FAFH purchase trends, nutrient demand trends, factors affecting these trends and to provide some idea of the possible effectiveness of proposed policy interventions in the area. In paper one of this study, a sample of Canadian FAFH purchases were analysed using a two stage demand model to examine the impact of industry advertising, households habit forming preferences and socio-demographic and economic variables. Given the unique method of restaurant categorization, results provide new and additional information of the impact of above variables in Canadian context. The second study examined the demand for selected nutrients in FAFH to understand factors affecting nutrient intake in FAFH foods focusing on chain restaurants. An innovative measure of nutrient content (nutrient density) was used in the analysis and study results provides interesting new information about nutrient consumption from chain restaurants in the FAFH market. The third study examined how some specific food industry changes in product formulations aimed at reducing trans-fatty acids (TFAs) could and have affected consumers overall diet quality and their demand for food away from home. This study provides some indications of effectiveness of the current trans-fat recommendations in Canada. In summary, this study is an empirical investigation of a number of questions related to Canadian FAFH consumption: What is the structure of the FAFH market in Canada? What are the households FAFH purchasing patterns? What is the impact of advertising and habit forming preferences and socio-economic and demographic factors on FAFH purchases? What are the nutrition profiles of the most popular menu items of chain restaurants? What are the factors affecting nutrient demand in FAFH foods? Would a specific food industry change in product formulation such as reducing TFAs have affect consumers overall diet quality and their demand for FAFH? In general, results from the three independent studies provide useful information to fill some of the gaps in our knowledge of FAFH consumption, especially on health and nutrition with implications for public policy. / Agricultural and Resource Economics

Over the past four decades, obesity in the United States has risen to record levels. Co-morbid conditions such as heart disease, diabetes, and stroke will impose over twenty trillion dollars of economic burden over the next two decades. More than half that sum will be direct medical expenses. Under current entitlement programs, governments, and ultimately taxpayers, will be responsible for about 43 percent of that. Even with all this spending, millions of lives will be cut short. Dietary factors are largely to blame. This thesis explores how policy interventions to encourage healthy diet and discourage healthy diet can be projected to affect future healthcare spending. It assesses six dietary factors to determine whether there is sufficient research to determine how much economic disease burden they will impose. Among those for which such research exists, the thesis estimates the cost-effectiveness of interventions such as education, subsidies, taxes and legislative bans.

No description available.