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Medical Forum / General / Cardiology / February 2009Controlling Cardiovascular Calcification
"Dietary lecithin promotes removal of lipid from established atherosclerotic plaque." "4 months 3% soya lecithin plasma cholesterol and LP distribution returned to normal" Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study. Full Abstract BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women. ------------------- Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Br J Exp Pathol 1985 Feb;66(1):35-46 Hunt CE, Duncan LA Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel diet containing 14% hydrogenated coconut oil and 0.06% cholesterol (approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the same ingredients but with no coconut oil or cholesterol. Rabbits fed atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months) and plasma lipoprotein (LP) distribution shifted from a pattern in which high-density lipoproteins (HDL) predominated to one in which very-low-density lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP distribution returned to normal in rabbits fed atherogenic diet for 18 months followed by atherogenic diet plus 3% soya lecithin for an additional 4 months. Rabbits fed atherogenic diet for 18 months had extensive, usually full circumference fibromuscular plaques in main branches of coronary arteries and all portions of aorta which compromised lumen area by almost 50%. These lesions were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked foam cells and cholesterol clefts, were less cellular with a distinct fibrous surface and occupied less space. Animals fed basal diet did not develop hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of plasma LP shifted slightly in favour of increased low-density lipoproteins (LDL) and decreased HDL compared with rabbits fed standard commercial diet. Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam cell lesions in proximal aorta. Liver injury including fatty change, cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus, rabbits fed appropriate diets low in cholesterol accumulate cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta and main branches of coronary arteries which are similar to those in man. Also, in this experimental model, dietary lecithin promotes a return to normal of the LP distribution profile and removal of lipid from established atherosclerotic plaque. PMID: 3970829, UI: 85122459 ---------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk And I thought the supplement vit K2 did all that work????? ;-) > "Dietary lecithin promotes removal of lipid from established > atherosclerotic plaque." [quoted text clipped - 111 lines] > DEAD PEOPLE WALKING > http://tinyurl.com/zk9fk And I thought the supplement vit K2 did all that work????? ;-) << You are for some reason of the belief one must learn how to milk a cow .. ? I believe you are mistaken about man needing to learn how to milk a cow .. I believe the vegetable lecithin .. logically .. would be the way man would get the vitamin K he needs. Vegetable lecithin is found in all your plant food and it contains vitamin K. I know for some reason you .. believe .. one must learn how to milk a cow .. but .. it is a stupid .. theory .. "Dietary lecithin promotes removal of lipid from established atherosclerotic plaque." "4 months 3% soya lecithin plasma cholesterol and LP distribution returned to normal" Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study. Full Abstract BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women. ------------------- Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Br J Exp Pathol 1985 Feb;66(1):35-46 Hunt CE, Duncan LA Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel diet containing 14% hydrogenated coconut oil and 0.06% cholesterol (approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the same ingredients but with no coconut oil or cholesterol. Rabbits fed atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months) and plasma lipoprotein (LP) distribution shifted from a pattern in which high-density lipoproteins (HDL) predominated to one in which very-low-density lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP distribution returned to normal in rabbits fed atherogenic diet for 18 months followed by atherogenic diet plus 3% soya lecithin for an additional 4 months. Rabbits fed atherogenic diet for 18 months had extensive, usually full circumference fibromuscular plaques in main branches of coronary arteries and all portions of aorta which compromised lumen area by almost 50%. These lesions were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked foam cells and cholesterol clefts, were less cellular with a distinct fibrous surface and occupied less space. Animals fed basal diet did not develop hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of plasma LP shifted slightly in favour of increased low-density lipoproteins (LDL) and decreased HDL compared with rabbits fed standard commercial diet. Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam cell lesions in proximal aorta. Liver injury including fatty change, cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus, rabbits fed appropriate diets low in cholesterol accumulate cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta and main branches of coronary arteries which are similar to those in man. Also, in this experimental model, dietary lecithin promotes a return to normal of the LP distribution profile and removal of lipid from established atherosclerotic plaque. PMID: 3970829, UI: 85122459 ---------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk >> And I thought the supplement vit K2 did all that >> work????? ;-) << > > "Dietary lecithin promotes removal of lipid from established > atherosclerotic plaque." -- Except, a higher dose of Vit K2 is not known to cause any major side effects, while supplementing too much lecithin can cause a great number of excess phosphate-related kidney conditions, including gout, or it could lead to dental problems, hypertension, or osteoporosis. So if someone does not know their Vit K2 status, they are not likely to cause themselves any harm by supplementing multiple times the recommended daily intake. However, if individuals are not aware of any existing kidney disorders, or if they are unable to monitor their calcium status (a major problem which even the best doctors have), they could create a cascade of severe calcium deficiency-related problems, by taking too much lecithin. supplementing too much lecithin can cause a great number of excess phosphate-related kidney conditions, including gout, or it could lead to dental problems, hypertension, or osteoporosis. << Don't believe ya .. "Dietary lecithin promotes removal of lipid from established atherosclerotic plaque." "4 months 3% soya lecithin plasma cholesterol and LP distribution returned to normal" Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study. Full Abstract BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women. ------------------- Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Br J Exp Pathol 1985 Feb;66(1):35-46 Hunt CE, Duncan LA Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel diet containing 14% hydrogenated coconut oil and 0.06% cholesterol (approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the same ingredients but with no coconut oil or cholesterol. Rabbits fed atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months) and plasma lipoprotein (LP) distribution shifted from a pattern in which high-density lipoproteins (HDL) predominated to one in which very-low-density lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP distribution returned to normal in rabbits fed atherogenic diet for 18 months followed by atherogenic diet plus 3% soya lecithin for an additional 4 months. Rabbits fed atherogenic diet for 18 months had extensive, usually full circumference fibromuscular plaques in main branches of coronary arteries and all portions of aorta which compromised lumen area by almost 50%. These lesions were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked foam cells and cholesterol clefts, were less cellular with a distinct fibrous surface and occupied less space. Animals fed basal diet did not develop hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of plasma LP shifted slightly in favour of increased low-density lipoproteins (LDL) and decreased HDL compared with rabbits fed standard commercial diet. Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam cell lesions in proximal aorta. Liver injury including fatty change, cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus, rabbits fed appropriate diets low in cholesterol accumulate cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta and main branches of coronary arteries which are similar to those in man. Also, in this experimental model, dietary lecithin promotes a return to normal of the LP distribution profile and removal of lipid from established atherosclerotic plaque. PMID: 3970829, UI: 85122459 ---------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk ESAD TROLL On Feb 26, 9:02 am, Ken <flakey...@aol.com> wrote: snip << Shteater .. you've been told to stay off my threads .. You don't seem to want to do that do ya .. shteater .. Maybe you should do it .. shteater .. Stay off my threads .. shteater .. "Dietary lecithin promotes removal of lipid from established atherosclerotic plaque." "4 months 3% soya lecithin plasma cholesterol and LP distribution returned to normal" Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study. Full Abstract BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women. ------------------- Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Br J Exp Pathol 1985 Feb;66(1):35-46 Hunt CE, Duncan LA Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel diet containing 14% hydrogenated coconut oil and 0.06% cholesterol (approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the same ingredients but with no coconut oil or cholesterol. Rabbits fed atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months) and plasma lipoprotein (LP) distribution shifted from a pattern in which high-density lipoproteins (HDL) predominated to one in which very-low-density lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP distribution returned to normal in rabbits fed atherogenic diet for 18 months followed by atherogenic diet plus 3% soya lecithin for an additional 4 months. Rabbits fed atherogenic diet for 18 months had extensive, usually full circumference fibromuscular plaques in main branches of coronary arteries and all portions of aorta which compromised lumen area by almost 50%. These lesions were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked foam cells and cholesterol clefts, were less cellular with a distinct fibrous surface and occupied less space. Animals fed basal diet did not develop hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of plasma LP shifted slightly in favour of increased low-density lipoproteins (LDL) and decreased HDL compared with rabbits fed standard commercial diet. Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam cell lesions in proximal aorta. Liver injury including fatty change, cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus, rabbits fed appropriate diets low in cholesterol accumulate cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta and main branches of coronary arteries which are similar to those in man. Also, in this experimental model, dietary lecithin promotes a return to normal of the LP distribution profile and removal of lipid from established atherosclerotic plaque. PMID: 3970829, UI: 85122459 ---------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk > On Feb 26, 9:02 am, Ken <flakey...@aol.com> wrote: snip << > [quoted text clipped - 5 lines] > > Stay off my threads .. shteater .. Tell me, FeChung, how does it feel that no one does as you say. Even this is a copy and paste of what you always repeat. Well, we know when it comes to repetition you are second to Chung. Chung is not mentally all there - what is your excuse? On Feb 26, 5:41 pm, J666 <j...@nowhere.com> wrote: snip << Shteater .. you've been told to stay off my threads .. Stay off my threads .. shteater .. "Dietary lecithin promotes removal of lipid from established atherosclerotic plaque." "4 months 3% soya lecithin plasma cholesterol and LP distribution returned to normal" Dietary linolenic acid is inversely associated with calcified atherosclerotic plaque in the coronary arteries: the National Heart, Lung, and Blood Institute Family Heart Study. Full Abstract BACKGROUND: High dietary intake of linolenic acid is associated with a lower risk of cardiovascular disease mortality. However, little is known about the association between linolenic acid and subclinical atherosclerosis. METHODS AND RESULTS: To examine the association between dietary linolenic acid measured by food frequency questionnaire and calcified atherosclerotic plaque in the coronary arteries (CAC) measured by cardiac CT, we studied 2004 white participants of the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study aged 32 to 93 years. The presence of CAC was defined on the basis of total CAC score of > or =100. We used generalized estimating equations to estimate odds ratios for the presence of CAC across quintiles of linolenic acid. The average consumption of dietary linolenic acid was 0.82+/-0.36 g/d for men and 0.69+/-0.29 g/d for women. From the lowest to the highest quintile of linolenic acid, adjusted odds ratios (95% CI) for the presence of CAC were 1.0 (reference), 0.61 (0.42 to 0.88), 0.55 (0.35 to 0.84), 0.57 (0.37 to 0.88), and 0.35 (0.22 to 0.55), respectively (P for trend <0.0001), after we controlled for age, gender, education, family risk group, smoking, fruit and vegetable intake, history of coronary artery disease, hypertension, diabetes mellitus, and statin use. When linolenic acid was used as a continuous variable, the multivariate adjusted odds ratio was 0.38 (95% CI, 0.24 to 0.46) per gram of linolenic acid intake. Use of different cut points for CAC score yielded similar results. CONCLUSIONS: Consumption of dietary linolenic acid is associated with a lower prevalence of CAC in a dose-response fashion in white men and women. ------------------- Hyperlipoproteinaemia and atherosclerosis in rabbits fed low-level cholesterol and lecithin. Br J Exp Pathol 1985 Feb;66(1):35-46 Hunt CE, Duncan LA Dutch-Belted rabbits were fed for 18 months an atherogenic semipurified gel diet containing 14% hydrogenated coconut oil and 0.06% cholesterol (approximately 0.15 mg/kcal) or a non-atherogenic basal gel diet containing the same ingredients but with no coconut oil or cholesterol. Rabbits fed atherogenic diet developed hypercholesterolaemia (means 733 mg/dl at 16 months) and plasma lipoprotein (LP) distribution shifted from a pattern in which high-density lipoproteins (HDL) predominated to one in which very-low-density lipoproteins (VLDL) were predominant. Total cholesterol/triglyceride ratio in d less than 1.006 LP changed from 0.3 to 1.8. Plasma cholesterol and LP distribution returned to normal in rabbits fed atherogenic diet for 18 months followed by atherogenic diet plus 3% soya lecithin for an additional 4 months. Rabbits fed atherogenic diet for 18 months had extensive, usually full circumference fibromuscular plaques in main branches of coronary arteries and all portions of aorta which compromised lumen area by almost 50%. These lesions were modified in rabbits fed atherogenic diet plus lecithin. The plaques lacked foam cells and cholesterol clefts, were less cellular with a distinct fibrous surface and occupied less space. Animals fed basal diet did not develop hypercholesterolaemia (means 86 mg/dl at 16 months), although distribution of plasma LP shifted slightly in favour of increased low-density lipoproteins (LDL) and decreased HDL compared with rabbits fed standard commercial diet. Basal diet rabbits had no coronary atherosclerosis and only minimal focal foam cell lesions in proximal aorta. Liver injury including fatty change, cholangitis and portal fibrosis occurred in animals fed atherogenic diet. Thus, rabbits fed appropriate diets low in cholesterol accumulate cholesterol-enriched LP in their plasma and develop lesions in abdominal aorta and main branches of coronary arteries which are similar to those in man. Also, in this experimental model, dietary lecithin promotes a return to normal of the LP distribution profile and removal of lipid from established atherosclerotic plaque. PMID: 3970829, UI: 85122459 ---------------------------------------------- Who loves ya. Tom Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh Man Is A Herbivore! http://tinyurl.com/4rq595 DEAD PEOPLE WALKING http://tinyurl.com/zk9fk |
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