Dr Mike Knapton, associate medical director at the British Heart Foundation, said the claims about saturated fat were "unhelpful and misleading".He added: "Decades of research have proved that a diet rich in saturated fat increases 'bad' LDL cholesterol in your blood, which puts you at greater risk of a heart attack or stroke."
Knapton states a fact coupled with an assumption. It's a fact that three chain lengths of saturated fat (12, 14, and 16) raise LDL cholesterol somewhat. http://ajcn.nutrition.org/cont... It is also a fact that 18 carbon chain stearic acid, which has no affect on LDL cholesterol levels is the most prominent fatty acid in unstable arterial plaques. http://circgenetics.ahajournal...
I mention unstable arterial plaques because of this. "Numerous studies have demonstrated that coronary atherosclerosis affects all eutherian animals with a body mass comparable to or larger than humans, regardless of diet specialization and LDL levels. Surprisingly, in these mammals, lipid accumulations in arterial walls were more common in herbivores than carnivores." https://www.ncbi.nlm.nih.gov/p...
So the debate should not be about LDL levels. It should center on what causes plaque build up and what generates unstable plaques. It's peculiar that nobody mentions mercury toxicity. Quite likely mercury toxicity contributed significantly to heart attack risk among middle aged men during the first half of the 20th Century. "Mercury activates phospholipase A2 (PLA-2) which increases the risk for coronary artery and cerebral plaque rupture with MI and CVA. In addition, mercury induces formation of arachidonic acid metabolites such as total prostaglandins, thromboxane B2 and 8 isoprostane in vascular endothelial cells and activates vascular endothelial cell phospholipase D. Even very low levels of chronic mercury exposure promote endothelial dysfunction (ED) as a result of increased inflammation, oxidative stress, immune dysfunction, reduced oxidative defense, reduction in nitric oxide (NO) bioavailability. Many of the cardiovascular consequences of mercury are mitigated by concomitant intake of fish containing omega 3 fatty acids and by the intake of selenium. All of these pathobiological findings will increase the risk of hypertension, CHD, MI, CVD and CVA." https://www.esciencecentral.or...
Note the mention of arachidonic acid metabolites. Why it that important? "Arachidonic acid (AA) in the diet can be efficiently absorbed and incorporated into tissue membranes, resulting in an increased production of thromboxane A2 by platelets and increased ex vivo platelet aggregability. Results from previous studies have shown that AA is concentrated in the membrane phospholipids of lean meats." https://www.ncbi.nlm.nih.gov/p...
"The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat." https://www.ncbi.nlm.nih.gov/p...
It is unfortunate that scientists debating the saturated fat issue ignore endocannabinoid system (ECS) research. "We now know that major changes have taken place in the food supply over the last 100years, when food technology and modern agriculture led to enormous production of vegetable oils high in -6 fatty acids, and changed a
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Dr Mike Knapton, associate medical director at the British Heart Foundation, said the claims about saturated fat were "unhelpful and misleading".He added: "Decades of research have proved that a diet rich in saturated fat increases 'bad' LDL cholesterol in your blood, which puts you at greater risk of a heart attack or stroke." Knapton states a fact coupled with an assumption. It's a fact that three chain lengths of saturated fat (12, 14, and 16) raise LDL cholesterol somewhat. http://ajcn.nutrition.org/cont... It is also a fact that 18 carbon chain stearic acid, which has no affect on LDL cholesterol levels is the most prominent fatty acid in unstable arterial plaques. http://circgenetics.ahajournal... I mention unstable arterial plaques because of this. "Numerous studies have demonstrated that coronary atherosclerosis affects all eutherian animals with a body mass comparable to or larger than humans, regardless of diet specialization and LDL levels. Surprisingly, in these mammals, lipid accumulations in arterial walls were more common in herbivores than carnivores." https://www.ncbi.nlm.nih.gov/p... So the debate should not be about LDL levels. It should center on what causes plaque build up and what generates unstable plaques. It's peculiar that nobody mentions mercury toxicity. Quite likely mercury toxicity contributed significantly to heart attack risk among middle aged men during the first half of the 20th Century. "Mercury activates phospholipase A2 (PLA-2) which increases the risk for coronary artery and cerebral plaque rupture with MI and CVA. In addition, mercury induces formation of arachidonic acid metabolites such as total prostaglandins, thromboxane B2 and 8 isoprostane in vascular endothelial cells and activates vascular endothelial cell phospholipase D. Even very low levels of chronic mercury exposure promote endothelial dysfunction (ED) as a result of increased inflammation, oxidative stress, immune dysfunction, reduced oxidative defense, reduction in nitric oxide (NO) bioavailability. Many of the cardiovascular consequences of mercury are mitigated by concomitant intake of fish containing omega 3 fatty acids and by the intake of selenium. All of these pathobiological findings will increase the risk of hypertension, CHD, MI, CVD and CVA." https://www.esciencecentral.or... Note the mention of arachidonic acid metabolites. Why it that important? "Arachidonic acid (AA) in the diet can be efficiently absorbed and incorporated into tissue membranes, resulting in an increased production of thromboxane A2 by platelets and increased ex vivo platelet aggregability. Results from previous studies have shown that AA is concentrated in the membrane phospholipids of lean meats." https://www.ncbi.nlm.nih.gov/p... "The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat." https://www.ncbi.nlm.nih.gov/p... It is unfortunate that scientists debating the saturated fat issue ignore endocannabinoid system (ECS) research. "We now know that major changes have taken place in the food supply over the last 100years, when food technology and modern agriculture led to enormous production of vegetable oils high in -6 fatty acids, and changed a