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Fats, Cholesterol, and Heart Disease
Doesn't a meat-based diet like our Stone Age ancestors promote high blood cholesterol and heart disease?
The fat quality and quantity in the wild animals our Stone Age ancestors ate was vastly different from the types and quantity of fat found in the fatty meats typically consumed in the US. A 100-gram serving of roast buffalo contains only 2.4 grams of fat, and 0.9 g of saturated fat, whereas a 100-gram, T-bone beefsteak contains a whopping 23 grams of fat, and 9 grams of artery clogging saturated fat. Additionally, the bison roast contains 215 mg of heart-healthy, omega-3 fatty acids whereas the T-bone steak contains a paltry 46 mg. The types of meats permitted on The Paleo Diet are lean meats (beef, pork, poultry, fish, seafood) trimmed of visible fat. These meats are healthful because they have nutritional characteristics similar to wild animals.
Recent clinical studies have shown that lean protein-based diets are more effective in improving blood cholesterol and other blood lipid levels than are low-fat, high-carbohydrate diets. High protein diets have also been shown to lower blood homocysteine levels, another risk factor for heart disease. When nutritionists abandoned meats as part of heart-healthy diets, they unknowingly threw out the baby with the bath water. It was the saturated fat that accompanied the lean protein that was harmful -- not the lean protein itself.
What would you say to people who disagree with your assertion that saturated fats cause heart disease?First off, let's get the record straight. I have never said that saturated fats are the sole dietary cause of "heart disease." Coronary heart disease (CHD) consists of myocardial infarctions (heart attacks) and angina pectoris and accounts for 54% of the deaths from a larger category of heart and blood vessel illnesses called cardiovascular disease (CVD) which accounts for 40.6% of all deaths in the U.S. CVD not only includes CHD, but also stroke, congestive heart failure, hypertension, rheumatic heart disease, congenital cardiovascular defects, artery diseases and others. The physiological mechanism underlying CHD is atherosclerosis, a complex process involving interactions among environmental factors (both nutritional and non-nutritional) and the genome. Environmental factors such as exercise, smoking, and inflammation clearly influence the development and progression of atherosclerosis. Numerous nutritional factors can serve to either (1) promote or (2) inhibit atherosclerosis via modulation of one or more of the steps involved in the atherosclerotic process.
Dietary saturated fats are nutritional elements that may promote atherosclerosis. As consumption of certain saturated fatty acids (12:0, 14:0, 16:0, but not 18:0) increases, the number of hepatic (liver) and peripheral low-density lipoprotein (LDL) receptors decreases which in turn causes serum concentrations of LDL cholesterol to rise (a process called down regulation). Down regulation occurs because internalization of 12:0, 14:0 and 16:0 within cells reduces the expression of genes which code for the LDL receptor protein. At low blood LDL cholesterol concentrations (20-50 mg/dl), LDL cholesterol molecules move freely in and out of the arterial intima (the portion of the artery where atherosclerosis arises). When blood levels of LDL cholesterol molecules rise, LDL molecules tend to become "stuck" in the intima where they undergo oxidation and glycation to become "modified LDL." Modified LDL stimulates arterial endothelial cells to display adhesion molecules which latch onto circulating monocytes and T cells. The endothelial cells then secrete chemokines which bring the monocytes and T cells into the intima where they mature into macrophages. T cells release cytokines causing inflammation and cell division within the artery. The macrophages are different from all other cells in the body in that they display a scavenger receptor which is not down regulated by LDL cholesterol molecules. The macrophages "feast" upon modified LDL cholesterol in the intima and become filled with these fatty droplets and become foam cells. Cytokines cause smooth muscle cells to grow over the lipid core of multiple foam cells forming a tough fibrous cap which becomes the characteristic plaque which defines atherosclerosis. Finally, inflammatory cytokines secreted by foam cells weaken the fibrous cap by digesting the collagen matrix. If the weakened cap ruptures, a substance secreted by the foam cells called "tissue factor" interacts with clot promoting elements in the blood causing a thrombus (clot) to form. If the clot is large enough to halt blood flow, it causes a myocardial infarction (heart attack).
Dietary saturated fats do not always elevate blood LDL concentrations. When consumed under hypocaloric (reduced energy) conditions they may improve most blood lipid parameters including total and LDL cholesterol, HDL cholesterol, and total triacylglycerol (TG). This phenomenon typically explains why Atkins-like diets (such as recently reported this spring in the New England Journal of Medicine) may be as or more effective than hypocaloric, low-fat, high-carbohydrate diets. However, under isocaloric (normal energy) conditions, studies of healthy normal subjects show increased consumption of saturated fats significantly raises blood LDL concentrations.
A further confounding factor in this scenario is the presence of a specific type of LDL cholesterol molecule in the blood called "small dense LDL." The rate of influx of LDL into the intima is not only related to the blood concentration of LDL cholesterol, but also to the size of the LDL molecule. Small dense LDL have a greater flux into the intima than normal LDL and they are more likely to get "stuck" in the intima because of increase binding to proteoglycans. The primary metabolic source of small dense LDL is very low density lipoprotein molecules (VLDL) whose blood concentration is greatly influenced by dietary carbohydrate, particularly high-glycemic-load carbohydrates. Hence foods with high glycemic loads such as those made with refined sugars and grains may also operate synergistically with high dietary saturated fats to promote atherosclerosis. Additionally, high-glycemic-load carbohydrates are positively correlated with plasma concentrations of C reactive protein, an important marker for systemic inflammation, a key element of the atherosclerotic process, as I previously noted.
The gold standard procedure for demonstrating cause and effect between diet and disease is called a dietary intervention. Subjects are either fed or not fed a certain food or nutrient and then either presence or absence of a disease or disease symptom is monitored over time. With CHD, the results of dietary interventions in which saturated fats have been lowered, frequently have been unable to demonstrate a reduced mortality from CHD. The problem with the majority of these studies is that they were conducted prior to the knowledge that high-glycemic-load carbohydrates were an important promoting factor in CHD etiology. Further, most of these studies did not control for inhibitory dietary factors such as omega-3 fatty acids, fiber, phytochemicals, antioxidants etc. Hence, the interpretation of whether or not dietary saturated fats cause CHD in these interventions is confounded by a number of crucial variables. In animal studies, including primates, these confounding dietary factors can be completely controlled and atherosclerosis is routinely induced by solely feeding high amounts of saturated fats. (Source: thepaleodiet.com)
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