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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)
