The following was written by Loren Cordain. I'm posting it for Loren as he
is having technical problems at the moment.
Those wishing to refer back to the messages Dr. Cordain is responding to
here may wish to see http://maelstrom.stjohns.edu/archives/paleodiet.html
and to do a search an "Enig" or "Fallon" to read the relevent messages.
Cordain's message follows:
-=-=-=-
This commentary represents my rebuttal to Dr. Enig's and Sally Fallon's
response of June 29. I realize that this rebuttal comes in rather late,
however I was unable to respond during the summer because I was out of
town. I have tried to preface the original questions so that our members
can determine what issues were being discussed.
1. Thank you for your followup comments on Dr. Voegtlin's book. We
are in agreement that an all animal based diet can provide all the known
nutrients needed for adequate nutrition. I am in complete agreement that
for optimal nutrition, diets based upon both plant and animal foods
probably provide superior nutrition than do diets based solely upon animal
derived foods. Not only do plant foods provide necessary vitamins,
minerals and soluable fiber, but they provide a source of phytochemicals
which are increasingly being found to benefit human health in a wide
variety of ways.
2. Dr. Enig and Sally Fallon say "We have consistently argued that the
current high levels of CHD have nothing to do with the consumption of
saturated fat from animal sources, but rather are due to foods relatively
new to the human diet--particularly excess polyunsaturates, hydrogentated
oils and refined carbohydrates".
I agree that there is now substantial evidence that hydrogenated
oils are atherogenic via their hypercholesterolemic effects (1); however
in terms of their cholesterol raising properties they may be worse than
saturated fats because they cause a decrease in HDL cholesterol (2).
Refined carbohydrates (sucrose in particular) has been known for more than
30 years (3) to be implicated in its CHD promoting effects, probably
through increases in VLDL, triglycerides, total cholesterol and perhaps
decreases in HDL (4). Recently it has been recognized that although
dietary polyunsaturates may lower serum cholesterol levels, they may
actually increase the risk for CHD by increasing the susceptibility of LDL
to oxidation (5).
So we are in agreement that hydrogenated fats, refined
carbohydrates and excessive polyunsaturated fats (primarily linoleic acid,
18:2n6) contribute to the development of CHD via hypercholesterolemic and
LDL oxidizing mechanisms. However, I cannot agree with the statement that
saturated fats from animals having nothing to do with CHD. It may be
possible that the hypercholesterolemic effects of saturated fats (12:0,
14:0. 16:0) can be negated or somewhat ameliorated by extremely low levels
of dietary carbohydrates (particularly in insulin resistant subjects) or by
high levels of dietary protein (>20% of total calories) via protein's VLDL
suppressing effects (6); however it is clear beyond a shadow of a doubt
that dietary saturated fats (12:0, 14:0 and 16:0) elevate serum cholesterol
levels within the context of the "average American diet". A recent meta
analysis of 224 published studies encompassing 8,143 subjects (many under
metabolic ward conditions) has unequivocally demonstrated the
hypercholesterolemic effect of dietary saturated fats (7). The cellular
basis for the this observation stems from the regulation of low density
lipoproteins. When the amount of cholesterol or saturated fat into the
body is increased, there is an expansion of the sterol pools within liver,
and to a lesser extent, peripheral cells, which causes a down regulation
of LDL receptors. As a consequence LDL in plasma increases (8).
Some have argued that increases in total plasma cholesterol and
LDL may not necessarily have a direct relationship to mortality from CHD
(9). Clearly, there are a wide variety of independent risk factors for CHD
including hypertension, homocysteine (vitamins B6, B12 and folic acid),
catecholamines, n6/n3 fatty acid ratio, antioxidant status (vitamins e, c
beta carotene, phytochemicals etc.)dietary fiber, cigarette smoking and
ethanol consumption which influence a variety of physiological systems
involved with CHD. However, there is powerful evidence (n = 356,222) to
indicate that the relationship between serum cholesterol levels and the
risk of premature death from CHD is continuous and graded (9).
Therefore, the recommendation to consume high levels of dietary saturated
fats within the context of the "average American diet" appears to not only
be erroneous, but probably deadly. Our hunter gatherer ancestors
consumed high levels of animal food (probably >55% of their total daily
calories), however the context under which this was done was much different
than present day conditions. As I have previously mentioned, the
carbohydrate content of the diet was low (~< 35 % of total calories) and
composed of plant foods with high soluble fiber and low starch content.
The protein content of the diet would have exceeded 20% and may have been
as high as 30-40 %. The fats consumed would have had a low n6/n3 ratio
and there would have been both ample levels of 20 and 22 carbon fats of
both the n6 and n3 variety. Since marrow contains, 70-75% monounsaturated
fats (MS) and was a favored food, it is likely that although the fat
content of the diet may have been as high as 40%, it was composed of higher
levels of MS and non atherogenic saturated fats such as stearic acid
(18:0).
3. Wholesale dismissal of the LDL/HDL ratio as a risk factor for CHD
without either rationale or references is difficult to respond to.
Perhaps Dr. Enig and Sally can provide further detail. Low HDL
cholesterol levels are strongly associated with coronary heart disease, and
many factors that produce lower HDL cholesterol levels increase the risk of
coronary heart disease; examples are smoking, obesity, lack of physical
activity, abstinence from alcohol and low levels of dietary ascorbate.
The induction of high HDL cholesterol levels in animals retards
atherogenesis, and the infusion of HDL protein retards the development of
fatty streaks (10).
I agree that the oxidized cholesterol in powdered milk, eggs and
aged cheeses is a powerful promoter of atherogenesis. In our
laboratories, we routinely induce atherosclerosis in miniature swine using
a diet with high levels of oxidized cholesterol.
Except for trans fatty acids which elevate Lp (a), Lp(a) is
remarkably unresponsive to dietary manipulations (11). I would enjoy
seeing the references showing that saturated fat consumption actually
decreases it.
4. Dr. Enig and Sally Fallon dismiss the idea that dietary protein has
any influence upon cardiovascular disease with the argument that there is
no difference in CHD incidence in populations consuming either "high
protein consumption (30-40%)" or "relatively low protein consumption
(15-20%)". Once again no references are cited to substantiate this
argument.
I would first like to point out that global surveys of the world's
populations indicate a remarkably limited range of protein consumption
that varies from about 10 to 15% of total calories (12). Further, except
for reports of Inuit and Eskimo diets, I know of no references showing any
contemporary populations consuming 15-20% of their calories as protein,
much less 30-40%. Please provide your sources.
Speth (12) has extensively studied protein intakes in contemporary
world wide populations and notes that most human populations today obtain
between 10-15% of their total energy requirements from protein. For
Americans the value is 14%, for Swedes it is 12%; for Italian shipyard
workers it is 12.5-12.8%; for Japanese, it is 14.4% and for West Germans it
is 11.1%. Even among athletes values rarely exceed 15%. Speth (12) shows
that Italian athletes consumed between 17-18% of their caloric intake as
protein; Russian athletes consumed 11-13%; Australian athletes competing at
the 1968 Olympic games consumed 14.4% of their daily calories as protein.
This data clearly demonstrates the relative homgeneity amongst contemporary
global populations in their protein consumption levels.
That protein consumption may have anything to do with the
atherosclerotic process and hence CHD is an obscure topic which has been
rarely examined by the medical and nutritional communities. I am not
surprised that Dr. Enig and Sally Fallon are unaware of the literature
which supports this concept. There are at least three human clinical
trials (13,14, 15) demonstrating that isocaloric substitution of protein
(daily caloric protein intakes ranging from 17-27% of total calories) for
carbohydrate reduces triglycerides, VLDL, LDL and total cholesterol while
increasing HDL cholesterol. Further, acute consumption of high levels of
beef protein without carbohydrate evokes an extremely small rise in serum
insulin levels and a concomitant substantial rise in glucagon (16). Both
of these acute responses would tend to be associated with a reduced risk
for CHD. Lastly, in animal models, high levels of protein are known to
dramatically inhibit hepatic VLDL synthesis (6). VLDL are the precursor
molecules for LDL cholesterol. In their classic study of Inuit, Bang and
Dyerberg (17) have shown that the serum cholesterol levels of the Inuit
were 0.48 mmol/liter lower than what would have been predicted by the Keys
equation which estimates plasma lipid levels from dietary saturated fats,
polyunsaturated fats and cholesterol . At the time (1980), it was
suggested that the paradoxically low serum cholesterol levels may have
resulted from the higher omega 3 (n3) fats found in the Eskimo's seafood
based diet. However after almost 30 years of research, meta analytical
studies have shown that n3 fatty acids, slightly elevate (5-10%) LDL
cholesterol concentrations, but do not materially affect total cholesterol
(18). Consequently, it may have been the higher dietary protein intake
(23-26% of total calories) in the Inuit compared to the Danish Controls
(11% of total calories as protein) which may have accounted for these
differences. However, since the Key's equation considers dietary
monounsaturated fats as neutral (which more recent research (19) indicates
is not the case), it is possible that the higher monounsaturared fat
content (57.3% of total fat) in the Inuit diet (Vs 34.6% in the Danes) may
have also contributed to the plasma cholesterol differences.
Many people on this list would argue that the cholesterol lowering
effect of the Eskimo diet stemmed from its low carbohydrate content.
However, in one of the few (and best controlled) metabolic ward trials of a
carbohydrate free (<20 gm/day) diet, Phinney and colleagues (20)
demonstrated a rather large rise in serum cholesterol (159 to 208 mg/dl)
in nine lean, healthy males who participated in this 35 day in patient
trial. The protein content of the diet was estimated to be 15%, whereas
the fat content of the diet represented between 83-85% of total daily
calories. Consequently, during the dietary trial, the protein content
remained similar to the average daily intake in the US and was not
increased. This experiment shows that a carbohydrate diet free diet
composed of "ground beef, breast of chicken, water packed tuna fish,
powdered egg solids, and cheddar cheese with mayonnaise, heavy cream , sour
cream, and cream cheese as primary lipid sources" was definitely
hypercholesterolemic. In a less well publicized , but highly controlled
clinical research center (CRC) study, Gray (21) showed similar results in a
3 week study of 10 healthy males who consumed a diet composed of 73-75%
fat, 7-9% CHO and 16-20% protein. Compared to their standard (normal
carbohydrate diet), the high fat diet increased total cholesterol from
156.5 mg/dl to 167.6 mg/dl and LDL cholesterol increased from 46.6 mg/dl to
55 mg/dl. The total CHOL/HDL ratio actually improved on the high fat diet
going from 3.36 to 3.20. High fat, low carbohydrate diets such as the
Phinney (20) and Gray (21) studies characteristically induce other
beneficial lipid profiles such as increased HDL levels and
(Continued in Part 2)
|
