Thank you all for the lively debate.  Following are answers to queries that
have come in.

A.  Replies to Dean Esmay:

1.  Our figures come from the USDA.  We stated that SATURATED fat intake
remained the same between 1935 and 1974--total fat consumption rose between
1935 and 1974 (from about 150 grams/capita/day to about 170 g/c/d.)  Animal
fat consumption actually declined (from 100 g/c/d to about 90 g/c/d) but
there was an increase in consumption of vegetable oils (from just over 50
g/c/d to over 80 g/c/d.)  We cannot say, however, that saturated fat intake
declined during this period, because vegetable oils contain some SFAs.

2.  The authors of the reference about SFAs reducing Lp(a) are Khosla and
Hayes.  Please let us know if you cannot find this on Medline.  You should
also be able to find it on Agricola.   As the abstract of this review article
does not mention the effect of SFAs on Lp(a), we will quote directly from the
relevant passage on page 330:  A subsequent analysis of frozen plasma from
this study revealed that the trans diet also resulted in significantly higher
concentrations of Lp(a) than those resulting from the oleic acid-rich diet.
 However, a surprising, but unheralded, aspect of the Lp(a) analysis was that
the saturated fatty acid-rich diet produced significantly lower Lp(a)
concentrations than the oleic acid-rich diet.

3.  The whole HDL/LDL hypothesis comes from the Framingham study, whose
coordinators utilized questionable methodologies and made many omissions in
reporting the data. For an excellent discussion of this issue see Smith,
Russell, L "Diet, Blood Cholesterol and Coronary Heart Disease:  A Critical
Review of the Literature" (1991) Volume 2, pp 3-78 to 3-100.  Smith
concludes:  "In 40 years of several hundred Framingham reports, this writer
has found neither an actual correlation coefficient published for either
total or LDL cholesterol nor a figure showing the CHD mortality and/or
morbidity rate as a function of LDL level . . . Examination of published
Framingham data. . . indicate that the correlation between CHD and total or
LDL cholesterol is probably under 0.3.  The objective and statistically
sophisticated scientist would consider these correlations as unrepresentative
of cause and effect relationships and would analyze the associated data base
to find reasons why the observed correlations occurred at all."  (pp1-2 to
1-3) An interesting sidelight to this issue is an item reported in a recent
newsletter from Dr. Atkins, who states that high HDL levels are indicative of
an underactive thyroid.  If this is the case, then the logical conclusion is
that high HDL predisposes to CHD, and not the reverse.

4.  Regarding your most recent contribution about milk consumption, one could
also say that man is the only animal that uses tools, lives in houses, wears
clothes, speaks and writes books--and uses milk products.  Is the use of milk
products thus one of those attributes that sets man apart from the beasts?
We reiterate that the use of milk produsts is associated with long and
healthy life in many parts of the world--Soviet Georgia, Hunza, Vilcabamba
in Equador, and the supremely healthy Swiss villagers studied by Weston
Price in the 1930s.

B.  To Robert Crayhon:

4.  Regarding stearic acid, we do mean that some studies have shown stearic
to raise blood cholesterol--some studies show it to be neutral and some
studies show 18:0 to lower cholesterol.  Thus nothing can be concluded about
the effect of stearic acid on cholesterol levels.  However, Dr. Cordain was
arguing that modern beef feeding methods lowered components that lower
cholesterol (stearic acid) and raised components that raise cholesterol (16:0
and 14:0).  We were merely demonstrating that no real conclusions can be
drawn  about the differences between wild and domesticated meat in regards to
its effect on serum cholesterol levels.

5.  Without giving specific references, we think it is a given that the
different fatty acids given in pure form would not have the same effect as
those fatty acids given as components of whole foods--this certainly is the
case with amino acids.  Remember also, that in many of the animal
experiments, animal fats were given to vegetarian animals (such as rabbits)
which of course led to pathological responses.

6.  We hope you will publish the results you have had with hyperlipidemic
clients using eggs, meat and other animal products while eliminating the
fabricated foods and refined carbohydrates.  We need to have more citations
in the literature about these kinds of real-world results.  What you have
here is a healthy lowering of cholesterol levels because the body does not
need to have as much cholesterol to serve as an antioxidant and protective
mechanism against rancid vegetable oils; rather than the kind of pathological
reduction that often temporarily occurs when individuals are put on a
high-PUFA diet.  This latter situation forces cholesterol into the tissues to
give them body and stability in the absence of sufficient SFAs.

C.  To Don Weiss and Dean Esmay:

Regarding the study by Kaneko et al.  The abstract is very clear.  When
27-year-old females ate meat, they absorbed more calcium.  Since they were
evidently in calcium balance, they excreted more calcium, i.e. the excess
that they did not need.  They also excreted the extra sulfur from the
sulfur-containing amino acids which are found in abundance in meat, but are
deficient in soy proteins (soy formula for infants must have added methionine
to overcome this deficiency.)  The results of the added meat is as would be
expected in normal homeostasis.  We would expect someone in appropriate
calcium balance to do just that.  When the soy protein was fed, there was no
increased absorption and excretion of calcium; this too is as expected since
the soy contains components that inhibit uptake of calcium.  We do not have
the actual paper so do not know if in fact the soy might have caused a
negative balance in some of the subjects.

Correctly interpreted, the abstract does not show that eating meat causes a
loss of calcium.  For further research on this subject, see the careful
studies of Herta Spencer, who did not find that eating meat caused calcium
loss.  (Spencer, et al "Effect of a high protein (meat) intake on calcium
metabolism in man" Am J Clin Nutr 31 (12):2167-2180 (Dec 1978); and Spencer
et al, "Further studies of the effect of a high protein diet as meat on
calcium metabolism" Am J Clin Nutr 37 (6):924-929 (Jun 1983.)