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To:  All Paleodieters
From: Mary and Sally Reply to Loren Cordain, Part II

7.  You cite a study by Artaud to support the assertion that the "highest
dietary correlates to CHD in world wide epidemiological studies come from
consumption of milk and dairy products."  This study was conducted by
dieticians (who are trained to dispense fabricated foods) and William E
Connor who is an avid supporter of the lipid hypothesis.  We note that the
study contains no tables of actual food consumption, so we are unable to
assess some of their surprising claims, such as the assertion that the
French consume much larger amounts of vegetable oil than the Finns.  In
fact, consumption of vegetable oil is remarkably low in France at 5 pounds
per person per year (compared to 18 in the US) with 8 pounds of trans fats
(compared to 24 in the US.)  As there are many societies that consume dairy
products and suffer little or no heart disease (not only France, but also
the Masai studied by George Mann and the primitive Swiss studied by Weston
Price), we would caution against basing any conclusions about milk on this
paper.  It should be noted that Switzerland and Austria have the longest
lifespan of the western countries, almost the same as Japan, consuming a
diet rich in dairy products. The Greeks are slightly behind, on a diet
containing lots of rich (and salty) feta cheese.  (Goat milk has 25% more
fat than cow's milk.)

You continue to argue that dairy fats as sources of 12:0, 14:0 and 16:0 are
"atherogenic."  Our question is this:  Why were these fats not atherogenic
at the turn of the century when the American diet was just loaded with
butter, whole milk and cream?  Why are they not atherogenic to the French?
Why are they not atherogenic to the Masai?  Why are they not atherogenic to
peoples in the tropics who consume large amounts of coconut?  Why are they
not atherogenic to the peoples of Soviet Georgia?  Why are they not
atherogenic to babies drinking mother's milk, which contains more medium
chain fatty acids (12:0 at 2.56 g/32 fl oz, 14:0 at 3.15 g/32 fl oz and
16:0 at 9.05 g/32 fl oz) than stearic acid (2.85 g/32 fl oz)? As we stated
earlier, just because these fats raise cholesterol levels in short term
metabolic ward studies does not mean that they cause heart disease.

You also argue that milk consumption results in an unfavorable Ca:Mg ratio.
The Ca:Mg ratio of cow's milk is about 9:1, which is "better" than the
ratio of 11:1 found in mother's milk, and very close to serum Ca:Mg ratios
of 8:1. Weston Price found that calcium levels in primitive diets were
about 4 times higher than the calcium levels in the American diet of his
day.  Those people who did not consume dairy products got their calcium
from preparations made from bone, particularly bone broths, which are a
distinguishing feature of traditional diets.  Small fish consumed with
their bones contain considerably more calcium than milk, and it is safe to
assume that insects, consumed with their hard shells, were also an
excellent source of calcium. Of course, it is likely that magnesium levels
were also higher in the Paleolithic diet. Magnesium is very important for
the health of the cardiovascular system--but so is calcium.  You give no
reference for your assertion that the Ca:Mg ratio in "pre-agricultural"
diet was 1:1.

The body's mechanism for regulating calcium intake is complex, involving
signals from the parathyroid gland when calcium is needed, and the action
of special calcium binding proteins in the gut to transport calcium across
the intestinal wall.  These mechanisms guard against overabsorption of
calcium should it be superabundant in the diet.  The emphasis in modern
diets should be on increasing magnesium from organically grown green
vegetables and nuts and grains that have been properly prepared to
neutralize phytic acid content (which can block magnesium absorption)--not
on decreasing calcium.

The theory that the lactose component of milk is a cause of CHD is an
interesting one and deserves more study.  It is one explanation for the
fact that France has a low incidence of CHD with a high consumption of
dairy products.  In France, dairy products are rarely consumed as milk, but
as fermented products such as cheese, yoghurt, butter and sour cream.
Alternative explanations are the relatively low fat content in modern milk,
leading to a vitamin A deficiency (18), and the addition of additives such
as powdered milk containing oxidized cholesterol to reduced fat milks.  Any
one of these explanations supports our argument that the problem lies not
with consumption of milk products per se, but in the abandonment of
traditional processing methods (cheese-making, natural yoghurt, natural
fermentation to make clabber, etc.) all of which do in fact reduce lactose
content.  Genetic selection in favor of low-fat-producing cows, use of
inappropriate feed, pasteurization (which destroys lactase) and
homogenization are other possible explanations.

The study you cite regarding copper deficiencies involved rats on copper
deficient diets that contained 62% fructose.  Feeding powdered lactoalbumin
exacerbated the effects of copper deficiency more than casein or egg
white--but lactoalbumin was not the cause of copper deficiency.  These
experiments have little relevance for populations that do not have a high
level of fructose consumption and that eat well-mineralized food and
properly processed dairy products.  Hunter/gatherers and traditional
societies got sufficient copper from frequent consumption of liver and
other organ meats.

7.  Regarding xanthine oxidase, an enzyme found all over the human body and
widely spread in animal products including milk, you might want to check a
web site on the subject
(http://www.bath.ac.uk/Departments/Biosciweb/roger2.htm) describing
research examining the possibility that IgM anti-XO antibodies have a
protective role in controlling free radicals and other reactive oxygen
species.  A study by White, et al, which found that high cholesterol
induced release of xanthine oxidase in non-milk drinking rabbits, is a
further indication that XO plays a protective role. (19)

As we have given many examples of healthy populations that consume dairy
products (usually fermented dairy products), we do not agree that foods
derived from milk "wreak havoc in human health."  But we do feel that
modern commercial milk--pasteurized, fat-depleted and adulterated with
additives--is best avoided.

Referring to Mann's 1972 study of the Masai, you state that "...autopsies
done on 50 Masai men (milk drinking populations) have revealed extensive
atherosclerotic lesions in coronary artery cross sections...[noting
that]...earlier reports of freedom from atherosclerosis in the Masai were
shown to be incorrect."  We find this statement rather curious.  In 1993,
George Mann quoted this same reference, which was Mann's own work, in the
first chapter of his book Coronary Heart Disease:  The Dietary Sense and
Nonsense (GV Mann, ed, Janus Publishing Co, London, 1993).  Mann said
"...and our autopsies of 50 adult males showed little evidence of
atheroma...[and also stated that]...these animal fat eaters show neither
hypercholesteremia, nor atheroma, nor heart attacks."  Two other references
you cite for their protein research (i.e., 13 and 14, Wolfe and Giovanetti,
1991 and 1992) happened to have referred to Mann's findings with the Masai
(as Mann had reported in 1964) as showing "...undetectable coronary heart
disease...and...undetectable arteriosclerotic heart diseases..."  Thus, we
are doubly perplexed by your statement, and we are inclined to accept
Mann's 1993 description of his own earlier work.

8.  We discussed SFA content of pre-agricultural man earlier.  As we
stated, the slightly higher PUFA content of the Eskimo diet is not typical
of other pre-industrial societies.  Most of the fat in the Eskimo diet
comes from marine mammals, not fish, which is rich in monounsaturated fatty
acids and also provides moderate amounts of saturates.

9.  Regarding the supposed calciuric effects of salt, Whiting et al found
that calcium excretion with sodium chloride or phosphate could not be
detected. (20) If salt causes osteoporosis, why do the Orientals, who
consume very high levels of salt, have low levels of osteoporosis?  Human
skeletons of Huguenot women ages fifteen to eighty-nine recently exhumed in
London showed no bone loss among the elderly.  The English diet at the time
was rich in salt, principally from salted meat and fish. (21)

10.  Your thesis is that we have not done any adapting to any of the post
agricultural diets, and that all of our modern ills are due to the fact
that we are not eating like the hunter=gatherers.  But we were not eating
like the hunter-gatherers a hundred years ago and we were not suffering
from all of the modern day chronic ailments, so obviously there are some
other variables to account for the increase in degenerative disease.  What
we are all trying to determine is what these variables are.

We think it is important to keep in mind that it is virtually impossible to
determine the overall health status (including infant mortality, length of
life, etc.) of Paleolithic man, particularly as he was subject to the
vagaries of the hunt, periodic famine, drought, etc., although the fossil
record indicates that the hunter/gatherer was in general well formed, well
muscled and had good bone mineralization.

We have better data about some Neolithic groups, principally from the
pioneering work of Weston Price who found 14 societies in which virtually
all members of the tribe or village were well formed, robust and enjoyed
freedom from degenerative disease including tooth decay.  The particulars
of these diets varied considerably.  Some contained milk products, some did
not.  Some contained grains and other plant foods; others were almost
devoid of plant foods.  Some were based on fish; others on animals of the
hunt.  Some contained much raw food and others consisted mostly of food
that was cooked. The underlying characteristics of these healthy diets are
summarized as follows:

1.  The diets of healthy primitive and nonindustrialized peoples contain no
refined or denatured foods such as refined sugar or corn syrup; white
flour; canned foods; pasteurized, homogenized, skim or low-fat milk;
refined or hydrogenated vegetable oils; protein powders; artificial
vitamins or toxic additives and colorings.

2.  All traditional cultures consume some sort of animal protein and fat
from fish and other seafood; water and land fowl; land animals; eggs; milk
and milk products; reptiles; and insects.

3.  Primitive diets contain at least four times the calcium and other
minerals and TEN times the fat soluble vitamins from animal fats (vitamin
A, vitamin D and the Price Factor) as the average American diet.

4.  In all traditional cultures, some animal products are eaten raw.

5.  Primitive and traditional diets have a high food enzyme content from
raw dairy products, raw meat and fish; raw honey; tropical fruits;
cold-pressed oils; wine and unpasteurized beer; and naturally preserved,
lacto-fermented vegetables, fruits, beverages, meats and condiments.

6.  Seeds, grains and nuts are soaked, sprouted, fermented or naturally
leavened before being consumed.

7.  Only about 4% of calories come from polyunsaturated oils naturally
occurring in grains, pulses, nuts, fish, animal fats and vegetables
(compared to modern diets with values as high as 30% from polyunsaturates.)
The balance of fat calories comes from monounsaturated and saturated fats.
(An exception is the Eskimos with higher total fat from polyunsaturates.)

8.  Traditional diets contain nearly equal amounts of omega-6 and omega-3
essential fatty acids.

9.  All primitive diets contain some salt.

10.  Primitive and traditional cultures use make use of animal bones,
principally by preparation and consumption of mineral- and gelatin-rich
bone broths.

11.  Traditional cultures make provisions for the health of future
generations by providing special nutrient-rich foods for parents-to-be,
pregnant women and growing children; by proper spacing of children; and by
teaching the principles of right diet to the young.

In summary, we feel that the debate over dairy products, saturated fat and
salt is misplaced.  The conquest of degenerative diseases need not entail
deleting nutritious and delicious foods like cheese, butter, sauces,
gravies, salt and whole grains from our diet.  Rather it requires more
wisdom in our application of technology to the entire chain of food
production, including the cultivation of plant foods so that they will be
rich in vitamins and minerals; humane and natural animal husbandry; the
delivery of fresh foods to the marketplace through a well-maintained
infrastructure and appropriate packaging (rather than sterilization,
pasteurization, additives and irradiation); a return to traditional
preservation and preparation techniques including lacto-fermentation and
the making of broth; and the elimination of refined, devitalized and
denatured foods including modern vegetable oils, trans fats, sugar and
white flour, soft drinks, most canned foods and protein powders. Rather
than "lean meat, occasional organ meats and wild fruits and vegetables,"
(and we wonder how we would obtain those wild fruits and vegetables and
still have time to participate in the paleodebate) may we suggest a varied
and interesting diet that includes juicy well-marbled steaks served with
Bernaise or a nice reduction sauce, sauteed liver with onions, traditional
(but not genetically engineered) cultivars of organic vegetables (lightly
steamed and dressed with butter or in salads with dressings composed of raw
vinegar, extra virgin olive oil and cold pressed flax oil), and a variety
of delicious fruits served with old-fashioned cream.

References

1.  Divi and George, Proceedings of the ISSX, 1996

2.  W. C. Willett et al, Intake of trans fatty acids and risk of coronary
heart diseases among women. Lancet 1993; 341:581-585; F.B Hu et al, Dietary
fat intake and the risk of coronary heart disease in women. N Engl J Med
1997; 337:1491-1499

3.  Harumi Okuyama, et al, Prog Lipid Res, Vol 35, No 4, pp 409-457 1997

4.  Tatu A Meittinen, et al, JAMA Oct 18, 1985 vol 254, No 15, pp 2097 -
2102; and Timo Strandberg, et al, JAMA September 4, 1991 vol 266, No 9 pp
1225 - 1229

5.  Loren Cordain et al, Abstract presented at the International Conference
on the Return of N-3 Fatty Acids Into the food Supply:  I. Land-Based
Animal Food Products. Natcher Conference Center, NIH, Bethesda, MD 1997.

6.  Trautwein et all, British Journal of Nutrition 77:605-620, 1997

7.  M. G Enig, "Health and Nutritional Benefits From Coconut Oil and Its
Advantages Over Competing Oils," 1995 Indian Coconut Journal 26:2-10

8.  J.K.G. Kramer et al, Lipids, Vol 17, No 5, 1982, pp 372-382

9.  David F. Horrobin, "The regulation of prostaglandin biosynthesis by
manipulation of essential fatty acid metabolism," Reviews in Pure and
Applied Pharmacological Sciences, Vol 4, pp 339 - 383, Freund Publishing
House, 1983.

10. Russell L Smith, "Diet, Blood Cholesterol and Coronary Heart Disease:
A Critical Review of the Literature," 1991, Vol 2, pp 3-18 to 3-100.

11. ìAmericans:  Then and Now,î Price-Pottenger Nutrition Foundation Health
Journal, Vol 20, No 4, 1996

12. P Khosla and K. C. Hayes, Dietary trans-monounsaturated fatty acids
negatively impact plasma lipids in humans: critical review of the evidence.
J Am Coll Nutr 1996; 15:325-339

13.  B. A. Clevidence et al, Plasma lipoprotein (a) levels in men and women
consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty
acids. Arterioscler Thromb Vasc Biol 1997; 17:1657-1661

14.  David J. A. Jenkins et al, Glycemic index of foods: a physiological
basis for carbohydrate exchange. Am J Clin Nutr 1981; 34:362-366

15. O. Rasmussen et al, Differential effects of saturated and
monounsaturated fat on blood glucose and insulin responses in subjects with
non-insulin- dependent diabetes mellitus. Am J Clin Nutr 1996; 63:249-253

16.  Okuyama, op cit.

17. M. G. Enig et al, "Comparisons of Fatty Acid Profiles Used in NHANES II
Data Base and Data Available in the Literature."  Abstract #2509, FASEB
73rd Annual Meeting; and M. G. Enig "Trans Fatty Acids in Diets and Data
Bases." 1996, Cereal Foods World 41:58-63

18. Sally Fallon, "Vitamin A Vagary" Price-Pottenger Nutrition Foundation
Health Journal, Vol 19, No 2, 1995

19. White et al, Proceed Nat Acad Sci 1996:93:8745-8749

20. Whiting et al, Am J Clin Nutr 1997:65:1465-72

21. B Lees et al, "Differences in proximal femur bone density over two
centuries," Lancet, March 1993, 341:673-675.

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