To:     All Paleodieters
From:   Mary and Sally

Following are some miscellaneous comments for the ongoing debate.

1.  George Mann did not find pathogenic build up of plaque in the Masai, but
rather the normal intimal thickening of the arterial wall that occurs in all
individuals, regardless of diet.  The pathologist William Stehbens has
reported on this and we quote from his work.  (The Pathology of
Atherosclerosis, in Coronary Heart Disease, George Mann ed., available from
the Price-Pottenger Nutrition Foundation (619) 574-7763):  For many years it
has been acknowledged that at birth the intima of the aorta is thickened, more
so distally than proximally, with similar intimal thickenings occurring at
forks of distributing arteries.  . . . It is also recognized that the intima
thickens throughout life progessively but not uniformly.  The process does not
cease at physical maturity, like other maturation phenomena, even though some
vessels remain unaffected or virtually unaffected for most of the subject’s
life.  This sclerotic change has been referred to as arteriosclerosis and is
often considered to be an aging phenomenon, while the accumulation of the
lipid-rich rich debris in the thickened intima was thought by some to be a
separate disorder, i.e. atherosclerosis.  However the two disorders have not
been satisfactorily differentiated, and so confusion has abounded for many
years over the use of the two terms. . . Logically, in seeking the cause of
atherosclerosis, we should investigate the earliest demonstrable lesions which
appears to be the intimal pads of cushions about arterial forks and junctions.
Ultrastructurally, these intimal proliferations exhibit evidence of granulo-
vesicular degeneration and loss of elastica even in the neonate, and their
localization is consistent with their being of hemodynamic origin.  These
thickenings progressively enlarge and exhibit evidence of considerable muscle
cell degeneration with the accumulation of myriads of vesicles in the cell
matrix and also plasma membrane fragments, abnormal collagen, loss of elastic,
and dystrophic basement membranes with separation of muscle and endothelial
cells from the multilaminated basement membranes.  The accumulation of lipid
and calcification is a later phenomenon. . .(end quote)

 In other words, atherosclerosis is initiated in the breakdown of normal
thickened arterial tissue that occurs in locations of pressure gradients due
to the fluid dynamics of blood flow.  Such breakdown may be due to nutritional
deficiencies or to irritations from viruses or free radicals from oxidized
cholesterol and rancid dietary fats.

2.  A 1962 study of coronary artery disease in Thailand is germane to our
discussion of saturated fats.  (A comparison of atherosclerosis of the aorta
and coronary arteries in Bangkok and Los Angeles, Am J Clin Path Vol 38, No 2,
pp162-170.)  Researchers  found that in Thailand, a diet which is low in total
fat [compared to Thai’s living in Los Angeles] but relatively high in the
proportion of saturated fat was found to be compatible with a low severity of
coronary atherosclerosis.  Sources of saturated fat in the Thai diet are lard
used in cooking; and coconut oil, which contains over 50% of total fat as the
supposedly atherogenic C-12, C-14 and C-16 fatty acids.  These fats strengthen
immune system function, which may by why Thailand has the lowest overall
cancer rate (for both men and women) of all the 50 countries included in the
National Cancer Institute surveys.

3.  Newly released USDA data show a decrease in the consumption of SFAs since
the turn of the century (57 grams per person per day in 1909 versus 52 in
1994.)  (CNI, February 13, 1998 pp 4-6.)  Levels for monounsaturated fatty
acids increased from 49 and 65 grams per capita per day and levels of
polyunsaturated fatty acids increased from 13 to 31 grams per capita per day.
Total fat contributions from red meat have generally declined throughout this
period.  In the early years, red meat contributed about one-third of the fat,
but by 1994 its contribution decreased by almost one-half.  However,
contributions from salad oils were 10 times higher in 1994 than in 1909.
Total fats and oils have increased from 41 pounds in 1909 to 70 pounds per
capita in 1994.  It is hard to conclude from this data that consumption of
saturated fats (from butter, tropical oils and animal sources) is the cause of
the steep rise in CHD that has characterized the 20th century.  In fact, these
statistics indicate that the so-called heart healthy monounsaturated fats
should be more closely examined as a possible contributing factor, at least in
the context of the American diet.

4.  We still lack one key piece of data, and that is the amount of adipose
tissue as a percentage of the total in a large wild ruminant such as an elk or
moose, during the late Summer and early Fall.  Without this we cannot make a
true comparison between the saturated fat available to Paleolithic man,
compared to his modern beef-eating counterpart.  Are there any hunters in the
group who can enlighten us?  Even a visual estimate would be helpful.  How
thick is the subcutaneous fat on such an animal at the height of its fat
stores?

5.  There was a question about traditional preparation of maize (corn) which
involves an alkaline treatment to release niacin.  This seems to contradict
assertions that grains should receive an acid treatment (lactic acid
fermentation) to neutralize phytic acid and other nutrients.  Actually, corn
in South American cultures was first treated with lye before cooking; but the
cooked gruel then underwent a long period of acid fermentation.  Examples are
Cherokee bread, made from a cooked gruel of corn and beans, wrapped in corn
husks and allowed to ferment for at least two weeks.  A similar preparation is
Pozol, from southern Mexico, made by wrapping cooked corn gruel in banana
leaves and allowing at least two weeks for fermentation.  The “bread” becomes
covered with green mold.  Pozol seems to be a complete food, supporting good
health without the addition of other foodstuffs (insect parts and the mold
itself would supply animal factors).  A high enzyme content and antibiotic
factors in the mold would provide protection against gastrointestinal distress
in the hot moist jungle environment.

6.  The politically correct interpretation of the Paleolithic diet is one of
lean meat, occasional organ meats, nuts, monounsaturated oils, fruits and
vegetables.  Some have found that their blood parameters worsen on such a
diet, and we submit that a likely cause is low levels of saturated fats, and
inadequate levels of fat soluble vitamins A and D, such as are found in dairy
fats, shell fish, egg yolks and organ meats.  We are especially concerned
about the use of this diet for growing children, who tend to dislike organ
meats and who have  traditionally obtained  vitamins A and D from dairy fats
and egg yolks.  Calcium deficiency is also a potential problem.  Traditional
societies obtained sufficient calcium either from dairy products or from
preparations made from bones--generally bone broths.  Vegetables will not
supply adequate calcium for growing children, due to a number of blocking
factors such as oxalic acid, and nuts will not be a good source either, unless
properly prepared to neutralize phytic acid content. Adequate vitamin A and D
are needed for calcium absorption.