Oxidized fats, oils and cholesterol have been known to induce greater
levels of atherogenesis in animal models than their non-oxidized
counterparts for at least 30 years (1,2,3).   Heating of fats, oils and
cholesterol increases the number and amounts of lipid peroxide products,
and these peroxides are thought to be the main reason why oxidized
lipids induce an elevated atherogenic response (3).
        When cholesterol containing diets were fed to rabbits, fried or
hard boiled eggs produced the highest serum cholesterol levels (10-14
times greater than pre-experimental values), scrambled or baked eggs
caused elevation of serum cholesterol to 6 to 7 time the
pre-experimental level.  Raw or soft boiled eggs only increased serum
cholesterol levels 3 to 4 times the pre-experimental level (4).
        There is little doubt that pre-agricultural man would have
consumed wild bird eggs when they were seasonally available, and for
most of man's history they would have been consumed raw, because fire
was not in use.    However, as I have pointed out in a previous post,
regular consumption of raw eggs can induce a number of nutritional
problems.    One of the functions of the egg white is to protect the
entire egg from decomposition by bacterial contamination.     Raw egg
white prevents bacterial contamination largely because of an iron
binding lectin (glycoprotein), called conalbumin (5).   Additionally,
raw egg white contains avidin, a substance which tightly binds certain B
vitamins including biotin.   Biotin deficiencies are routinely induced
in animal models via avidin feedings.    Therefore, regular consumption
of high levels of raw eggs can potentially impair human nutrition.
Because, pre-agricultural man only consumed eggs on a seasonal basis,
there would be no chronic health problems associated with their sporadic
consumption.
        I know of no epidemiological studies contrasting the effects of
goat vs. cow milk consumption upon human health.    The percentage
composition of major components in goat's milk resembles that of cow's
milk , although there tends to be more variability in the total amount
of fat and in the fatty acid profiles (6).    Therefore, from a purely
lipid/atherogenesis perspective, one would not expect to find
differences.    I have never seen data on the Ca/Mg ratio for goats
milk, and am therefore unable to comment upon its potential for
atherogenicity in this regard.   The same can be said for its xanthine
oxidase levels, although because of its ubiquitous nature in mammals, I
suspect that goat's milk also contains significant amounts of this
enzyme.    Whether or not there is cross reactivity between goat and
human xanthine oxidase is not known.    The only milk which humans have
evolutionary experience in drinking  is mother's milk and this only for
the 2-4yr period prior to weaning.

                                REFERENCES
1.      Taylor CB et al.  Spontaneously occurring angiotoxic derivatives
of cholesterol. Am J Clin Nutr 1979;32:40-57.
2.      Kummerow FA.  Nutrition imbalance and angiotoxins as dietary
risk factors in coronary heart disease. Am J Clin Nutr 1979;32:58-83.
3.      Kubow S.  Lipid oxidation products in food and atherogenesis.
Nutr Rev 1993;51:33-40.
4.      Pollak OJ.  Serum cholesterol levels resulting from various egg
diets  -- experimental studies with clinical implications. J Am Ger Soc
1958;6:614-18.
5.      Alderton G et al.  Identification of the bacteria inhibiting,
iron binding protein of egg white as conalbumin.  Arch Biochem
1946;11:9-13.
6.      Lawton R.  Goat's milk.  In: Health Hazards of Milk, DLJ Freed
(Ed), Bailliere Tindal, London, 1984, 150-56.