jaym1212

Here are some considerations that I have found. I do not know their
validity.

1. Milk is among the top allergens for humans, possibly causing or
aggrevating autism,

2. Oxidized Cholesterol in milk, increased by pasteurization, may be a
significant factor in formation of arterial plaques.

3. Lactose in milk induces copper deficiencies that in turn reduce the
levels of the bodies natural antioxidants such as the Cu-Zn form of
superoxide dismutase. Lowered levels of endogenous antioxidants
presumably increase the susceptibility of LDL to oxidation and
therefore increase the risk for CHD. Most become latose intolerance
(LI) with age and genetics is a significant factor. According to 50
autopsies, even the Masai (famous for living on meat, milk and blood)
had atherosclerotic lesions.

4. Xanthine oxidase (XO) found in milk, apparently magnified by
homogenization, may enter the circulation. Because XO is routinely
used to induce LDL oxidation in vitro, it may be that part of milk's
pro atherogenic effect stems from its ability to increase LDL
oxidation.

5. Raw milk is alkaline. Homogenized milk is acidic. Some say a
persons diet should be mostly alkaline.

6. Some say the high amount of protien in milk results is calcuim
loss.

7. Some say casein looks like protein in pancreas. When casein enters
the body human body attacks it and damages the pancreas.

To be on the safer side, may limit dairy consumption with emphasis on
fermented products such as yogurt and kefir which have less lactose.

jaym1212

The above logic does not guarantee that milk is unacceptable for
humans under some conditions.

don wiss

There has been some recent discussion of dairy on the PaleoDiet list. See
these: http://maelstrom.stjohns.edu/CGI/wa.exe?A1=ind0310&L=paleodiet#5

The first in that group (5.) by Edward Thompson includes:

"Note: Regarding milk consumption, I would have to say that it appears
"guilty as charged" regarding prostate cancer (a "probable" cause)."

He doesn't follow up with this accusation. I'd like to know more about this
connection. Maybe a Medline search would have more.

Then in the first article by Roland Rohde it discusses how milk causes
leaky gut, which is why the Samburu and the Masai never mix milk and meat.
And the origin of the appropriate jewish kashrut. Following articles by
Roland discuss this more.
Don <donwiss at panix.com>.

jeff

Unproven conjecture, at best.

Skim milk is low in choelstrol. Not relevant to question.

Can you supply the references, please?


Maybe? The XO would be almost totally digested. Please provide the
references that show that a significant amount enters the blood stream.

Some say? So what?

The fact is I have these two things that take care of acid base balance.
They are called kidneys. Milk clearly doesn't hurt.

Soem say? See above. Milk has lots of calcium.

Some say? References please.

What safer side? You have yet to demonstrate that milk is not good for you.

Jeff

trent duke

Hi Ken,

First, why do you drink so much?

A quart a day or 4 cups is okay giving you about 1000mg of calcium. If you
eat alot of other calcium products such as cheese or a supplement that
contains calcium, I would cut back a little on the milk. Any long term
consumption of calcium over 2000mg can develop problems. You and others can
go here to see a long list of other vitamins and minerals dosages @
http://1stholistic.com/Nutrition/hol_nutr-toxic-dosages.htm

Milk is not bad for you despite what many neo anti-milk zealots say.

Drink it!

Trent


-- Look and Feel Great! FREE weight loss and anti-aging group. Join now @
http://groups.yahoo.com/group/weightloss_health

jaym1212

The below from an old google post:

Lactose as an
epidemiological risk factor for CHD, independent of its saturated fat,
I cite the following references (4,5,6,7,8,9,10). There are numerous
animal experiments to show that added lactose increases the severity of
atherosclerosis in animal models (10,11,12,13). As I mentioned in my
original post, the most likely explanation for lactose's atherogenicity
is that high milk diets induce copper deficiencies (15,16) presumably
via high levels of lactose (10,14). Copper deficiencies in turn reduce
the levels of the bodies natural antioxidants such as the Cu-Zn form of
superoxide dismutase (13,14,17). Lowered levels of endogenous
antioxidants presumably increase the susceptibility of LDL to oxidation
and therefore increase the risk for CHD.

References

4. Segall JJ. Dietary lactose as a possible risk factor for
ischaemic heart disease: review of epidemiology. Int J Cardiol
1994;46:197-207.
5. Segall JJ. Lactose. In: Health Hazards of Milk. DLJ Freed
(Ed.). Bailliere Tindall, London, 1984,229-39.
6. Segall JJ. Hypothesis: is lactose a dietary risk factor for
ischaemic heart disease. Int J Epidemiol 1980;9:271-76.
7. Lember M et al. Lactose absorption and milk drinking habits in
Estonians with myocardial infarction. Brit Med J 1988;296:95-96.
8. Popham RE et al. Variation in mortality from ischemic heart
disease in relation to alcohol and milk consumption. Med Hypotheses
1983;12:321-29.
9. Pearce RJ. Correlation of coronary heart disease with milk
consumption: is protein or some other factor involved? Med Hypothesis
1984;14:259-63.
10. Strain JJ. Milk consumption, lactose and copper in the
aetiology of ischaemic heart disease. Med Hypotheses 1988;25:99-101.
11. Wells WW, Anderson SC. The increased severity of
atherosclerosis in rabbits on a lactose containing diet. J Nutr
1959;68:541-49.
12. Wostmann B et al. Effect of dietary lactose at levels
comparable to human consumption on cholesterol and bile acid metabolism
of conventional and germfree rats. J Nutr 1976;106:1782-90.
13. Carville DGM et al. The effect of copper deficiency on blood
antioxidant enzymes in rats fed sucrose or sucrose and lactose diets.
Nutr Rep Int 1989;39:25-33.
14. Lynch SM et al. Effects of copper deficiency on hepatic and
cardiac antioxidant enxyme activities in lactose and sucrose fed rats.
Brit J Nutr 1989;61:345-54.
15. Stemmer KL et al. Copper deficiency effects on the
cardiovascular system and lipid metabolism in the rat; the role of
dietary proteins and excessive zinc. Ann Nutr Metab 1985;29:332-47.
16. Fields M et al. Copper deficiency in rats: the effect of type
of dietary protein. J Am Coll Nutr 1993;12:303-06.
17. Lynch SM et al. Effects of skimmed milk powder, whey or casein
on tissue trace element status and antioxidant enzyme activities in rats
fed control and copper deficient diets. Nut Res 1990;10:449-60.

jaym1212

From an old post:

....autopsies done on 50 Masai men (milk drinking
populations) have revealed extensive atherosclerotic lesions in
coronary artery cross sections "which equaled that of old U.S. men"
(44). Thus, the earlier reports of freedom from atherosclerosis in
the Masai were shown to be incorrect.

44. Mann GV et al. Atherosclerosis in the Masai. Am J Epidemiology
1972;95:26-37.

jez

These folks don't seem to like milk much.......

http://www.notmilk.com/


--
Ho hum
Jez
"Few of us can easily surrender our belief that
society must somehow make sense. The thought
that the State has lost its mind and is punishing so
many innocent people is intolerable. And so the
evidence has to be internally denied."
- Arthur Miller

jaym1212

From an old post:

....Milk also contains significant quantities of xanthine oxidase(37)
which has been shown to enter the circulation (37,38). Because
xanthine oxidase is routinely used to induce LDL oxidation in vitro
(39), it may be that part of milk's pro atherogenic effect stems from
its ability to increase LDL oxidation. Alternatively, there is
increasing recognition of the involvement of the immune system in
atherosclerosis, and there is now substantial evidence to indicate the
presence of activated macrophages and T-lymphocyte in human arterial
fatty streaks indicating a cell mediated immune response (40). In
milk drinking populations, human sera has been shown to exhibit
extraordinarily high concentrations (20 to 100 times higher than for
other autoantibodies) of IgG antibodies to xanthine oxidase which are
specifically directed against the xanthine oxidase antigen present in
endothelial cells of capillaries and arterioles (41). Specificity
for xanthine oxidase has been demonstrated by immunoblotting in
capillary endothelium, and there is cross reactivity with the human
and bovine xanthine oxidase polypeptide (41). Further, IgA antibodies
to bovine xanthine oxidase are significantly elevated in patients with
severe atherosclerosis when compared to controls (42). It is quite
possible that the high titers of xanthine oxidase specific
auto-antibodies in human serum (41) are induced by bovine milk xanthine
oxidase that has been taken up with dairy products and which has
escaped digestion. Because the ba*****t membranes of arterial
endothelial cells may share epitopes with xanthine oxidase, the initial
lesion to the endothelial lining which is characteristic of the first
stage of atherosclerosis, likely occurs because of an immune response
directed against the bodies own tissues. The loss of self tolerance
occurs because there is molecular mimicry (similar amino acid
sequences) between bovine xanthine oxidase and proteins within the
endothelium. Activated T-lymphocytes therefore cannot distinguish
self from non self and cause continual damage to endothelial linings of
arterioles. The hypothesis that a cow milk protein may be involved
in an autoimmune response related to CHD is not new and Davies has


37. Deeth HC. Homogenized milk and atherosclerotic disease: A
review.=20
J. Dairy Sci 1983;66:1419-35.

38. Muscari A et al. Association of serum IgA antibodies to milk
antigens with severe atherosclerosis. Atherosclerosis 1989;77:251-56.

39. Napoli C et al. Human low density lipoproteins are peroxidized by
free radicals via chain reactions triggered by the superoxide radical.=20
Cardiologica 1991;36:527-32.

40. Munro JM et al. An immunolohistochemical ****ysis of human aortic
fatty streaks. Hum Pathol 1987;18:375-80.

41. Bruder G. et al. High concentrations of antibodies to xanthine
oxidase in human and animal sera. J Clin Invest. 1984;74:783-94.

42. Muscari A et al. Association of serum IgA antibodies to milk
antigens with severe atherosclerosis. Atherosclerosis 1989;77:251-56.

43. Davies DF et al. Antibodies to reconstituted dried cow's milk
protein in coronary heart disease. J Atherocler Res 1969;9:103-07.

jaym1212

Influence of type of carbohydrate on atherosclerosis in baboons fed
semipurified diets plus 0.1% cholesterol
D Kritchevsky, LM Davidson, HK Kim, DA Krendel, S Malhotra, D
Mendelsohn, JJ van der Watt, JP duPlessis and PA Winter

Five groups of six (three male, three female) baboons (Papio ursinus)
were maintained for 17 months on a semipurified diet containing 40%
carbohydrate, 25% casein, 13.9% coconut oil, 0.1% cholesterol, 15%
cellulose, 5% salt mix (USP XIV) and 1% vitamin mix. The carbohydrates
fed were: fructose, sucrose, starch, glucose, and lactose. A fifth
group was used as control and was fed bread, fruit, and vegetables.
Serum, liver, and tissue lipids were ****yzed at the end of the
feeding period as were cholesterol absorption (as 3H-cholesterol) and
synthesis (from 14C-mevalonic acid). Serum cholesterol and
beta-lipoprotein levels were elevated in all the test groups compared
to final control levels or to starting levels for all the baboons.
Average serum cholesterol levels of the test groups were not
significantly different. Liver lipids were elevated in all test groups
except that fed glucose. Baboons on the test diets absorbed more
exogenous cholesterol (3H) but biosynthesis of this sterol was not
inhibited. The ratio of biliary primary/secondary bile acids was below
normal levels only in the animals fed fructose and sucrose.
Cholesteryl ester fatty acid spectra of serum and liver reflected the
dietary fat. Fecal weight was 69% higher in lactose fed animals and
31% lower in sucrose fed animals than in the controls. The ratio of
endogenous or exogenous neutral/acid steroids was considerably lower
in the fructose-fed baboons than in the other animals. On this diet
average aortic sudanophilia (percentage of surface) was: fructose,
11.3; sucrose, 10.4; starch, 21.3; glucose, 17.2 lactose, 65.8; and
control, 1.4. Gross atheromatous lesions were seen in five of six
baboons fed lactose; three of six baboons fed fructose; two of six
baboons fed sucrose, and one of six baboons fed starch. In a second
experiment three groups of baboons were fed the control diet, the
semipurified diet in which the carbohydrate was lactose, and the
semipurified diet containing lactose plus 0.1% cholesterol for 8.5
months. Serum lipids were elevated in the two test groups but liver
lipids were not significantly different from control levels. Average
aortic sudanophilia (percentage of area) was: lactose, 2.2;
lactose-cholesterol, 20.8; and control, 0.3%. One of the six baboons
in the lactose-cholesterol group had visible atherosclerotic lesions.
These experiments represent the first successful attempt to produce
severe atherosclerosis in baboons by dietary means alone.


My Note: Coconut oil which is highly saturated didn't seem to be a
significant factor in creating atherosclerosis.