Progesterone from Milk of Pregnant Cows and Disease

by Elisabeth Rieping

last update 2008-07-20

first written 2008-01-01

rev. by mr 10.11.2010

In the sixties the appearance of fetal proteins in cancer patients was already discovered (Abelev GI 1965) and described for Time table
liver cancer. Up to now fetal or embryonic proteins are described in many cancers and for many of them it is known that
they are produced under the influence of progesterone, which is the typical steroid hormone of pregnancy. This knowledge J Tatarinov discoverd alpha fetoprotein as an
obviously did not lead to a search for progesterone in patients with cancer, though most of them are outside the age of antigen of hepatomas and embryos described by
pregnancy or they are men or children. (Abelev GI 1965) in english

A hint to the origin of progesterone comes from the well known observation that many types of cancer, most prominent 1965 Phil Gold and Samuel O. Freedman
breast, prostate and colon cancer were extremely rare in peoples who did not use milk as food. These are especially the East discovered the Carcino Embryonic Antigen
Asians. Even Japanese who reach an age comparable or higher than those of Western industrialized countries did not get CEA and described that it is a fetal protein
much of these diseases before adopting the habit of using milk-based foods. expressed between the second and sixth month
of fetal life (Gold P 1965)

Why? At the end of pregnancy progesterone production ceases and subsequently milk production starts, one would assume
as a person with no knowledge and experience in dairying.

To think so is naive. For it is possible to gain milk during pregnancy also. And because it is possible, it is done by all dairy
farmers. About 70% of today’s produced milk comes from pregnant cows (Rollinger M 2004).This milk is mainly the Progesterone and disease, old text
origin of the ingested progesterone (Sato A 2006). Additionally to progesterone there are estrogenes in the same food
(Courant F 2008) which often act synergistically in induction of tumor promoting markers.

After eating foods like ice cream, cheese or butter a big increase in progesterone levels can be detected a day later in the
saliva (Goodson WH 2007). In rats it was shown that the mRNA, a precursor of IGF-1, a hormone linked to many kinds of Letter to Naomi Allen corresponding author of
tumors is produced in the liver of rats fed with casein instead of plant protein (Miura Y 1992). But not only rats, human the Epic study
breast cancer tissue starts to produce IGF-1 under the influence of progesterone (Milewicz T 2002).
We ingest it with dairy products like milk, cheese, butter or cream in cakes, sweets, drinks and so on and so it comes out
that children, not pregnant women and men produce fetal proteins. Especially for cancer patients progesterone is dangerous
because it is an immune modulation hormone which stops the immune reactions against the embryo. Natural killer cells
have progesterone receptors and the contact between progesterone and this receptors leads to apoptosis, the organized death
of the natural killer cells by a caspase mediated mechanism (Arrovito L 2008).

The same happens, if cancer cells - under the influence of progesterone - start to produce embryonic proteins stopping the
immune answer.

Embryonic Proteins are often called Tumor Markers

CA15-3

The tumor marker CA15-3 mostly used to follow breast cancer is an embryonic protein called MUC1. MUC1 is produced
under the influence of progesterone (McGuckin et al. 1998, Horne AW 2006) and protects the embryo (Braymann MJ
2007) by inhibiting cell lysis by natural killer cells (Zhang K 1997). In cancer patients it stops the immune reaction against
cancer cells and so the tumor is not disturbed in proliferation. CA15-3 is analysed also in other cancers but breast cancer,
for example prostate cancer, where it is better known as MUC1 (Li Y 2007). In Japan it is called Kl-6 and is used to
monitor non small cell lung cancer (Ishikawa N 2008) among others.

PIBF - The Proegesterone Induced Blocking Factor

The more recently discovered “Progesterone Induced Blocking Factor” PIBF, a tumor marker found not only in cancers but
also in leukemia cells, blocks the natural killer cells as well (Check JH 2007). Here, one finds a hint to the fetal or
embryonic origin by writing or reading the full name of the tumor marker. With other tumor markers it is similar, for
example CEA the often used tumor marker in colon cancer is the “Carcino-Embryonic Antigen”.

PIBF under physiologic conditions plays its role in pregnancy, changing the regulation of the immune response, which is
necessary to allow successful pregnancy (Canellada A 2008).
c-myc

Another protein, conventionally not called tumor marker but oncogene is c-myc. It also is more abundant in squamous cell
cervical cancer patients with high progesterone levels (Lindstrom AK 2007).

VEGF

Another fetal protein, the Vascular Endothelial Growth Factor VEGF, which is also produced progesterone dependent
(Mirkin S 2005, Hyder SM 2006) helps to acquire blood vessels in the tumor. Today we fight this in many diseases like
colon cancer with antibodies like Bevacizumab. But as these antibodies work only against one of the many progesterone
dependent proteins, the success is limited. The same VEGF associated process occurs during late diabetes where patients
suffer from aberrant vascularization of the retina resulting in blindness or aberrant vascularization of kidney tissue resulting
in the dependency on dialysis.

Of cause this process is not limited to diabetes or cancer patients which often do not live long enough to experience it. We
see the same process in the eye of otherwise healthy people. There it is called wet age-related macular degeneration or
macular edema and treated with a lot of VEGF directed antibodies (Tremolada G 2007). Other progesterone induced
proteins might provoke insulin resistance known as diabetes type 2, which we often see in breast cancer patients during
disease progression. The today produced milk is so rich in progesterone that it induces insulin resistance, hyperglycemia
and glucosuria in calves (Hostettler-Allen RL 1994), which today therefore have to be fed by milk replacer, because the
milk of their mothers causes disease. In the pregnant women this change in metabolism may be necessary to keep the
glucose in the blood in favor of the fetus. But, maybe, even for the pregnant women the additional progesterone from food
is deleterious. Many women on Western diet develop gestational diabetes and keep it after pregnancy.

To find the diseases which might be involved one should look for progesterone dependent proteins. One easily finds VEGF
in the medulloblastoma of children, of cause in breast cancer, in colon cancer, where anti-VEGF antibodies are approved
for treatment and there is a wide array of other diseases. For example in the skin of persons with atopic disease there is a
25-fold increase in VEGF (Zhang Y 2006).

Osteopontin
A further new discovered protein trying to make a career as a tumor marker for mesothelioma is osteopontin, progesterone
inducible too (Mo SX 2007, Qu X 2008). In lung cancer its expression is linked to disease progression (Guy SY 2007) and
in breast cancer to the lack of homone receptors (Wang X 2008). It seems to promote metastasis of mammary tumors
(Chakraborty G 2008) and it is associated with metastasis in renal cell carcinoma (Ramankulov A 2007).Like VEGF
osteopontin is not only elevated in cancer, but in diabetes type 2 (Belovici M 2007) where it is linked to calcification of
blood vessels. Prednisolone, an immun supressing medication, is probably competing for progesterone binding sites,
provides a certain relieve to osteopontin linked conditions like Erdheim-Chester disease (Taguchi T 2008).

uPA, MMP-2, MM-9

Elevated expression of osteopontin in higher grades of breast carcinoma correlates with enhanced expressions of several
oncogenic molecules like uPA, MMP-2 and -9 (Chakraborty G 2008) which can also be stimulated by progestins
(Carnevale RP 2007).

Right now uPA is tested as a marker for therapeutic decision making in breast cancer. Women bearing breast cancer with
low uPA are unlikely to develop metastasis are encouraged to skip adjuvant chemotherapy. It might be more interesting to
teach breast and other cancer patients to change their cancer phenotype to a favorable one by avoiding progesterone rich
uPA inducing foods.

Alkaline phosphatase

Alkaline phosphatase is mainly used as a tumormarker for prostate cancer. The effect of progesterone on progesterone
sensible cells can be measured (Zava DT 1998). During pregnancy bone alkaline phosphatase of the mother increases
(Hellmeyer L 2006). The same occurs in patients with rheumatic arthritis (Oelzner P 2007) and in cancer patients with bone
metastases (Lein M 2007).

TPS - tissue polypeptide-specific antigen

TPS also called cytokeratin-18 is a protein found in maternal serum during pregnancy (Protonotaiou E 2006) and used as a
tumor marker.

HLA-G

Similar to the trophoblast protecting the embryo, tumor-cells in vivo produce the progesterone inducible leucocyte antigen
HLA-G (Urosevic 2008). This HLA-G is a progesterone inducible protein (Yie SM 2006), not unlikely for a protein
important during pregnancy. In tumor-cell-lines growing in vitro HLA-G cannot be observed (Polakova K 2000) as the
culture medium does not contain progesterone.

The HLA-G gene has a unique progesterone responsive element PRE with homology to the RNA tumor virus PREs (Yie
SM 2006) some suspicious, some proven to induce human and animal tumors.

P-glycoprotein and breast cancer resistance protein

P-glcoprotein and breast cancer resistance protein protect cancer cells by making them resistant to exogenous poisons
administered during chemotherapy for cancer treatment. During embryonic development they perform this task in the
placenta (Mathias AA2005).

Transforming growth factor-beta 1

Transforming growth factor-beta 1 (TGF-beta-1) is released progesterone dependent (Kim MR 2005). Its production by
tumor cells kills dendritic cells in sentinel lymph nodes, draining breast cancers rendering the lymph nodes tolerant to
invading tumor cells (Ito M 2006). Elevated plasma TGF-beta1 levels correlate with decreased survival of metastatic breast
cancer patients (Ivanovic V 2006).

Proteins - Repressed by Progesterone - which are often inactiv in Tumor Cells

p53

A very interesting protein is p53. Generally it is not called a tumor marker, because it is often absent or not working in
tumor cells. It seems as if it is repressed in persons with high progesterone levels (Lindstrom AK 2007).

Heat shock protein 70

It is not the only protein negatively controlled during pregnancy. Heat shock protein 70 is diminished in pregnant women
(Molvarec A 2007 ). In breast cancer patients it was shown to be most diminished in those women who quickly succumb
their disease (Torronteguy C 2006).

Consumption of Milk Proteins and Cancer

In April 2008 the Epic study on milk protein consumption and development of prostate cancer was published (Allen NE
2008). It was done in many European countries. Data from 1142 520 men got analyzed. It could be shown that prostate
Cancer development increases 32% for every 35g of milk protein consumed.

Of cause, the researchers do not think that the protein itself is responsible for the development of cancer. They speculate
about which hormone of the milk might be to blame. But IGF-1 a suspicious candidate increasing in blood after milk
consumption will probably be destroyed in the stomach as proteins are in general. So the researchers cannot explain their
results. As professional physicians and epidemiologists they are not familiar with modern milk production which is
occurring mainly during the progesterone rich pregnancy of cows. Progesterone is not destroyed in the stomach and it
seems to induce IGF-1 (Queiroga FL 2008. So - IGF-1 a potent growth hormone - might be one more progesterone induced
protein.

What to do?

First of all it is necessary to avoid milk products and for many additionally progesterone rich eggs in the foodstuff. And of
cause the future milk should be produced outside of the pregnancy of cows. That should be possible and quickly
implemented and will improve on one hand the situation of seriously ill people and on the other of those still healthy who
later might suffer under milk-born progesterone contamination.

Studies are necessary, but as long, as there are none, one can act for one's own health. A patient for example, with breast
cancer will see a rapid decline in tumor markers like CA 15-3, a progesterone dependent protein which during pregnancy
protects the embryo from natural killer cells. If all milk products are kept away from food, this diet, also known as Jane A.
Plant Diet works, as long as cortisons are not used. For cortisones also protect the tumor cells (Mattern J 2007). This diet
works not only for breast cancer patients. For instance, more quickly declines CA-125, the marker for cancer of the ovary
(own experiences).

Discussion

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