Anything on Creutzfeldt-Jakob Disease
betty at noel.pd.org
Tue Aug 15 19:58:15 EST 1995
You say just because the dwarfs in the 1950's got bovine growth hormine
injections (bovine=cow) and the dwarfs got a "cow" disease, how do we
know they got Creutzfeldt-Jakob Disease from this? Isn't that sort of
like saying you don't get rose petals from roses?
As to the references I'll be glad to go over them. The insulin growth
factor is the regulator of cancer! Milk is an enzyme inhibitor and
hormones survive digestion.
The most recent research would tend to support the dramatic role that IGF
plays in cellular growth. Kleinman report that IGF-I is found to be
involved in the growth regulation of endometrial tumor cells and is 30
fold more potent than insulin, suggesting the effects of these growth
factors are mediated by the IGF-I receptor. D-Errico notes that results
obtained using molecular biology techniques suggest a possible role for
insulin-like growth factor II (IGF-II) in the pathogenesis of
hepatocellular carcinoma (HCC). Kwok has found that the biological
effects of IGF-I are initiated by its binding to the IGF-I receptor,
which is able to transduce mitogenic and metabolic signals, supporting
the hypothesis that the IGF-I receptor is involved in the development of
diabetic vascular complications. Wimalasena found IGF-I to increase cell
growth, and a maximal effect of 3-5 fold increase in cell number was
There is evidence that IGF functions on a nanomolecular level. MCF-7
cancer cells proliferate in response to nanomolar concentrations of IGF-I
and IGF-II. De-Leon reported that the actions of both peptides are
mediated through the IGF-I receptor concluding that IGF-I and IGF-II are
potent mitogens in MCF-7 cells and can stimulate cell proliferation
through all three receptors. Martin reports that IGF-II stimulates cell
proliferation via the type I IGF receptor. The type I IGF receptor
mediates IGF-II induced autocrine neuroblastoma cell growth.
Ambrose observed that the interaction of insulin-like growth factors with
the IGF-I receptor is an important step in the control of cell
proliferation and development. In particular, IGF-I and IGF-II are key
regulators of central nervous sytem development and may modulate the
growth of glital tumors. Nielsen noted that the transcription of IGF-II
genes lead to the production of significant amounts of IGF-II which
stimulate the proliferation of MSRCT (cancerous growths) by interaction
with IGF-I receptors on the cells.
FDA, based upon Monsanto's research, continues to proclaim that IGF in
milk has no effect on human metabolism. IGF-I is a mitogenic growth
factor. Prager found rat cells responding so in vitro IGF-I treatment by
increased proliferation and DNA synthesis. Tumor cell assays confirmed
continued expression of IGF-I receptors. Raile observed similar
effects. Insulin-like growth factor I and II were implicated in the
growth promotion of in vivo tumors and tumor cells in vitro. Tumor cells
responded to an addition of exogenous insulin growth factor with an
increase of DNA synthesis.
Langford found that IGF-I has multiple metabolic actions and effects on
the differentiation and proliferation of a wide variety of cell types.
IGF-I and II have been identified as autocrine and endocrine growth
regulators which accelerate various types of carcinomas. IGF-I is
considered to play an important role in the proliferation of pancreatic
cancer cells, according to Gillespie.
Glick noted that IGFs play an important role in the regulation and
glucose metabolism in CNS tumors.
It was reported by Atig that insulin-like growth factor II is associated
with human primary colorectal tumors and colincarcinoma cell lines.
Yashiro found IGF-bp activity was significantly higher in cancer
extracts, suggesting that higher IGF-bp activity in cancer tissue is
involved in regulating growth of thyroid papillary carcinoma cells.
Robbins (Genentech, Inc.) found IGF-I increased lymphocyte numbers in all
of the peripheral lymphoid organs examined. This increase had functional
significance, and Robbins concluded that IGF-I produced locally by thymic
and bone marrow cells may be a natural component of B and T cell
Yun demonstrated that IGF transcripts were 32-64 fold more abundant in
Wilms tumors than in the adjacent uninvolved kidneys. IGF-II is
suggested as playing a role in transforming growth factor in Wilms
Minniti concluded that insulin-like growth factor II (IGF-II) acts as an
autocrine growth and motility factor in human rhabdomyosarcoma cell
lines. Analyses of tumor biopsy specimens demonstrate high levels of
IGF-II mRNA expression. All tumor specimens examined expressed the gene
for IGF-II, and this expression was localized to the tumor cells and not
to surrounding stroma. These data suggest that the IGF-II autocrine loop
may be operating not only in vitro but also in vivo.
Developing osteogenic sarcoma were researched by Kappel who wrote that
this type of cancer is the most common bone tumor of childhood and
typically occurs during adolescent growth spurts when growth hormone and
insulin-like growth factor-I (IGF-I) may be at their highest lifetime
levels. He noted that human osteogenic sarcoma cell lines are dependent
on signaling through IGF-I receptors for invitro survival and
proliferation. Furthermore, they suggest modulation of the growth
hormone IGF-I axis may affect the growth of these tumors in vivo.
Lippman, as early as 1991, had implicated IGF-I as being critically
involved in the aberrant growth of human breast cancer cells.
Lee observed the processing of insulin-like growth factor by human breast
tissue and commented:
"This indicates, for the first time, that oestrogen regulation of IGF-I
peptide in breast cancer cells would support the hypothesis that IGF-II
has an autocrine regulatory function in breast cancer.
Chen notes that IGFs are potent mitogens for malignant cell proliferation
in the human breast carcinoma cell line.
Figueroa confirmed that insulin-like growth factors (IGFs) are potent
mitogens for breast cancer cells and their activity is modulated by high
affinity binding proteins.
Li treated breast cancer cells (MCF-7) with IGF-I and observed a 10-fold
increase in mRNA levels of cancer cells and concluded that IGF-I
modulation of gene expression appears to be an important step in cellular
proliferation. Krasnick furnishes another clue to this puzzle by
revealing that IGF-I may have a role in the regulation of human ovarian
cancer. His data support a role for IGF-I in proliferation of ovarian
cancer and suggests that IGF-I and estradiol interact in a synergistic
manner and regulate this malignancy.
Musgrove states that growth factors play a major role in the control of
human breast cancer cell proliferation.
Here's your missing link:
On November 8, 1994 the New York Times published a story written by Gina
Kolata which revealed:
1. There is good reason to believe that many very early cancers never
become clinically significant.
2. Although 1% of women between the ages of 40 and 50 are diagnosed with
breast cancer, autopsy studies reveal that 39% of women in that age group
have tumors in their breasts.
3. Forty-six percent of men between the age of 60 and seventy have
prostate cancer although only 1% are clinically diagnosed.
4. Virtually all people over 50 have thyroid tumors.
5. Cancerous tumors are the ones that have somehow thrown off the
usually tight genetic controls on unwanted divison and growth. (Remember
the match I mentioned?!)
The FDA now has information indicating that data was manipaulated and
withheld from peer review. In addition, new information has surfaced
indicating that the product which was approved for use after many years
of testing is not the smae product that is now being used. (Remember the
freak amino acid - epsilon-N-acetyllysine - in place of lysine in the
Armed with the knowledge that virtually all humans hae tumors waiting to
proliferate, and milk hormones (IGFs) cause proliferation of cancer, and
that treatment of cows with recombinant bovine growth hormone causes an
increase in IGF levels in milk, it is now time for science, industry and
the FDA to re-investigate and re-evaluate this controversy.
Consumer's Union says the government bought up 9 billion lbs of surplus
milk and spent $2 billion to kill 1.5 million cows. Obviously, we don't
need a hormone to produce more milk - and one that has an increase in IGF
that will trigger the spread of cancer is very unwelcome. With spleens
in lab animals increased up to 46% you know this will cause a
According to Sciene News in 1988 when human growth hormone was given to
dwarfs some got leukemia.
Monsanto doesn't want it labeled because consumers won't buy it. That's
why in 10 or 11 major cities of the U.S. on Thursday there will be
protests sponsed by PURE FOODS in Washington. The one in Atlanta is in
cooperation with Mission Possible and includes aspartame, another
Monsanto monster. (10:30 A.M., Thursday, August 17 in front of Return to
Eden, Cheshire Square Shopping Center at Cheshire Bridge and LaVista).
Robert Cohen who has done this research is trying to stop this insanity
and save our children who are drinking this milk.
I hope this further information is helpful. I know that scientists are
only interested in peer review journals but many times data is compromised.
It certainly is in this case. This post is already too long or I would
quote the letter Robert Cohen sent today to the FDA. He did meet with
them on April 21 and they did admit that the IGF increases in milk and
that IGF bypasses digestion and is absorbed intact by the intestinal
lumen. They just didn't like that we made their comments public!
Regards Betty OPERATION MISSION POSSIBLE
Domain: betty at pd.org
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