Anything on Creutzfeldt-Jakob Disease

Betty Martini betty at noel.pd.org
Tue Aug 15 19:58:15 EST 1995


Dear Andy:

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 
observed.

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 
lymphopoiesis.

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 
tumorigenesis.

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 
peptide chain?!)

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 
pre-leukemic condition.  

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  


Betty Martini
Domain:  betty at pd.org
UUCP:  ...!emory!pd.org!betty




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