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Understanding the scope of BSE danger

flounder

Well-known member
Understanding the scope of BSE danger
By Terry S. Singeltary, Sr.
Feb 11, 2007





IN reply to:

Latest Alberta BSE case leaves little doubt: Canada has a problem By R-CALF USA media release
Feb 10, 2007

Billings, Mont. - On Wednesday, the Canadian Food Inspection Agency (CFIA) announced yet another case of bovine spongiform encephalopathy (BSE) discovered in a "mature bull" in Alberta.

"Although Canadian headlines tend to say this is Canada's ninth case of BSE, it is important to note that this latest incident is actually the 10th case of BSE in native Canadian cattle, because the BSE-positive cow discovered in Washington state in December 2003 was imported into the U.S. from Canada," noted R-CALF USA Vice President and Region VI Director Max Thornsberry. "In addition to the 10 native Canadian cases, in December 1993, BE was discovered in a cow imported into Canada from England.

Thornsberry also is a veterinarian and chairs R-CALF USA's Animal Health Committee.

"This demonstrates just how ridiculous and premature it is for our government to be considering even further relaxations of our import standards that would allow into the U.S. imports of Canadian cattle older than 30 months (OTM) of age, as well as the government's intention to allow into the U.S. beef products from Canadian cattle of any age," Thornsberry continued. "OTM cattle in a BSE-affected country bear an inherently higher risk for the disease, so R-CALF calls for the immediate withdrawal of this proposed rule.

"Furthermore, in light of the clear ongoing problem with BSE in Canada, we question whether Canada meets the regulatory requirements of a so-called 'BSE Minimal Risk Region' under the regulations issued by USDA in January 2005 regarding imports of cattle and beef from countries affected by this disease," Thornsberry emphasized.

R-CALF USA currently has an appeal before the 9th U.S. Circuit Court of Appeals in litigation filed by cattle producers in January 2005, which challenges the regulations issued by USDA as arbitrary and capricious, and not based on what scientists actually know about BSE. If R-CALF USA is successful in court with this challenge against USDA, the agency will be forced to address the problem of BSE in Canadian cattle and reduce the chance of spreading the disease in the United States.

"Canada is still not doing sufficient BSE testing to ascertain the magnitude of its problem with this disease," added R-CALF USA Region II Director Randy Stevenson, who also co-chairs the R-CALF USA Marketing Committee. "Because we don't already have COOL (country-of-origin labeling), and because we are currently commingling Canadian cattle and beef with U.S. cattle and beef, this case will further complicate U.S. efforts to restore beef export markets lost since 2003."

"Additionally, Canada has not yet implemented improvements to its 1997 feed ban, which were announced in July 2006, despite the obvious and increasing evidence of the widespread exposure of Canadian cattle to this disease," said R-CALF USA Region VII Director Eric Nelson. "Canada has had four known cases of BSE born after the 1997 implementation of its original feed ban, three of which were known to have been born years later."

R-CALF USA (Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America) is a national, non-profit organization and is dedicated to ensuring the continued profitability and viability of the U.S. cattle industry. R-CALF USA represents thousands of U.S. cattle producers on both domestic and international trade and marketing issues. Members are located across 47 states and are primarily cow/calf operators, cattle backgrounders, and/or feedlot owners. R-CALF USA has more than 60 affiliate organizations and various main-street businesses are associate members. For more information, visit www.r-calfusa.com or, call 406-252-2516.

© Copyright 2002-2006 by North Texas e-News, llc




http://www.ntxe-news.com/artman/publish/article_40341.shtml



Understanding the scope of BSE danger

http://www.ntxe-news.com/artman/publish/article_40385.shtml

By Terry S. Singeltary, Sr.
Feb 11, 2007



This is like the pot calling the kettle black.

I agree with Dr. Thornsberry's assessment that Canada has a problem with BSE, the EFSA BSE GBR risk assessment says this. BUT what Dr. Thornsberry fails to tell you is that the USA has the same problem, the EFSA BSE GBR risk assessment says this, along with Mexico, that they are all BSE GBR III.

You see this is why the BSE MRR policy was brought forth. Commodities and Futures, and the legal trading of all strains of TSE (Transmissible Spongiform Encephalopthy) globally. THE BSE MRR policy, a legal tool that the OIE and the USDA (GW Bush) brought forth to legally get around the attempt to eradicate BSE globally i.e the BSE GBR's and the trade policy surrounded it. THEY knew the attempted BSE firewalls had failed terribly in the USA. THEY knew there were serious problems, and they did the 'end around', the BSE MRR policy.

IF not for the Honorable Phyllis Fong of the OIG, no other mad cow in the USA would have been documented but that Washington BSE cow back in Dec. of 2003. THIS has all been proven in hearings, testimony, and Dr. Paul Brown of the CDC has been highly critical of the USDA and Canadian Food Agency about this, along with Dr. Linda Detwiler and many others.

CJD in the USA has been on the rise also. THE UKBSEnvCJD mad cow hamburger food only theory, is a small part, of a much larger problem. The medical, surgical, and pharmaceutical industry plays a huge role in this. You may not hear much about it, but believe me, behind closed doors and at meetings, they have been concerned for years. sporadic Creutzfeldt Jakob Disease i.e. sporadic CJD, simply means CJD of unknown origin, and it has been on the rise in the USA over the years, and we have atypical strains that are being documented, with some being documented in the young. Its the undocumented ones I am worried about, the medical, surgical, and dental ramifications surrounding them, who they may have exposed?

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and Scrapie in the USA has run rampant for decades. We know that scrapie transmits to primates through their non-forced oral consumption. We know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. All of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. USA is still feeding cows to cows as late as 2006. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.

These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I lost my mother to the hvCJD. I do not pretend to have all the answers, but I do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting theit TSE-tainted products until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. All we are doing is the exact same thing the UK did with ther BSE mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing.

This BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. FOR R-Calf, or anyone else to pretend that Canada has a more serious problem with BSE than the USA, with the way cattle and feed has been transported back and forth over the years, with the way the USDA has stumbled, bumbled, and fumbled the football with BSE surveillance, fed bans, firewalls, and triple firewalls, testing protocols flawed, downer testing flawed, it was like they were doing everything they could NOT to find and document it. Even the SRM ban that Canada has will surpass that of the USA when it goes into effect this year in 2007. TO even suggest that Canada has a worse problem with BSE under the present circumstances is a hoot, one that should be taken with great suspicion.

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518


REFERENCE


18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.

snip...

64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

http://www.seac.gov.uk/minutes/95.pdf


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***
© Copyright 2002-2006 by North Texas e-News, llc



http://www.ntxe-news.com/artman/publish/article_40385.shtml



TSS
 

Kathy

Well-known member
Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.

Something very fishy here, flounder!

"...none of the BSE-inoculated mice appear to be infected after more than 2 years."

This statement goes against every experimental transmission study with BSE to humanized mice, in the past.

It shows that experimental transmission studies are not reliable.
 

flounder

Well-known member
1: J Infect Dis 1980 Aug;142(2):205-8



Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their


nonforced consumption of known infectious tissues.


The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract


TSS
 

Kathy

Well-known member
Monkey's are not "humanized - PrP expressing" mice!



Health Phys. 1983;44 Suppl 1:411-7.

Can information on the gastrointestinal absorption of actinide elements by neonatal rats, guinea pigs, dogs and swine be extrapolated to man?

Sullivan MF, Gorham LS.

Neonatal mammals that acquire passive immunity by absorbing immunoglobulins from mother's milk (colostrum), as well as species that develop immunity prenatally, absorb macromolecules from the gut. This permeability of the GI tract to large molecules also serves as a route of entry for actinides in quantities greatly in excess of adult absorption. Administration of 238Pu nitrate to piglets results in absorption that is 1000 times the adult value but neonatal dogs, guinea pigs and rats absorb only 100 times more 238Pu than adults. Neonatal pigs and rats retain as much as 60% of the dose in the gut mucosa for several days but dogs and guinea pigs retain much less. We have also found this difference in GI tract 238Pu retention to occur after inhalation, indicating that the gut is an important route of entry for actinides that are inhaled by neonates. Although retention of different gavaged actinides by suckling rats is within the same range (1-3%) we found retention by piglets to range between 35% for 233U and about 2% for 237Np, 244Cm and 241Am nitrate. Piglets that were gavaged with 238Pu nitrate retained 19% in the liver and carcass a week later. After one year, half of that still remained. Neonatal rats, on the other hand, retained 3% initially and only 0.1% at one year. While the GI tract of the human infant is probably not nearly as permeable to macromolecules as that of the swine, it is known to be more permeable to macromolecules than that of the adult human. If actinide absorption is also increased in the child, the retention of these elements would probably be more like that in swine than in rats, because of the greater similarity between man and swine in skeletal maturation, in retention of actinides in liver and their longer life span. These studies suggest a need for further information on neonatal absorption of actinides in a large animal species that has a developing GI function more similar to that of humans.

PMID: 6305879
 

flounder

Well-known member
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.

look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;


Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa



It is clear that the designing scientists must

also have shared Mr Bradley’s surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley’s answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradley’s surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf



2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml



Natural and experimental oral infection of nonhuman primates by BSE agents
PNAS Vol. 96, Issue 7, 4046-4051, March 30, 1999
full text for subscribers, single articles not purchasable.
http://www.pnas.org/cgi/content/full/96/7/4046

N–elle Bons, Nadine Mestre-Frances, Patrick Belli, FranÁoise Cathala, D. Carleton Gajdusek, and Paul Brown The work was funded by the Region Languedoc-Roussillon, the Ministry of National Education, Research and Technology, and the Mediterranean Association for the Study on Cerebral Aging.

The first author is a neurobiologist at the Ecole Pratique des Hautes Etudes, Laboratoire de Neuromorphologie Fonctionnelle, UniversitÈ Montpellier II, Montpellier,ÝFrance with 46 publications at Medline, 3 others of which concern TSE in primates [abstracts below] and 14 of which concern other amyloidoses in primates. Contact information is email: [email protected], Tel: (33) 04.67.52.40.08, Fax:(33) 04.67.63.33.27. [fluent in English]

The second author, Nadine Mestre-Frances, co-authored the group's 4 articles on primate TSE and 7 other papers on primate amyloidoses, and is apparently a post-doc in the lab the first author.

The third author, FranÁoise Cathala, has 60 publication on scrapie and familial CJD dating back to 1971, including 4 earlier concerning primates. In 1985, she dscribed a case of CJD in a 19-year old girl [Eur J Epidemiol 1985 Mar;1(1):42-7. In 1981], later 'transmission to primates of a CJD-like disease from two familial cases of Alzheimer disease' is discussed [Neurology 1981 Mar;31(3):323-5].

The fourth author, Patrick Belli, is affiliated with the Centre National d'Etudes Veterinaires et Alimentaires, Pathologie Bovine, Lyon,ÝFrance. He has 5 earlier TSE papers, including 2 on BSE, 2 on scrapie, 1 on the French zoo cheetah. The CNEVA Web site exists but is dysfunctional.

Gajdusek and Brown have well-known histories of research in this area.

Abstracts of earlier work on prion disease in French primates and zoo animals:

Spongiform encephalopathy in an imported cheetah in France.
Baron-T, Belli-P Madec-J-Y Moutou-F Vitaud-C Savey-M.
Vet Rec 1997 Sep 13;141(11):270-1 Spongiform encephalopathy iy in an imported cheetah in France.

Prion immunoreactivity in brain, tonsil, gastrointestinal epithelial cells, and blood and lymph vessels in lemurian zoo primates with spongiform encephalopathy.
C R Acad Sci III 1997 Dec;320(12):971-9
Bons N, Mestre-Frances N, Guiraud I, Charnay Y

We report on two animals of a non-human primate species Eulemur fulvus mayottensis, housed in the local zoo and fed over a number of years with a food containing cattle meat, that developed serious neurological symptoms associated with prion immunoreactivity in brain and various viscera. Microscopy of the brains showed neuronal vacuolation with patchy/perivacuolar immunolabelling with an abnormal isoform of prion protein (IR-PrP), an important characteristic of spongiform encephalopathy. For the first time, we report the presence in the same severely ill animals of IR-PrP in the gastrointestinal tract, detected by immunocytochemistry with mono- and polyclonal antibodies directed against various parts of the PrP.

Strong PrP labelling was observed in the epithelial cells lining the pharyngeal and gastrointestinal lumen. The tonsils and the walls of the lymph and blood vessels below the intestinal epithelium were also labelled. There were no such immunoreactions in healthy lemurians killed as controls, i.e. a younger congener of the same species housed under the same conditions, and others belonging to the smaller species Microcebus murinus, reared in the laboratory and never fed on commercial food products containing cattle meat. These results demonstrate a strong PrP accumulation in the brain, the gastrointestinal tract and underlying lymphoreticular structures in these primates living in a zoological park and suffering from a spongiform encephalopathy.

Spontaneous spongiform encephalopathy in a young adult rhesus monkey.
C R Acad Sci III 1996 Aug;319(8):733-6
Bons N, Mestre-Frances N, Charnay Y, Salmona M, Tagliavini F

This paper reports the occurrence of a spongiform encephalopathy (SE) in young adult monkeys housed in a zoological park. Three rhesus monkeys (Macaca mulatta) acquired from the same zoo and maintained on feed containing animal protein, developed a progressive neurological disorder with behavioural abnormalities and physical deterioration and died at the age of 10-year-old. Neuropathological examination of one of these animals revealed a spongiform encephalopathy similar to that observed in monkeys following experimental transmission of Creutzfeldt-Jakob disease (CJD). In particular, several brain regions exhibited vacuolation of nerve cell bodies and processes accompanied by astrogliosis. Immunohistochemical analysis showed prion protein (PrP) immunoreactivity at the periphery of vacuolated neurons. The spontaneous occurrence of a SE in these young monkeys might be related to consumption of protein of animal origin.



snip...





TSE in non-human primates
In non-human primates a naturally occurring TSE comparable to Creutzfeldt-Jakob disease (CJD) in humans has never been diagnosed. A large number of non-human primate species, however, is susceptible to experimental infection with various TSE strains. It was shown that Saimiri monkeys are highly susceptible to CJD infection; this species is therefore favoured in experimental studies on CJD.
A number of non-human primates in British, French and possibly other European zoos were exposed to BSE infectivity through primate feed that was produced in the UK with risk tissue such as brain and spinal cord. In some of these monkeys, a spongiform encephalopathy was diagnosed after several years of incubation, and strain typing confirmed the similarity with cattle BSE. In immunhistochemical examinations of a range of tissues of infected monkeys, detectable PrPSc accumulation was found in the brain, spinal cord, tonsils, various sections of the gut and gut-associated lymphatic tissues as well as in the spleen.

...TSS
 

bse-tester

Well-known member
Kathy wrote:

Something very fishy here, flounder!

"...none of the BSE-inoculated mice appear to be infected after more than 2 years."

This statement goes against every experimental transmission study with BSE to humanized mice, in the past.

It shows that experimental transmission studies are not reliable.

Kathy, all this means is that the "Base" mice incubation period was approximately 19 months and that the "bse-inoculated" mice incubation period did not go over 24 months. The study showed that the "Base" was a more virulent form of infection due to the shorter incubation period.

Nothing fishy here Kathy, just poor expression on the part of the original writer in the study.
 

Kathy

Well-known member
Yes, Mr. Bradley... The same guy who worked for MAFF, while he worked for ICI - the manufacturer of "Phosmet", the OP used in the government mandated warble eradication program that STARTED in 1982.

[note: the Gabriel Horne Report of the UK stated that no cattle that developed BSE were likely treated with Phosmet because the warble erad. program ENDED in 1982 - yes, Bradley is a word smith and puppet for the chemical companies, thanks for bringing him up again. The GHR is echoed by the Harvard Risk Assessment and the Canadian/Alberta TSE risk assessment. Nobody wants to correct this ERROR.

Note that studies of animals exposed to radionuclides shows that high levels of these products, including uranium, lead 210, polonium 210 can accumulate in the kidneys and bones. If animals are fed kidney and bones, regularly, who knows what will happen; but, we saw what happened to the ex-Russian spy in London. Seems his tea was a little "too hot" [210Po]

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Oh yah, the study by the Commission Energie L'Atomique et al. Maybe this was the study that Dr. Broxmeyer mentioned where-in Dr. Lasmezas found that 55%of the mice inoculated with BSE homogenized brain tissue, that also developed neurological symptoms, showed NO SIGNS OF PRIONS (PrPSc).

I see that the scare mongering tactics are increasing. I'm sure all these worries will have American cattle producers lining up at the store for their new electronic identification ear tags.

I don't know what the "foot and mouth" comment was about in the article you posted flounder [another thread]. We can't have a foot and mouth outbreak, we sent all our railway ties to the UK so they could burn their carcasses. You remember, the hundreds of thousand of cattle that were destroyed under their FM scare. None of them were tested for BSE.

Of course the origins of the Foot and Mouth were linked to a missing vial of the stuff from a secure government lab.

Bradley, also testified that there were no prions in the pancreas. Seems he was wrong there too. Diabetes increases are being linked to the usage of DU weapons (testing and war zones). Seems the DU alters the pancreas. Too much of a coincidence for me. This might explain why naturally derived insulin was yanked [even though alot of it came from pigs]. Metal contamination of these products, just like iatrogenic transmissio/contamination with growth hormone.
 
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