My Photo
Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Sunday, December 18, 2011

A blood test for variant Creutzfeldt‐Jakob disease: briefing note for patients, carers and health professionals

A blood test for variant Creutzfeldt‐Jakob disease: briefing note for patients, carers and health professionals

A blood test for variant Creutzfeldt‐Jakob disease (vCJD) has been an important goal of medical research laboratories and companies around the world for many years. It has been very difficult to achieve because the infectious agent (germ) causing vCJD, known as a prion, has unique features that mean that the sensitive methods doctors normally use to detect the presence of a germ (detecting the body’s antibody response to the germ or the germ’s own genetic material) do not work.

The Medical Research Council (MRC) Prion Unit, working with the NHS National Prion Clinic at the National Hospital for Neurology and Neurosurgery (NHNN) in London, has now developed an entirely new type of test following a number of years of intensive research.

The test is at an early (prototype) stage but is able to correctly identify the large majority of patients with symptoms of vCJD and has not yet given any false results in patients with other brain diseases or in healthy individuals. We think this is an important breakthrough and it raises a number of issues which need to be carefully considered. Details of the test have been published by the leading medical journal, the Lancet, on 3rd February 2011. The full text of the paper is available here.

This brief article describes CJD and other so‐called prion diseases, why a blood test is important, how the test works and how to approach us at the National Prion Clinic to inquire further about this test. It is important to be cautious about this news, because although the results so far are very encouraging, we want to go on to look at blood samples from much larger numbers of healthy people and those with other brain diseases to get a better idea of how specific the test is in practice. This will be vital before a version of this test could be considered to routinely screen healthy blood donors.

What are prion diseases? Also known as transmissible spongiform encephalopathies, prion diseases are a group of rare fatal conditions affecting the brain. Prion diseases are caused by one of the body’s normal proteins, called the prion protein, changing its shape and forming clumps of protein in the brain. This process damages and eventually kills brain cells. In humans, there are three different ways these diseases can start. The commonest form is called sporadic CJD and this form is seen all over the world and appears to occur at random as an unlucky event when the production of prions in the brain is triggered spontaneously. Secondly, the disease can be passed down from generation to generation as a genetic condition in some families with a faulty prion protein gene. Thirdly, and most importantly from the point of view of this new test, someone can “catch” a prion infection by being exposed to infectious prions.

These illnesses affect both animals and humans. The animal prion diseases include scrapie, a common prion disease affecting sheep and goats which is not thought to pose a threat to human health and bovine spongiform encephalopathy (BSE or mad cow disease) in cattle which can jump species to infect humans. BSE prions are responsible for variant CJD which was first recognised in 1996 and which has so far affected about 200 people, most from the UK. It is thought that people become infected by BSE prions by eating food containing material from BSE‐infected cattle, although other sources of exposure are possible. Much of the UK population born before 1996 (when rigorous measures to limit exposure were enforced) have potentially been exposed to BSE‐contaminated food and the number of people who may carry the infection but remain healthy is unknown.

Why is a blood test important? vCJD (as with other forms of CJD) tends to be diagnosed only when the patient has had the disease for some time and has developed symptoms that are associated with extensive damage to the brain. There are several reasons why this is the case. The early symptoms of the disease (such as anxiety, depression and tingling pains in the legs) have many much more common causes and so doctors will understandably not attribute these symptoms to something much more serious until other features such as difficulty with movement or balance and loss of mental abilities occur. At this stage, it will be apparent there is a serious brain condition but a series of tests are required to make the diagnosis and these take time to organise and interpret. Because the disease itself typically progresses quite rapidly (over weeks and months), the patient is likely to be showing quite advanced symptoms by the time a confident diagnosis is reached. A simple blood test gives us an opportunity to make the diagnosis at a much earlier stage. While at present there is no treatment we know is effective in stopping progression of these diseases, an early diagnosis does avoid the need for other tests and gives the patient and their family a clear answer. This enables them to make the best use of their time together and spend less of this precious time in hospital. However, experimental drugs are being developed at the MRC Prion Unit and elsewhere with a view to clinical trials in the next few years and we would want to try such treatments at the earliest stage before irreversible brain damage has occurred.

It is now known that vCJD can be passed on by blood transfusion. Several vCJD patients had been blood donors before they developed symptoms of the disease. To date, three individuals who had received blood transfusions from such donors have themselves developed and died from the disease. A further individual, who had also received prion‐infected blood, died of unrelated causes but showed evidence of prion infection at autopsy examination.

Only a very small number of individuals are definitely known to have received such potentially infected blood transfusions. However, several thousand individuals have been notified by the Health Protection Agency that they have received possibly infected blood products such as plasma, clotting factors, or purified antibodies. One individual who had received a clotting factor from a donor who went on to get vCJD died of unrelated causes but showed signs of vCJD infection at autopsy. It is not known whether this individual would have gone on to develop the disease had he not died of other causes.

Prion diseases are known to exist in “carrier states” in laboratory animals and these would be expected in humans too. A “carrier” is a person infected with prions but who does not show any signs of disease in their natural lifetime. Such carrier states are well recognised with other infectious diseases in humans. In the UK population, following an anonymous study of archived tissue specimens, the Department of Health uses an estimate that 1 in 4000 individuals may be silently infected with vCJD prions in its risk calculations. There is considerable uncertainty about this figure, that is, the true number could be significantly higher or lower than 1 in 4000. It is also not known how many of those infected will eventually go on to develop the disease itself. We do know that incubation periods in human prion diseases can be very long, over 50 years in some cases. As these infected but healthy individuals cannot currently be identified in the population, many will be active blood donors and could pass on infection to other people in this way or by medical and surgical instruments used on them becoming contaminated by prions (since prions are quite resistant to normal sterilisation methods). The National Blood Service has taken several actions to try to minimise this risk, for example, by removing white cells from blood, however it is uncertain how effective these measures are at reducing risk, or indeed whether they are really justified should the real number of infected people turn out to be extremely small.

A future development of our blood test may allow us to screen donated blood and further increase the safety of blood transfusions. Also it may in the future allow individuals who have been exposed to vCJD infection to find out if there is evidence that the infection has taken hold in their body. However, considerable further research will need to be done first to find out how specific the test is when tested on large numbers of health donors and to understand how good the test will be at detecting infected blood from healthy individuals rather than those with the established disease.

How well does the test work? It has been hard to develop a test for prion disease because the body’s immune system does not fight off prion infection by making antibodies (that can be readily detected in a blood test) in the same way it does against germs like bacteria or viruses. It has been challenging to develop a test that can distinguish between the normal prion protein, which we all have in our blood, and the abnormal form linked to the disease which is chemically very similar.

Scientists in the MRC Prion Unit have developed a prototype test. This involves taking a small blood sample from a patient as with any other blood test. A small sample of blood is mixed with special metal beads to which the rogue prion proteins stick tightly. These are then washed to remove the normal prion protein and other blood components that would interfere with the test. Finally, the amount of rogue prion protein attached to the beads is measured using antibodies we have developed that bind very tightly to the prion protein.

The test was applied to a number patient samples including from patients with vCJD, those with sporadic CJD, other neurological diseases that might be confused with vCJD and a number of healthy blood donors. As vCJD is a rare disease, only relatively small numbers of samples were available for this testing. All samples were given code numbers and the scientists carrying out the test in our laboratory did not know which sample was which. We were able to try the test on 21 samples from different vCJD patients. 15 of these 21 patient samples (around 70%) were shown to be positive by the test. So far, all samples from other neurological diseases or healthy blood donors have tested negative but only relatively small numbers of these have been looked at so far (about 200). We are testing larger numbers of samples now. At present the test does not work in other forms of prion disease such as sporadic CJD but we are hoping this will be possible with further work in the future.

What happens now and how is the test going to be made available? We are ready to use the test to assist with diagnosis of patients who are suspected of having vCJD or other diseases that might be mistaken for vCJD. Working with neurological colleagues to begin to use the test will also help us get more information on the test itself and hopefully lead to further improvements and understanding of its usefulness. A request card needs to be completed which can be obtained here. We require at least 2 x 5ml EDTA vacutainer tubes. For sample delivery please see further details here. While we are working to increase the throughput of the test, at this stage it remains relatively labour intensive. Whilst we will attempt to return results at the earliest opportunity, clinicians should allow up to four weeks for results. Please call the Clinic for further details.

The National Prion Clinic at the National Hospital for Neurology is happy to take telephone enquiries about suspected prion disease patients. We are particularly interested in referrals of patients at an early stage of their illness when diagnosis is most difficult.

Please visit the NHS National Prion Clinic website for more details and telephone/email contact details.

hmmm, most all of the iatrogenic CJD cases have been sporadic type iCJD. only the 5 or so cases (documented) has been associated with blood transfusion from vCJD. seems it would be more important to find a blood test for the sporadic CJD types that pass it on via the friendly fire and or pass if forward mode. why is it the UK scientist can develop and implement a test for their vCJD cases, but yet it can’t be done for the sporadic CJD cases in North America and or the UK ?

from the iatrogenic aspect, and considering that 85%+ of all human TSE is of the sporadic CJD strains, and the potential of iatrogenic transmission there from, seems to me we should be testing for sporadic CJD, considering also now that science has linked atypical BSE and atypical Scrapie to the sporadic CJD in humans, and most likely some cases from CWD once science crawls along and finally admits..............oops, I mean proves it.

you know the rest of the story $$$


Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study

Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria

Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.

Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.

Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).

Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.

Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.

Saturday, September 5, 2009



Wednesday, June 29, 2011

TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products

Transmission of sporadic Creutzfeldt-Jakob disease by blood transfusion: risk factor or possible biases

Maria Puopolo, Anna Ladogana, Vito Vetrugno, Maurizio Pocchiari

Article first published online: 7 JAN 2011

DOI: 10.1111/j.1537-2995.2010.03004.x

© 2010 American Association of Blood Banks

BACKGROUND: The occurrence of transfusion transmissions of variant Creutzfeldt-Jakob disease (CJD) cases has reawakened attention to the possible similar risk posed by other forms of CJD.

STUDY DESIGN AND METHODS: CJD with a definite or probable diagnosis (sporadic CJD, n = 741; genetic CJD, n = 175) and no-CJD patients with definite alternative diagnosis (n = 482) with available blood transfusion history were included in the study. The risk of exposure to blood transfusion occurring more than 10 years before disease onset and for some possible confounding factors was evaluated by calculating crude odds ratios (ORs). Variables with significant ORs in univariate analyses were included in multivariate logistic regression analyses.

RESULTS: In the univariate model, blood transfusion occurring more than 10 years before clinical onset is 4.1-fold more frequent in sporadic CJD than in other neurologic disorders. This significance is lost when the 10-year lag time was not considered. Multivariate analyses show that the risk of developing sporadic CJD after transfusion increases (OR, 5.05) after adjusting for possible confounding factors. Analysis conducted on patients with genetic CJD did not reveal any significant risk factor associated with transfusion.

CONCLUSION: This is the first case-control study showing a significant risk of transfusion occurring more than 10 years before clinical onset in sporadic CJD patients. It remains questionable whether the significance of these data is biologically plausible or the consequence of biases in the design of the study, but they counterbalance previous epidemiologic negative reports that might have overestimated the assessment of blood safety in sporadic CJD.;jsessionid=656FB07EE4507FB2632BA3E691D3B824.d03t02

Wednesday, March 2, 2011

Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript

Posted: 3/2/2011 Posted: 3/2/2011

Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

Thursday, July 21, 2011

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

August 2011 - Volume 70 - Issue 8 - pp 698-702

Wednesday, August 24, 2011

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

Wednesday, August 24, 2011

There Is No Safe Dose of Prions

Saturday, December 3, 2011

Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies

Volume 17, Number 12—December 2011

Friday, December 16, 2011

Creutzfeldt-Jacob Disease Question Asked by Lord Walton of Detchant P-Capt filter

Wednesday, May 11, 2011 House of Commons CJD May 2011 UPDATE

Monday, December 12, 2011

Second iatrogenic CJD case confirmed Korea

Thursday, December 08, 2011

A case of Iatrogenic Creutzfeldt Jakob Disease (iCJD) in a patient who had received a German-manufactured human dura mater graft 23 years ago

Saturday, November 19, 2011

Novel Prion Protein in BSE-affected Cattle, Switzerland

Saturday, December 3, 2011

Isolation of Prion with BSE Properties from Farmed Goat

Volume 17, Number 12—December 2011

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...


When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

2011 Monday, September 26, 2011

L-BSE BASE prion and atypical sporadic CJD

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ; Monday, October 10, 2011 EFSA Journal 2011 The European Response to BSE: A Success Story snip... EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential. snip...

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)

Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)

Saturday, March 5, 2011


Tuesday, November 01, 2011

Could we face the return of CJD? Experts fear it may lie dormant in thousands

Tuesday, November 08, 2011

Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011

Original Paper

Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.

Thursday, August 12, 2010

USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010

Sunday, August 01, 2010

Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010

Saturday, August 13, 2011

Sensitive detection of prion proteins in blood

Friday, July 8, 2011

Blood Test Could Quickly Detect Prion Diseases

Prion Diseases

Monday, February 7, 2011

FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

Tuesday, September 14, 2010

Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)

Saturday, October 24, 2009

SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs 2nd Public Meeting 27 October 2009


Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

Sunday, July 27, 2008

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

-------- Original Message --------

Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

Date: Sun, 11 Jul 2004 21:34:22 –0500

From: "Terry S. Singeltary Sr."

To: CC:,

Response to Public Comments

on the

Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005


The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:

Suppressed peer review of Harvard study October 31, 2002.

October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024

Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Thursday, April 09, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed

Greetings FDA et al,

I kindly wish to comment on the following ;

[Docket No. FDA-2002-N-0031] (formerly Docket No. 2002N-0273) RIN 0910-AF46

[Federal Register: April 9, 2009 (Volume 74, Number 67)] [Proposed Rules] [Page 16160-16161] From the Federal Register Online via GPO Access [] [DOCID:fr09ap09-18]

Owens, Julie

From: Terry S. Singeltary Sr. []

Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006

Greetings FSIS, I would kindly like to comment on the following ;



Terry S. Singeltary

From: Terry S. Singeltary Sr. []

Sent: Thursday, September 08, 2005 6:17 PM


Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.

who will watch our children for CJD for the next 5+ decades ???

WAS your child exposed to mad cow disease via the NSLP ???



you can check and see here ;

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305

Comment Number: EC –254

Accepted - Volume 11

Sources: World Trade Atlas What is the level of passenger traffic arriving in the United States from the affected country? Approximately 185,000 direct flights from Greece arrived to US airports in fiscal year 2000. Also, an unknown number of passengers from Greece arrived via indirect flights. Under APHIS-PPQ's agriculture quarantine inspection monitoring, 584 air passengers from Greece were sampled for items of agricultural interest in fiscal year 2000. Of these passengers, 14 carried meat (non-pork) items that could potentially transmit pathogens that cause BSE; most passengers carried from one to two kilograms (kg) of meat, although one passenger in November 1999 carried 23 kg of meat in a suitcase. Florida, Massachusetts, and New York were the reported destinations of these passengers. None of the passengers with meat items reported plans to visit or work on a ranch or farm while in the US. Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

Greetings list members, i just cannot accept this;

> 23 kg of meat in a suitcase (suitcase bomb...TSS)

> The data do not provide a species of origin code for these

> products, therefore they may not contain any ruminant product.

what kind of statement is this? how stupid do they think we are? it could also very well mean that _all_ of it was ruminant based products !

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a

Comment Number: EC –2

Accepted - Volume 7

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7


what did Paul Brown say about this previously;

i bring your attention to (page 500) Dr. Paul Brown statements;

253 1 DR. BOLTON: I have an additional question about 2 that. What is the assurance that additional locally sourced 3 tracheas are not added into that manufacturing process, thus 4 boosting the yield, if you will, but being returned to the 5 U.S. as being produced from U.S.-sourced raw material? 6 DR. McCURDY: Are there data to indicate how many 7 grams, or whatever, of infected brain are likely to infect 8 an organism, either animal or man, when taken orally? 9 DR. BROWN: If I am not mistaken, and I can be 10 corrected, I think a half a gram is enough in a cow, orally; [FULL TEXT ABOUT 600 PAGES] 3681t2.rtf


Unregulated "foods" such as 'nutritional supplements' containing various extracts from ruminants, whether imported or derived from 3 US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or at least very seriously regulated.

(neighbors Mom, whom also died from CJD, had been taking bovine based supplement, which contained brain, eye, and many other bovine/ovine tissues for years, 'IPLEX').

my plight with metabolife and there 'bovine complex' about risk factors of TSE in there product ;

Terry S. Singeltary Sr. wrote:

######## Bovine Spongiform Encephalopathy #########

1. Dietary Supplements: Review of Health-Related Call Records for > Users of Metabolife 356. GAO-03-494, March 31.

-------- Original Message --------


Date: Thu, 01 May 2003 11:23:01 –0500

From: "Terry S. Singeltary Sr."

To: NelliganJ at

The General Accounting Office (GAO) today released the following reports > and testimonies:


1. Dietary Supplements: Review of Health-Related Call Records for > Users of Metabolife 356. GAO-03-494, March 31.


> i was suprised that i did not see any listing of bovine tissue in metabolife > on it's label. have they ceased using these desiccated tissues???

> > i see that the lable on this product METABOLIFE 356, > does not state that it has any tissues of desiccated bovine organs? i no the product use to, so i am curious if they have

> ceased the use of the tissues of cattle they _use_ to use (see below)???





> > i tried warning them years ago of this potential threat of CJD/TSEs;

> > From: Randy Smith

> To: "'flounder at'"

> Subject: Metabolife

> Date: Mon, 7 Dec 1998 14:21:35 –0800

> > Dear Sir,

> > We are looking at reformulation. I agree that slow virus diseases > present a problem in some areas of the world.

> > Our product uses healthy USDA inspected cattle for the glandular > extract.

> > If you have any links to more information on this subject I would like > to examine them.

> > Thank you for your interest and concern,

> > Dr. Smith

> ============

> > From: Randy Smith

> To: "'flounder at'"

> Subject: RE: [Fwd: Your submission to the Inquiry]

> Date: Wed, 9 Dec 1998 10:37:07 –0800

> > Terry,

> > Thank you for your note and the information links you forwarded to me. > I am new to Metabolife International, however hopefully as my role here > enlarges I well have a greater impact on formulation and product > development.

> > Metabolife International does believe in placing safety first. And I am > going to do my best to see that we continue to do so.

> > Sincerely,

> Dr. Smith

> ============

> -----Original Message-----

> From: Terry S. Singeltary Sr. [mailto:flounder at]

> Sent: Wednesday, December 09, 1998 5:49 PM

> To: rsmith at

> Subject: [Fwd: Your submission to the Inquiry]

> > Dr. Smith, I am truly impressed with you honesty, THANKS.....I am not > just spouting off about the potential dangers, here. THEY ARE REAL.....I > have forwarded an e-mail from the BSE Inquiry, in which I made a > statement about them........You might want to go to the site and read > through it........IT WILL TAKE A WHILE........ THINGS ARE HAPPENING HERE > SIR, THAT YOU ARE NOT AWARE OF, AND AS MOST PEOPLE ARE > NOT...............I JUST HOPE, THAT THE REFORMULATION YOU SPEAK OF, IS > IN FACT GOING TO TAKE PLACE.

> The Department of Health, here in the U.S., is also worried about the > potential dangers involved hear............Terry/MADSON

> ================================================== =======

> From: Randy Smith

> To: "'flounder at'"


> Date: Fri, 18 Dec 1998 09:55:17 –0800

> Return-Receipt-To: Randy Smith

> > Thanks very much for the info. I appreciate all these articles I can > get. It does sound very familiar - just follow the green ($) trail.

> > -----Original Message-----

> From: Terry S. Singeltary Sr. [mailto:flounder at]

> Sent: Friday, December 18, 1998 5:15 PM

> To: rsmith at


> > Randy, thought you might be interested in this...............MADSON!!!!!1

> > snip...

> ===============================

> Sender: "Patricia Cantos"

> To: "Terry S Singeltary Sr. (E-mail)"

> Subject: Your submission to the Inquiry

> Date: Fri, 3 Jul 1998 10:10:05 +0100

> > 3 July 1998

> Mr Terry S Singeltary Sr.

> E-Mail: Flounder at

> Ref: E2979

> > Dear Mr Singeltary,

> > Thank you for your E-mail message of the 30th of June 1998 providing the > Inquiry with your further comments. Thank you for offering to provide the > Inquiry with any test results on the nutritional supplements your > mother was taking before she died.

> > As requested I am sending you our general Information Pack and a copy of the > Chairman's letter. Please contact me if your system cannot read the attachments.

> > Regarding your question, the Inquiry is looking into many aspects of the > scientific evidence on BSE and nvCJD. I would refer you to the > transcripts > of evidence we have already heard which are found on our internet site at >

> > Could you please provide the Inquiry with a > copy of > the press article you refer to in your e-mail? If not an approximate date > for the article so that we can locate it? > In the meantime, thank you for you comments. Please do not hesitate to > contact me on 0171 261 8332 should you have any queries.

> > Yours sincerely

> Patricia Cantos

> Families Team Leader

> Attachments


> ==============

> -------- Original Message --------

> Subject: re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''

> Date: Thu, 01 May 2003 16:04:35 –0400

> From: "Marcia G Crosse"

> To:

> CC: "Charles W Davenport" , "Carolyn Feis Korman" > , "Martin Gahart" >

> Mr. Singletary,

> > We were informed by representatives of Metabolife, Inc. that Metabolife

> 356 was reformulated to remove bovine complex as an ingredient in the

> product, approximately September 2001. We did not independently verify

> the contents of the product.

> > Sincerely,

> Marcia Crosse

> Acting Director

> Health CarePublic Health and Science Issues

> U.S. General Accounting Office

> 441 G Street, N.W.

> Washington, D.C. 20548

> ===================

> > -------- Original Message --------


> Date: Thu, 01 May 2003 15:48:52 –0500

> From: "Terry S. Singeltary Sr."

> To: Marcia G Crosse

> CC: Charles W Davenport , Carolyn Feis Korman > , Martin Gahart > References: >

> THANK YOU! > > MIRACLES DO HAPPEN! ;-) > > now all we need to do is; >

> snip......

> > one small step for man, one giant leap for mankind ;-)

> > however; >

> ''We did not independently verify the contents of the product''

> > ???


> TSS >

Could you get mad cow from a pill ? Some doctors say a class of pills that promise smarts, energy, and sexual vitality may cause mad-cow disease.

The government isn't worried. Should you be?

June 1, 2001

Health Magazine

by Susan Freinkel


BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehörden sind lax.,1518,119306,00.html

From: Terry S. Singeltary Sr. []

Sent: Tuesday, July 29, 2003 1:03 PM

To: fdadockets@oc.fda.govCc:;; BSE-L

Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSIONTO DOCKET 2003N-0312]

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to load...TSS]

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2


Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;

Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7

Dockets Entered On October 2, 2003 Table of Contents, Docket #,Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. Vol #: 1, ...

Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...

Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

Freas, William

Terry S. Singeltary Sr. []

Monday, January 08,200l 3:03 PM


CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)

[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1

Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ...

Tuesday, February 8, 2011 U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001

Friday, December 16, 2011


FDA faulted over state inspections

Sunday, November 13, 2011

California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock




Post a Comment

Subscribe to Post Comments [Atom]

<< Home