Tuesday, December 17, 2013

Alzheimer's Disease U.K. diagnosed by region in each of the last five years [179852]

Alzheimer's Disease U.K. diagnosed by region in each of the last five years. [179852]


Alzheimer's Disease

David Simpson: To ask the Secretary of State for Health how many people in each region of the UK were diagnosed with Alzheimer’s disease, by region in each of the last five years. [179852]

Norman Lamb: The number of people recorded on practice disease registers is available in the quality and outcomes framework (QOF), published by the Health and Social Care Information Centre (HSCIC). The number of diagnoses are not available but the number of people on the dementia register are available. This is a measure of prevalence rather than incidence.

QOF does not have any information specifically on Alzheimer’s disease and the HSCIC only has information for England.

The numbers on the dementia register in the last five years are given in the following tables. Information for 2008-09 to 2011-12 (table 1) is presented at strategic health authority level and for 2012-13, under the new NHS structure, at commissioning region level (table 2).

QOF registers are constructed to underpin indicators on quality of care, and they do not necessarily equate to prevalence as may be defined by epidemiologists. For example, prevalence figures based on QOF registers may differ from prevalence figures from other sources because of coding or definitional issues. It is difficult to interpret year-on-year changes in the size of QOF registers, for example, a gradual rise in patients on a QOF register could be due partly to epidemiological factors (such as an ageing population) or due partly to increased case finding.

Table 1: Number of patients on the QOF dementia register by strategic health authority in England, 2008-09 to 2011-12
  2008-09 2009-10 2010-11 2011-12
England 232,430 249,463 266,697 293,738
North East 13,198 14,034 15,014 16,568
North West 34,057 35,952 38,230 42,158
Yorkshire and the Humber 24,844 26,755 28,845 31,908
East Midlands 20,089 21,625 23,423 25,953
West Midlands 23,866 25,622 27,735 30,386
East of England 25,315 27,591 29,578 31,975
London 24,859 26,745 28,255 31,160
South East Coast 21,442 23,037 24,284 26,419
South Central 18,840 20,044 21,085 23,114

16 Dec 2013 : Column 516W

South West 25,920 28,058 30,248 34,097

Table 2: Number of patients on the QOF dementia register by commissioning region in England in 2012-13
England 318,669
North of England 98,768
Midlands and East of England 96,274
London 33,333
South of England 90,294
Source: Health and Social Care Information Centre.






Tuesday, November 26, 2013


Transmission of multiple system atrophy prions to transgenic mice





Tuesday, May 21, 2013

IS ALZHEIMER’S DISEASE A PRION DISEASE? the possible secondary transmission by blood transfusion are posed



Segarra C and Coste J

Etablissement Francais du Sang Pyr en ees-M editerran ee R&D TransDiag, Montpellier,


Alzheimer’s disease (AD) is the most common type of senile dementia, mainly affecting individuals over 65 years old. Disease manifestation is characterized by progressive impairment of memory and cognition, mainly produced by synaptic dysfunction and neuronal loss. This fatal neurodegenerative disease is a matter of great interest because since its first description in 1906 by the psychiatrist A. Alzheimer the AD cases doesn’t stop to increase and more than 90% of disease arise sporadically. Cerebral accumulation of misfofded protein aggregates composed of amyloid b (Ab) proteins and hyperphosphorylated tau protein have been associated to the disease. In the past decade, there has been renewed interest in the possibility that the proteins causing neurodegenerative disorders are all prions. Recently, the origin of the disease, described until now as linked to aging, was re-evaluated by S. Prusiner (Nobel Prize). In animal models he has shown that, when the neurodegenerative process had been started, it propagates over all the brain, by a prion-like mechanism – prion is the responsible agent of Transmissible Spongiform Encephalopathy (TSE) such as Creutzfeldt-Jacob Disease (CJD).

The misfolding and aggregation mechanisms and structural intermediates are very similar in both AD and TSE. The starting point would be a normal protein, PrPC (Cellular Prion) for TSE and APP (Amyloid Precursor Protein) for AD, which would be converted into pathological misfolded proteins (MFP): PrPSc (scrapie Prion) and Ab protein respectively. These MFP would be then implicated in a process of selfaggregation, leading to the formation of amyloid plaques in the brain. Moreover the mechanism of aggregation follows the same seeding-nucleation process.

Several studies in animal models had shown that:

1 For TSE, the PrPSc aggregates generated by this process were infectious.

2 Ab deposition can be induced by injection of AD brain extracts into animals which without exposure to this material will never develop brain alterations.

3 The transfusion of blood from mice with amyloid plaques in brain accelerates the neuro-degenerative phenomenon and the memory loss in two different models of healthy transgenic mice.

In conclusion, questions on the infectivity of Ab protein in Alzheimer’s disease and the possible secondary transmission by blood transfusion are posed.

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.


Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.


I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.


There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.



Wednesday, May 16, 2012

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Proposal ID: 29403

Subject: [BLOODCJD] Alzheimer's Association 2013 Alzheimer's Disease Facts and Figures Today, an American develops Alzheimer's disease every 68 seconds. In 2050, an American will develop the disease every 33 seconds.

An estimated 5.2 million Americans of all ages have Alzheimer's disease in 2013. This includes an estimated 5 million people age 65 and older and approximately 200,000 individuals younger than age 65 who have younger-onset Alzheimer's.

The number of Americans with Alzheimer's disease and other dementias will grow as the U.S. population age 65 and older continues to increase. By 2025, the number of people age 65 and older with Alzheimer's disease is estimated to reach 7.1 million—a 40 percent increase from the 5 million age 65 and older currently affected. By 2050, the number of people age 65 and older with Alzheimer's disease may nearly triple, from 5 million to a projected 13.8 million, barring the development of medical breakthroughs to prevent, slow or stop the disease.


Alzheimer's disease is the 6th leading cause of death in the United States overall and the 5th leading cause of death for those aged 65 and older. It is the only cause of death among the top 10 in America without a way to prevent it, cure it or even slow its progression. Deaths from Alzheimer's increased 68 percent between 2000 and 2010, while deaths from other major diseases, including the number one cause of death (heart disease), decreased.

While ambiguity about the underlying cause of death can make it difficult to determine how many people die from Alzheimer's, there are no survivors. If you do not die from Alzheimer's disease, you die with it. One in every three seniors dies with Alzheimer's or another dementia.

Impact on Caregivers

In 2012, 15.4 million family and friends provided 17.5 billion hours of unpaid care to those with Alzheimer's and other dementias — care valued at $216.4 billion, which is more than eight times the total sales of McDonald's in 2011. Eighty percent of care provided in the community is provided by unpaid caregivers.

Nearly 15 percent of caregivers are long-distance caregivers, living an hour or more away from their loved ones. Out-of-pocket expenses for long-distance caregivers are nearly twice as much as local caregivers.

More than 60 percent of Alzheimer's and dementia caregivers rate the emotional stress of caregiving as high or very high; more than one-third report symptoms of depression. Due to the physical and emotional toll of caregiving, Alzheimer's and dementia caregivers had $9.1 billion in additional health care costs of their own in 2012.

Cost to the nation

In 2013, the direct costs of caring for those with Alzheimer's to American society will total an estimated $203 billion, including $142 billion in costs to Medicare and Medicaid. Total payments for health care, long-term care and hospice for people with Alzheimer's and other dementias are projected to increase from $203 billion in 2013 to $1.2 trillion in 2050 (in current dollars). This dramatic rise includes a 500% increase in combined Medicare and Medicaid spending.

Nearly 30 percent of people with Alzheimer's and other dementias are on both Medicare and Medicaid, compared to 11 percent of individuals without these conditions.

The average per-person Medicare costs for those with Alzheimer's and other dementias are three times higher than for those without these conditions; the average per-person Medicaid spending for seniors with Alzheimer's and other dementias is 19 times higher than average per-person Medicaid spending for all other seniors.

Alzheimer's disease facts in each state

The 2013 Alzheimer's Disease Facts and Figures report contains data on the impact of this disease in every state across the nation. Click below to see the effect that Alzheimer's is having in your state.

very sad, and very disturbing figures...tss

2013 Alzheimer’s disease facts and figures Includes a Special Report on long-distance caregivers

Transmission of Prions and Alzheimer’s disease Abeta Amyloid

Claudio Soto, PhD

Mitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept of Neurology

University of Texas Medical School at Houston

Tuesday, March 19, 2013

Alzheimer's Association 2013 Alzheimer's Disease Facts and Figures

Today, an American develops Alzheimer's disease every 68 seconds. In 2050, an American will develop the disease every 33 seconds.

Sunday, February 10, 2013

Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder?

Saturday, October 13, 2012

On the issue of transmissibility of Alzheimer disease: A critical review.

Tuesday, October 4, 2011

Molecular Psychiatry

advance online publication 4 October 2011; doi: 10.1038/mp.2011.120

De novo induction of amyloid-ß deposition in vivo

Our results suggest that some of the typical brain abnormalities associated with AD can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding. These findings may have broad implications for understanding the molecular mechanisms responsible for the initiation of AD, and may contribute to the development of new strategies for disease prevention and intervention. Keywords: amyloid; prion; protein misfolding; disease transmission

see more here ;

Wednesday, September 21, 2011

PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)

Published Date: 2011-10-03 19:22:21 Subject: PRO/AH/EDR> Prion disease update 2011 (09) Archive Number: 20111003.2983



Ann N Y Acad Sci. 1982;396:131-43.

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.


Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.

CJD1/9 0185 Ref: 1M51A


Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray


1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:

i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;

ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and

iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1

BSE101/1 0136


5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992


1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.

2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?

3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.

92/11.4/1-1 BSE101/1 0137

4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.

JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2

BSE101/1 0136



From: Dr J S Metters DCMO

4 November 1992


CJD1/9 0185

Ref: 1M51A


From: Dr. A Wight Date: 5 January 1993


Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray


Wednesday, January 5, 2011


David W. Colby1,* and Stanley B. Prusiner1,2

01:33 PM on 10/07/2011

what concerns me here, is the potential for the iatrogenic transmission of Alzheimer's disease. if proven, and there is other science showing the likelihood of this being true, but this would explain a great deal, and would explain the high increase of Alzheimers disease over the last decade. the medical, surgical, dental, blood, tissue, would all be a canidate for potential transmission. we must fund all these TSE prion disease research, and pursuit the cause and cure of these neurological mad cow type TSE prion disease...

Tuesday, October 4, 2011

De novo induction of amyloid-ß deposition in vivo

Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120

Saturday, January 22, 2011

Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011

Wednesday, April 27, 2011


Friday, September 3, 2010

Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE

'Harmless' prion protein linked to Alzheimer's disease

Saturday, March 22, 2008

Thanks Terry Singeltary, Sr. for your post. First time I have ever bookmarked a comment page before.

2009-02-26 09:43:47 PM Posted by: David Deal

#17057 Thursday, December 23, 2010

Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom



2010-12-24 07:09:49 PM Posted by: Terry S. Singeltary Sr.

10 Million Baby Boomers to have Alzheimer's in the coming decades 2008 Alzheimer’s disease facts and figures

14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

T. Singeltary

Bacliff, TX, USA


An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


12 years independent research of available data


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Friday, October 05, 2012

Differential Diagnosis of Jakob-Creutzfeldt Disease

Monday, August 20, 2012


see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;

Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis

full text with source references ;

re-Human Prion Diseases in the United States Posted by flounder on 01 Jan 2010 at 18:11 GMT

I kindly disagree with your synopsis for the following reasons ;

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.

Views & Reviews

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD

+ Author Affiliations

From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.

Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.

26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported 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. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT

The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI

Tracking spongiform encephalopathies in North America


Xavier Bosch

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...

2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

Saturday, October 13, 2012

On the issue of transmissibility of Alzheimer disease: A critical review

A VERY IMPORTANT FACTOR that must be weighed in on, HEALTH INSURANCE COMPANIES. IF there is not a provision, clause, that stipulates that being placed AT RISK OF CREUTZFELDT JAKOB DISEASE, would NOT blackball you i.e. MARK you, that NOT in any way can discriminate against you because of the disease, that NOT in any way would jeopardize or enhance cost for health insurance for anyone being placed 'AT RISK'.

Subject: Lord Lucas asked Her Majesty's Government about insurance company's and CJD???
Date: Thu, 6 Apr 2000 09:49:14 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy ######### Greetings Everyone, I am deeply concerned about the answer given to Lord Lucas on CJD and
insurance company's. In Her Majesty's reply, the reason given for
insurance company's _not_ being able to require candidates for life
insurance to be tested for incipient nvCJD or any human TSE, was because there is no test to date, that would allow them to test.
My question to Her Majesty's Court would have been;
when such a test is available, will the insurance company's be allowed
to test for human TSE's?
It seems Lord Lucas question was not answered fully, it seems Her
Majesty's Court just went around the question.
If in fact, the insurance company's are allowed to do this, once again
the people would have been deceived by their government, for the sake
of money, greed, and corporate industry$$$ This would be devastating
to the people, not only have they been murdered by corporate greed,
but they then would be sold out, for corporate greed. It's a no-win
situation for public consumers...
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA

April 4, 2000
Lord Lucas asked Her Majesty's Government:
Whether they will permit insurance companies to require that candidates for life insurance be tested for incipient
new-variant CJD.[HL1661]
Lord Hunt of Kings Heath: Insurance companies would be unable to
introduce such a step, as no acceptable test currently exists for the demonstration of infection before the onset of clinical

Subject: Re: re-Lord Lucas U.K. Government sells out CJD victims (and others)'again' / U.K. Government O.K.'s Genetic testing for Insurers, looking for hereditary illnesses
Date: Fri, 13 Oct 2000 09:37:22 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
References: 1
######### Bovine Spongiform Encephalopathy ######### first Huntington's, then CJD, then another, and so on.
what needs to take place, is everyone drop their insurance.
once you give these people an opening, it's like a hole in
a dam, there is no closing it, and it just gets bigger and
bigger. This is a serious breach of human ethics, all for the
almighty dollar$$$
kind regards,

The Genetics and Insurance Committee (GAIC) has today announced that
the reliability and relevance of the genetic test for Huntington's
Disease is sufficient for insurance companies to use the result when
assessing applications for life insurance.
Professor John Durant, Chairman of GAIC said: "Genetic test results are already used in certain circumstances by
insurers and the Committee was asked to look at the reliability and
accuracy of the genetic test for Huntington's Disease. We have
considered carefully the application received from the Association of
British Insurers for approval of the use of these tests.
The evidence presented demonstrates that the two tests for the
Huntington's gene are reliable and that an abnormal result is
associated with significant clinical effects and with an increased
probability of a claim on a life insurance policy. This decision
will mean that those with a negative test result will not be asked to
pay more for life insurance because of their family history of
HuntingtonÆs disease.
"This decision does not mean that individuals will be asked to have a
genetic test for Huntington's Disease before obtaining insurance but,
where individuals have already been tested as part of their medical
care, then there is nothing to prevent insurance companies asking for
that information.
"Many who have a family history of a genetic disorder such as
Huntington's Disease have difficulty in obtaining insurance because
of their family history. The approval of the two tests for
Huntington's Disease will allow insurance to be provided at normal
rates to those who have a normal test result."
A significant amount of data has been collected concerning the
effects of Huntington's Disease on life expectancy and on mortality
risk as part of the process of reviewing this application. The
Committee hopes that the insurance industry will use this information
to look at the problems of those who have an abnormal genetic test
result and of those who have chosen not to have a genetic test (who
have a 50 % chance of carrying the abnormal gene if they have an
affected parent).
The GAIC was asked to examine the actuarial evidence for using
individual genetic tests. The insurance industry, through the main
trade body the Association of British Insurers, has agreed to abide
by GAIC decisions. If GAIC decides that the evidence on the
reliability and relevance of a particular test is insufficient to
justify its use, the Association have agreed to stop using them and
retrospectively reassess affected individual insurance premiums. The
broader social and ethical issues surrounding the use of genetic
tests in insurance and employment have been referred to the new Human
Genetics Commission.
An application for approval of two genetic tests for Huntington's
Disease was submitted to GAIC by the Association of British Insurers
(ABI) in July 2000. The application was sent to a clinical
geneticist and an independent actuary for expert review and also to
support groups for Huntington's Disease and to the Genetic Interest
Group (GIG) for their comments. At their meeting on 28 September,
GAIC considered the application, in the presence of observers from
the ABI, GIG and Huntington's Disease Association. Their decision is
announced today.
The committee recognises that this complex subject is an important
issue to the public, industry and government alike. GAIC will work
closely with the new Human Genetics Commission when they begin their
inquiry into the use of genetic data including in insurance and
employment later this year.
Notes to Editors: A summary of the decision and further details about GAIC and the
application process are available on the Department of Health web
site at www.doh.gov.uk/genetics/gaic.htm
The establishment of the Genetics and Insurance Committee (GAIC) on
12 April 1999 fulfilled the Government's commitment to establish an
independent review body, to evaluate the scientific and actuarial
evidence presented in support of the use of specific genetic tests
for insurance products. This was made in response to the Human
Genetics Advisory Commission (HGAC) report on the Implications of
Genetic Testing for the Insurance Industry, issued in December 1998.
GAIC is a non-statutory Advisory Committee and has a UK-wide remit.
Its terms of reference are:
- to develop and publish criteria for the evaluation of specific
genetic tests, their application to particular conditions and their
reliability and relevance to particular types of insurance;
- to evaluate particular tests against those criteria and promulgate
its findings;
- to report to Health, Treasury and Department of Trade and Industry
Ministers on proposals received by GAIC from insurance providers and
the subsequent level of compliance by the industry with the
recommendations of GAIC.
The core membership of GAIC is: Professor John Durant, Chief Executive of At-Bristol as Chairman,
appointed from amongst the members of Advisory Committee on Genetic
Professor Sandy Raeburn, a geneticist nominated by the Association of
British Insurers (ABI);
Professor Dian Donnai a geneticist nominated by CMO (England); Dr David Muiry, an Actuary nominated by the Faculty and Institute of
Mr Anthony OÆLeary, an Insurance Practitioner nominated by the ABI; Mrs Susan Watkin and Mrs Barbara Carmichael, members of Patient
Support Organisations nominated by the Genetic Interest Group;
Professor Tim Bishop, an academic with a background in epidemiology
and genetics nominated by the Director of Research, Department of
GAIC has published evaluation criteria covering the details of the
genetic condition being tested for, the accuracy and reliability of
the tests used to detect it and the relevance of the test results to
decisions about insurance underwriting. GAIC expects that
applications will be for genetic conditions caused by changes in a
single gene, that are very likely to lead to serious ill health or
disability and that are therefore most relevant to the setting of
premiums for life and health insurance.
Over the next few months, GAIC will consider applications relating to
the conditions currently covered by the Association for British
Insurers' Code of Practice on Genetic Testing. These include
Huntington's Disease, myotonic dystrophy, the early-onset form of
Alzheimer's disease and rare inherited cancers. The intention is to
complete review these applications by June 2001.
The Human Genetics Commission, chaired by Baroness Helena Kennedy,
was created in 1999 to provide the Government with strategic advice
on the wider implications of human genetics. It replaces three former
committees and is responsible for making links between all the other
relevant bodies in the advisory and regulatory framework. Further
information can be found at www.hgc.gov.uk
HGC has been formulating a public consultation exercise on the
storage, protection and use of personal genetic information which
will include the use of genetic data for insurance purposes. The
issues are due to be discussed at a public consultative meeting at
the Centre for Life, Newcastle-upon-Tyne in November 2000.
"Terry S. Singeltary Sr." wrote:
> ######### Bovine Spongiform Encephalopathy #########
> Greetings List,
> Talk about something that really stinks, this does. First
> the U.K. Government allows the Industry's involved to continue
> to murder (God only knows how many). Then they don't support them,
> and to top it off, they then allow the only hope one has to
> get any kind of medical care, they allow the insurers to bail
> out on victims of this man-made blunder. I thought Lord Lucas
> asked this question to Her Majesty's Court, and Her Majesty's
> Court said;
> ######### Bovine Spongiform Encephalopathy
> #########
> They replied that as there was no test they could not test, so the
> question did not arise!
> Ralph
> > Did I miss something or have they not yet responded to this one?
> >
> > Question 20: Whether they will permit insurance companies to require > that
> > customers be tested for incipient nvCJD.
> Dear Lord Lucas,
> the question has arised again, and should be confronted.
> may i suggest that you ask this question again. it would seem,
> with a test so close to come about for the testing of TSE's,
> one would think, they are just preparing for the worse, and
> covering their butts, at the same time.
> Politics as usual, but my God, have not these people suffered
> enough, without the Governments completely stripping them
> from any help at all. Hell, you should just take them out back
> and shoot them........
> kind regards,
> Terry S. Singeltary Sr., Bacliff, Texas USA
> ===========================================
> Thursday, 12 October, 2000, 11:28 GMT 12:28
> UK Genetic test first for UK
> Genetic tests can predict future illness
> Insurers in the UK are to be allowed to use
> genetic test results to identify people with
> hereditary illnesses.
> The government will announce on Friday that
> insurers will be able to use those results to
> refuse cover or to push up premiums for those
> born with genes that could lead to fatal
> conditions.
> The decision makes Britain the first country to
> approve the commercial use of gene
> technology in this way.
> The Genetics and
> Insurance Committee,
> an advisory body
> reporting to the
> Department of Health,
> has decided that a test
> used to identify a
> hereditary risk of
> contracting the disease
> Huntington's chorea is
> technically reliable.
> Tests covering several other conditions,
> including hereditary breast cancer and
> Alzheimer's disease, are also awaiting approval.
> Two years ago another advisory body, the
> Human Genetics Advisory Commission,
> recommended a moratorium on the use of
> information from such tests.
> However, that advice was rejected by the
> government, which decided insurers should be
> able to use such information, subject to the
> Genetics and Insurance Committee agreeing a
> test's technical reliability.
> The announcement is likely to fuel the ethical
> debate over the use of genetic information.
> Critics fear that vulnerable groups could find it
> difficult to get a mortgage or life insurance, or
> face higher premiums.
> But the insurance industry dismissed that
> suggestion.
> No compulsion
> Professor John Durant, chairman of the
> Genetics and Insurance Committee, told the
> BBC that nobody would be asked to take a
> genetic test by an insurance company.
> Rather they would be
> expected to disclose
> the results of any
> genetic test for
> Huntington's disease
> they had taken in the
> past.
> Professor Durant said
> this would not be a
> legal obligation, but
> insurance companies
> would have the right to
> refuse to offer
> insurance if a customer
> refused to reveal details.
> He said: "It is not a punitive step. This will
> actually benefit very many people seeking
> insurance.
> "The only people who are likely to have taken
> a test for Huntington's disease are people with
> a family history of this disease.
> "Many of those people will actually have had
> results which show that they are fortunate
> enough not to have inherited the gene, so
> those people will be able to get insurance, at
> the moment they may well find it difficult."
> Mary Francis, the Director-General of the
> Association of British Insurers, said that
> companies already asked potential customers
> about family history of disease.
> She said: "This is really an extension of what
> already does happen."
> Sue Watkin, chair of
> the Huntington's
> Disease Association,
> also said insurance
> companies were already
> using genetic test
> results to calculate or
> refuse premiums.
> She said: "Our main concern is that people at
> risk of late onset genetic disorders should be
> able to get insurance of some kind up to a
> certain level.
> "At present, many people are made offers they
> just cannot afford."
> Ms Watkin said that a person at 50% risk of
> developing Huntington's often found their
> insurance premium loaded by as much as
> 300%.
> She called on the government to establish a
> fund to be used to provide insurance for
> people at risk.
> The National Consumers' Council is concerned
> people will be put off having tests because
> they feared that the results might count
> against them - with a possible knock-on effect
> on their health.
> A spokeswoman said: "A person might think if I
> take a test I will know information that I don't
> know now, and maybe ignorance is bliss.
> "If you don't know the information you can't
> put it on the form."
> The Human Genetics Commission, another
> government advisory body overseeing
> developments in the use of genetic
> technology, said that it would launch shortly a
> major public consultation exercise about the
> use and protection of genetic information,
> which would include insurance issues.
> The exercise would eventually result in the
> Commission making recommendations to
> ministers.
> http://news.bbc.co.uk/hi/english/health/newsid_968000/968443.stm

Subject: Re: CJD $ BLOOD $ Schmerr test$$$
Date: Wed, 18 Oct 2000 11:01:01 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
References: 1
######### Bovine Spongiform Encephalopathy ######### Greetings again List Members, it just hit me about the blood testing. bought knocked me out of the
chair. could it be, the reason they have stalled the blood testing, they
are waiting for the genetic testing to be perfected for the insurance
company's. once perfected and implemented, and no risk of any type
medical insurance coverage for TSE patients, then they will be allowed
to go ahead with the blood tests for human TSE's. pretty smart huh, they
don't pay all these Gov. Officials just to cram BSE tainted hamburgers
down the throat of their daughters, or just for nothing. They pay a good
portion of them to think up schemes, to get them out of man-made
environmental death sentences. I would love to know, who thought
up the scheme, to brain-wash everyone into believing the 'CHOSEN ONES'
are the only ones tied to this man-made death sentence? Probably the
one to think up the genetic testing for insurance companies.
Oh, well, this pretty much does it for me today. Probably already
over-loaded myself today. Now i know why Mr. Schmitt only allows 4
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA
Department of Health Statement - Genetic Testing and Insurance kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA
"Terry S. Singeltary Sr." wrote:
> ######### Bovine Spongiform Encephalopathy #########
> Greetings again list members,
> Has anyone heard of any further development of the Schmerr test???
> I knew of powers within, that were trying to inhibit the progress
> of this testing (from a _most_ reliable source), but did not think they
> actually would stop the research.
> hmmmm, who knows???
> Here are a few links some may find informative;
> Opinion On
> Update of the Opinion given by the Scientific Committee on Medicinal
> Products and Medical Devices on The Risk Quantification For CJD
> Transmission Via Substances of Human Origin;
> 2. Screening assays
> It is assumed that although there is no proven or even probable case of
> transmission by blood or blood products the identification and exclusion
> of donors in the preclinical phase of CJD or vCJD would contribute to an
> increase in the safety margin and, probably, an increase in the
> confidence in blood and blood products by potential recipients.
> Therefore, the SCMPMD in its Opinion of October 1998 emphasised the need
> for "the development of a simple readily available ex vivo diagnostic
> test for preclinical nvCJD/CJD". In addition it stated: "When a
> validated test for TSE infectivity in donor blood becomes available, it
> should be implemented in routine donor screening as soon as possible and
> donors found to be positive should be excluded from donation. Member
> Statos should, in the interest of public health, warrant availability of
> TSE tests for blood screening in collaboration with possible patent
> holders."
> During the "WHO Consultation on Diagnostic Procedures for Transmissible
> Spongiform Encephalopathies: Need for Reference Reagents and Reference
> Panels" held in Geneva on March 22 and 23, 1999, M.J. Schmerr presented
> results of a new assay that may be able to detect the pathological fbrm
> of ption protein in blood of animals in the clinical as well as in the
> preclinical phase of TSE (serapie in sheep and chronic wasting disease
> in deer, Schmerr 1999, Schmerr et al. 1999). The basic reaction is the
> competition of the proteinase K treated sample with a labelled peptide
> derived from the sequence of prion protein binding to an antibody mised
> against this peptide (Schmerr et al. 1998). The test material is
> extracted from buff), coat prepreed from a sample of peripheral blood.
> >From the relation between ti'ee and bound peptide as determined by
> capillary electropheresis the amount of corn?ting protein i.e. protease
> resistant prion protein, is calculated.
> In contrast to other tests used for the detection of TSE infected
> animals or lbr confirmation of CJD/vCJD in humans the assay proposed by
> Schmerr uses for the first time as test material a body fluid, namely
> blood, which is eaqily availahl,~ In thi~ respect, this assay fulfils a
> prerequisite for a screening assay which could be used in the blood
> donation setting. However, it has to be stressed that this assay is far
> from ir~ing vaildated tidier in animals or in humans. On the contrary,
> preliminary tests with haman material performed in several laboratories
> have not yet validated this test.
> There is no doubt that the assay has the potential to be developed into
> a screening assay, but this developmere will need a number of carefully
> designed studies. Use in donor screening will not be possible until
> there is more information on the sensitivity, specificity and validity
> of the assay.
> The SCMPMD repeats its recommendation to support efforts in the
> development of easily applicable screening tests for CJD/vCJD.
> The SCMPMD would also like to draw the attention to an ethical aspect of
> the expected introduction of a screening assay for CJD/vCJD. The
> information of a positive test result would confront the individual with
> the diagnosis of an inevitably fatal disease without any reliable
> prediction of the duration of the preclinical phase. Such information
> could cause severe psychological stress and would demand careful
> counselling. In such a situation, it would not be surprising if donors
> would stop donating il' such a test for CJD/vCJD were introduced. If the
> number of those dollors is high the introduction of a screening assay
> would lead to a significant loss of donors who would have to be replaced
> by first time donors who are at higher risk of well known blood borne
> infections. This situation should be considered well in advance.
> 3. Exclusion of donors at risk for TSE infection by ruminant derived
> material
> Until the end of 1998 vCJD cases were observed only in the United
> Kingdom (UK), with one single exception. Therefore, residency in UK was
> described as one of the known risk factors for vCJD (the others being
> young age (i.e. below 53 years) and homozygosity of methionine at codon
> 129 of the prion protein gene). The exclusion of donors who resided for
> some time in the UK could, therefore, be considered as contributing to
> minimising the theoretical risk of vCJD transmission by blood and blood
> products.
> The first recommendation of this kind was given by the Ottawa based
> Bayer Advisory Council on Bioethics which stated in his working paper
> "Creutzfeldt-Jakob disease, blood and blood products: A bioethics
> framework" (1998):
> "The differences between classical CJD on the one hand and nvCJD on the
> other creme differences in the quality of the hypothetical risk. As
> discussed earlier, the new variant form appears to have crossed the
> species barrier from cattle. It has an earlier age at onset, and the los
> of pathological ptiohs is much greater than in classical forms of the
> disease. The anatomical distribution of nvCJD infectivity is also
> different, which raises the plausible possibility that it is more likely
> to have infectivity in the blood. Therefore, nvCJD is the wild card that
> warrants special vigilance. The disease appears to be isolated, at
> present, to parts of Europe. The number of people in affected countries
> who are currently incubating the disease is ankhown. The Council
> therefore recommends:
> 20. That persons who, at any time since 1980, have resided in a
> geographic area with a significant incidence of BSE or nvCJD not be
> permitted to contraute blood or plasma until the hypothetical risk of
> accepting donations from such persons can be evaluated."
> http://europa.eu.int/comm/food/fs/sc/scmp/out28_en.pdf
> also, for those interested, here are more documents on this and
> other issues;
> http://europa.eu.int/comm/food/fs/sc/scmp/out12_en.pdf
> http://europa.eu.int/comm/food/fs/sc/scmp/out20_en.html
> http://europa.eu.int/comm/food/fs/sc/scmp/out25_en.html
> http://europa.eu.int/comm/food/fs/sc/scmp/out29_en.pdf
> kind regards,
> Terry S. Singeltary Sr., Bacliff, Texas USA

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