Monday 21st March 2011

Many of the young victims of vCJD are a similar age, some share the same birthday months and some were even born on the same day. There appears to be a clustering of individuals roughly the same age, who also became sick around the same time of year, winter months and Christmas is usually cited by families as when symptoms first became apparent.

Many of these younger victims would have started their education the same time, several attended the same schools, some even lived in the same street, I have visited these families and talked to them at length. Yet with all these co incidences the UK government has not been able to find a link? Two young men received oral polio vaccines from the same batch roughly the same time at educational facilities within a few miles of each other, these young guys died within weeks of each other of vCJD. .

Many of the victims would have been babies, infants at the same time and shared similar lifestyle, medical and food choices. These include commercially prepared baby food, formula milk, school meals, medicines and vaccines. Although some victims may have died several years apart, I have discovered if they had lived they would have all been roughly the same age. This points at a common source of infection with perhaps some victims ingesting more infected material so incubation periods are shorter.

Baby Food and school meals have been quoted by experts from the CJD/Prion unit as a likely source of vCJD infection. During my extensive investigations I have found that many victims never ate commercially prepared baby food and/or school meals. Some victims through religious and cultural beliefs were strict vegetarians. These include Sikhs and Hindus, one lady didn’t even eat cheese gelatin or any part of the cow……and yet these people still died of vCJD? The odds of these victims eating one ‘stray burger’ or a total vegetarian eating one yoghurt or contaminated food product infected with sufficient rogue prions to develop vCJD is astronomical… …..

My Andrew hardly ate beef and from the age of 6 years old all beef and beef products were banned from my home and my family never touched any of these products again during Andrews childhood, and yet he still developed vCJD. My Andrew was a very fussy eater and even when he was dying he asked a friend who was cooking for us ‘ ‘Don’t use beef because of mad cows disease’….the terrible irony makes me weep. When he visited friend’s houses he would refuse anything that looked like meat or beef so the actual odds of him eating a ‘stray burger’ during his childhood and teenage years is also astronomical…... My daughter Emma who was born in 1990 told me ‘ I can never remember us ever eating or having beef or beef products in our home or ever eating these products outside the home’. When my children attended birthday parties or outside events they never wanted to eat or consume these products either. So how did my Andrew become infected with vCJD?

What is Whitehall keeping secret…..? What important piece of the picture is being withheld from us? What made my Andrew develop vCJD and the boy next to him at school didn’t?, why haven’t siblings and other family members not succumbed to vCJD?

There is one case in Spain where a pensioner and her 40 year old son died within a year of each other from vCJD. This case could hold lots of answers but once again publication of papers and information about this mother and son are not transparent or fully in the public domain…..why?

Perhaps younger vCJD victims succumbed to a variety of sources of infection?. Some baby food, some school meals and some vaccines? But I have been assured by experts that what killed my son and all victims of vCJD ‘was a hugely toxic dose of BSE infected material’…..’ a stray burger….didn’t kill my Andrew…….or the other victims.

When Andrew was initially diagnosed with vCJD his Consultant at Southampton General Hospital Mr Monaghan told me very angrily: ‘A stray burger didn’t cause this’ ( Andrew developing vCJD) when I suggested another source such as vaccines, .there was a deathly silence in the room which contained another consultant, registrar, doctor and two nurses. When I asked if a ‘stray burger’ didn’t cause my Andrew to develop vCJD and asked Mr Monaghan ‘ What did?’. There was another long silence…..there was a definite sense of the medical team knowing more about how my Andrew had become infected than they were admitting to me. I felt like they knew a lot more than they were telling me…and was told again that ‘ a stray burger’ could not possibly have caused him to develop vCJD and the damage that was occurring to Andrews brain. At the time of diagnosis Mr Monaghan did not know that as a family we had not eaten beef for decades so his comments were not influenced, they were I believe an honest, professional and expert opinion.

Andrew hadn’t eaten beef or burgers for over 14 years so if a ‘stray burger’ is not the source of vCJD what is? Since my Andrews death Mr. Monaghan has moved to work in another country where he still practices as a Consultant Neurologist, I would say he was an honest man who really cared about my Andrew and was really angry at my sons avoidable dying.

Lots of half truths and lies have been spun to the public and families of victims of vCJD about the source and route of the infection…….this is to continually muddy the waters, pile on the already terrible guilt suffered by parents but also to take the heat off the real culprit and culprits……

Conflicting research and findings are encouraged by Whitehall to further confuse and take the focus away from the truth. One paper will say ‘one stray meal can cause vCJD’ another ‘baby food causes vCJD’ and yet another ‘root fillings and going to the dentist may cause vCJD’……These are then peddled into the media so the public become even more confused and unsure.

I continue to uncover ‘red herrings’ disregard them and focus on the path which is taking me ever nearer to the source of the infection and truth behind BSE and vCJD. At present much of my work is sensitive not only to its ongoing development but to the people who are helping me not only would their careers be in jeopardy so could their lives.

I would like to share with you some of the many differing facts and research that has been pumped into the public arena to continue the mystery surrounding BSE/vCJD. Whilst there is manufactured uncertainty the truth can be blocked and sidelined……

So is this article and research below ‘fact or fiction?’ Dr Desly has been rewarded for his findings by the UK Department of Health and now sits on the Oversight Committee. a prestigious UK CJD group deciding which scientists and medics receive blood samples from vCJD victims. (Including my Andrews). This committee can effectively block any outside companies or scientists developing medication or treatments by withholding these precious samples so validation cannot take place. Dr Desly has been brought into the fold of the UK Department of Health and within the firm grip of Whitehall and the UK Government.

In a article dated 27^th January 2005 Dr Desly a scientist researching BSE/vCJD told BBC1 ‘To become infected (with vCJD) you would have to eat an enormous amount of brain material which is just not possible’. His research using primates found ‘A person would have to eat at least 1.5kg of neural (brain and spinal) tissue to be at risk of developing vCJD’ Dr Jean Philippe Desly conducted his research for the Commissariat an l’Engerfie Astoronomique.

So what or who do we believe?

In the SE1736 test carried out secretly at a farm in the UK. Over many years cattle were fed BSE material.

‘All the 1g infected cattle died, either as part of random sampling or euthanasia because of symptoms. Surprisingly, 2 of the 100g exposed animals survived beyond the end of the experiment’.

What happened to those 2 cows that didn’t develop the disease and more crucially why did they survive to the end of the experiment? .

Off the record scientists who worked at these experimental farms have told me the higher the dose of infected material  fed to cows the quicker the incubation period and the faster cattle died of BSE. Yet some cattle fed 100g of BSE material never developed any symptoms by the end of the experiment. Too many questions remain, too much significant data is being hidden...too much conflicting information is being put into the public domain.....to confuse....and to conceal not reveal. This is deliberate and there has been a manufacturing of information and data to continue the mystery surrounding BSE.  

Primates are our closest match for DNA, it was known in 1966 that if you fed monkeys with cjd material they became ill and died of cjd, but these primates had also cut, scratched and lacerated their hands with the infected material, this proved to be a much quicker and easier route to infect primates. 

Yet in the 1980s and 1990s those named and shamed on this website allowed BSE into the human food and medicine chain, despite knowing the scientific findings of 1966.

So what does Desly and SE1736 experiment prove? Significant findings and facts have been withheld or manipulated and kept from the public domain. Whilst half truths and findings that will muddy the waters are pumped out to an unsuspecting public in much the same way as facts/figures were distorted throughout BSE.

What is a fact that during the SE1736 experiment and other experiments some cattle that were infected with BSE did not develop the disease? Why? Perhaps those cattle did not have abrasions in their mouths or on their bodies?

What is a fact is what killed those BSE cows killed my Andrew and all victims of vCJD , the symptoms and chemical makeup of BSE exactly replicates vCJD in humans. I have witnessed cattle dying and infected with BSE and the symptoms are the same as my Andrew and all the other victims of vCJD who I have met, spoken too and spent time.

Even different genotypes have the same and generalised symptoms of BSE infected cattle. Once you have met and seen a person even at the earliest stages of vCJD it’s unmistakable from any other disease.

What is a fact is my son and all victims of vCJD where unlawfully ‘killed’ by an acquired disease that could and should have been prevented by those ministers named on this website. They had a duty of care to the UK population including my son , but Kenneth Clarke, John Gummer and those listed put their careers and allegiance with the ‘beef and drug companies’ instead of protecting the UK public health and well being….

Experts in prion disease employed by the Department of Health declare that BSE material was in virtually everything we ate during the 1980s and 1990s and probably beyond……and yet so far millions haven’t succumbed to the deadly disease which killed my only son….(though millions of us could be ‘silently carrying the disease)

This points at a specific source of infection to which my son Andrew and other victims past present and unfortunately those to come have been exposed.

Is there something that was different from my son and the other victims of vCJD which made them more vulnerable? Apparently not all tests conducted on my Andrew came back healthy and normal, his heart, lungs, liver and all other major organs apart from his brain were healthy and disease free..

According to all the experts I have quizzed on this matter including Professor John Collinge University College London ‘Andrew was a fit healthy young man…no different from any other fit healthy young guy in his early twenties living in the UK’. …So why did Andrew develop Vcjd…what huge toxicity was he exposed to that would kill him so horrifically…? And why was this allowed for over 14 years into the human food and medicine chain?

I was asked if my family had any dementia or related neurological illnesses and can state that none of my or Andrews relatives have died or developed any neuro or dementia type illnesses so there was and is no susceptibility. Also my Andrew never had any blood transfusions, dentistry, operations, not even a stitch for a wound or a cut he was a totally fit young man. He also never ate beef or beef products from the age of 6 and throughout his childhood and teenage years.

The same experts that tell us that every one over 14 has eaten at least 50 BSE infected meals also declare ‘How difficult it is to infect animals orally with BSE’ Once again we have the conflicting press articles, scientific papers…used to conceal not reveal.

Theoretically it’s more difficult to become infected via food than it is intravenously such as vaccines or blood products, through wounds or cuts. Transmitting the rogue prions that cause vCJD is much easier through blood or intravenous drugs.

Why haven’t other family members including a twin contracted and died of vCJD?

There is only one case officially recognised of a mother and son dying within months of each other in Spain…from vCJD…..this has never been fully or publicly explored or explained. Apparently the villagers where this Mother and Son lived regularly ate cow’s brains as a local delicacy…but the whole village and area would have indulged in this practice…and yet so far these are the only local cases of vCJD?

What about the Spanish pathologist working with cjd who also developed vCJD, his Post Mortem, genotype and the route of his infection has also remained clothed in secrecy with just the bare minimum of details being published and these details are not complete or the full picture. .

My research has shown a common thread which indicates why predominately young people have died and continue to die of vCJD.

Because this group of society were exposed specifically to a common source…..

Several top experts have told me they suspect a rogue batch of vaccines/medicines is the source of at least some of the younger victims of vCJD …..

Babies, infants and younger children are probably more susceptible to BSE material

What is also clear is that many of the older individuals who died of vCJD, had ‘high risk’ jobs or lifestyles and either worked on farms, at abbatoirs, or worked as health care professionals, within catering, armed forces or jobs that would have given them access to frequent vaccines such as tetanus, polio, BCG, meningitis, flu and other inoculations.

What is the Department of Health keeping from the public? What do they know about the exact source of the infection that has killed so many innocent people? And continues to kill!

Why is so much information about BSE ‘commercially sensitive’, been shredded or is kept under lock and key and top secret?

Why are the same drug companies that manufactured those suspected vaccines/medicines in the 1980s 1990s and beyond…now hold the purse strings regarding funding research into vCJD here in the UK?

Why are many of the top and scientific experts in the UK manacled to these drug companies by this funding? So that any research they conduct into vCJD is overseen by the very people who developed these dodgy vaccines/medicines in the first place?

Why are young people still dying of vCJD in 2011?

If a ‘stray burger’ didn’t kill my Andrew what did?

What really made my Andrew develop vCJD?

What really killed my Andrew? .. I continue to uncover the truth and in the future all will be revealed…….

Tuesday 15th March 2011

A Canadian resident has been diagnosed with vCJD, it would appear the victim was exposed to BSE outside of Canada and never received a blood transfusion or blood products. This individual immigrated to Canada in 2010, was born in the Middle East and had limited history of traveling outside these two countries approximately 3 months.

There have been previous cases of vCJD in individuals from the Middle East, many countries in this location have strong links with the UK, many UK nurses, medics and medical supplies are based and sent to Middle Eastern Hospitals. Vaccines made in the UK derived from BSE infected cattle and human albumen were exported to this region.

I would challenge the stance that this person became infected before safety measures were implemented here in the UK, I would assume this paper is talking about the SBO ban in 1989 which stopped specified bovine offal apparently entering the human food and medicine chain. As some of the latest victims of vCJD were not even in the UK till after that time and with a rough incubation period of 10-11years….it would appear that victims who are developing the disease in the 21^st century were probably according to prion experts and the UK DOH infected in the 1990s…….and maybe much later….possibly late 1990s and beyond…...

If this victim is MM genotype it would appear that they were infected much later…which raises many concerns and significant health issues. How long was BSE infected material; allowed into the human food and medicine chain here in the UK and in our exports to the global community? When is the public going to be told the whole and real truth behind BSE and vCJD….how much longer can the UK government and its Whitehall minions keep these secrets?

My thoughts are with this victim and their family…and to all our brothers and sisters in the Middle East , Canada and the 12 countries who have lost loved ones to vCJD. We are a global family and community and BSE continues to wreck lives and steal futures……

We must remain vigilant and continue with our cohesive alliance…….the truth will be heard and there will be justice for all victims of vCJD and their families…….

Infectious Diseases News Brief - March 11, 2011

[Current Issue - Table of contents]

Variant Creutzfeldt-Jakob Disease in a Canadian resident Canadian Creutzfeldt-Jakob Disease Surveillance System, National Microbiology Laboratory, Public Health Agency of Canada Working closely with Canadian clinical specialists, the Public Health Agency of Canada's Creutzfeldt-Jakob Disease Surveillance System (CJDSS) has identified a probable case of variant Creutzfeldt-Jakob disease (variant CJD, also called vCJD) in a Canadian resident. The diagnosis is supported by several lines of clinical, paraclinical and laboratory evidence, in keeping with internationally accepted surveillance case definitions for human prion disease.(1, 2) This is the second case of variant CJD reported in Canada to date. The first such case occurred in 2002, in an individual who is believed to have contracted the disease outside of Canada.(3) As explained in more detail below, evidence to date strongly indicates that (i) the risk exposure in the second case also occurred outside Canada; (ii) there are no negative implications for the safety of the Canadian food supply; and (iii) the case poses no secondary risks to the health of Canadians.

Variant CJD belongs to a group of rare, fatal degenerative brain disorders called prion diseases that affect humans and animals and can arise sporadically, genetically, or through infectious transmission.(4) Prion diseases are marked by brain tissue vacuolation (spongiform change), neuronal loss, and presence of a pathologically altered form of a host-encoded glycoprotein, PrP, that is considered to constitute the transmissible agent, or prion.(5) Among classic types of human prion disease, the most common and widespread is sporadic CJD, which occurs without an apparent infectious or genetic cause mostly in persons 50+ years of age and accounts for 80-90% of the remarkably uniform annual prion disease mortality of ~1-2 per million population.(6) Most of the remaining 10-20% of classic human prion diseases are caused by mutations in the PRNP gene that encodes PrP.(7) Fewer than 1% of classic cases of CJD are attributed to accidental transmission through surgical and medical pr ocedures such as dura mater grafts, and use of therapeutic hormone preparations that were derived from prion-contaminated cadaveric pituitary tissue.(8)

Variant CJD is the only known zoonotic human prion disease, resulting from dietary exposure to a feedborne prion disease of cattle, bovine spongiform encephalopathy (BSE, also known as "mad cow disease"), that emerged internationally in the 1980s and 1990s.(9) Most human exposure to BSE is thought to have occurred before regulatory controls were implemented to control BSE in animals and to eliminate the inclusion of high-risk bovine tissues in human food.(10) A small number of secondary cases of variant CJD have also been linked to transfusion of fresh blood components (erythrocytes) from pre-symptomatic donors who later developed the disease.(11) By October 2010, a total of 222 definite and probable variant CJD cases had been reported worldwide in residents of 12 countries.(12) The total numbers of clinical cases of variant CJD that will ultimately emerge remains uncertain, as does the frequency of long-term asymptomatic carriage during which apparently healthy individuals could transmit infection for example through blood donation or invasive medical procedures.(13)

Importantly, based on extensive interviews with family members there is no indication that the current patient was ever a blood donor, received a blood transfusion, or underwent a surgical procedure that was not managed to prevent prion transmission as per the Public Health Agency of Canada's CJD Infection Control Guidelines.(14) This indicates the absence of secondary risks to the health of Canadians as a result of this case. Health Canada issued directives to Canadian blood operators in 1999, 2000, 2001 and 2005, requiring deferral of blood donors with a history of residence and/or travel in the United Kingdom (UK), France and Western Europe in the period 1980-1996, as well as other criteria including receipt of blood transfusion in the UK, and has committed to review these deferral policies if new scientific information becomes available. Canada has also reported a small number of cases of BSE,(15) and Health Canada and the Canadian Food Inspection Agency have implemented regulations to prevent both the transmission of BSE in animal populations and human exposure to it. Given (i) these protective measures, (ii) the observation that acquired prion diseases have long incubation periods (years to often a decade or more), and (iii) the fact that the current patient experienced onset of symptoms just prior to immigrating to Canada in early 2010, the possibility of BSE exposure in this country can essentially be ruled out as the cause of illness. The patient was born in the Middle East, and also resided in several other countries before arriving in Canada. Apart from a few visits totalling less than three months in duration, there was no history of travel to the UK or Europe.

In Canada, all human prion diseases are both legally reportable at the provincial/territorial level and nationally notifiable, and despite their rarity the public health importance and economic impacts of these diseases have maintained a need for timely diagnosis, reporting, and surveillance. To help meet these requirements the CJDSS has conducted prospective national surveillance of human prion diseases continuously since 1998, and working collaboratively with a network of health professionals sponsors detailed diagnostic and epidemiologic investigation of any suspected case of human prion disease in Canada. Supporting laboratory services are provided for autopsy, neuropathologic examination, molecular genetics, and biochemical testing for 14-3-3 protein in cerebrospinal fluid. Test results are reported directly to referring health professionals, with CJDSS case files maintained centrally to facilitate diagnostic assessment and final case classification. Full patient enrolme nt with the CJDSS takes place with written informed consent. The CJDSS surveillance protocol has been approved by the Health Canada Research Ethics Board (Certificate REB-2009-0036), and by numerous REBs at collaborating healthcare institutions. For further information on human prion diseases, available services and how to access them, interested health professionals are invited to contact the CJDSS toll-free, at 1-888-489-2999 1-888-489-2999 .

References 1.World Health Organization (WHO). WHO manual for surveillance of human transmissible spongiform encephalopathies including variant Creutzfeldt-Jakob disease. 2003. http://whqlibdoc.who.int/publications/2003/9241545887.pdf . 2.Heath CA, Cooper SA, Murray K et al. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010;67(6):761-770. 3.Jansen GH, Voll CL, Robinson CA et al. First case of variant Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2003;29(13):117-120. 4.Aguzzi A, Calella AM. Prions: protein aggregation and infectious diseases. Physiol Rev 2009;89(4):1105-1152. 5.Prusiner SB. Prions. Proc Natl Acad Sci USA 1998;95(23):13363-13383. 6.Ladogana A, Puopolo M, Croes EA et al. Mortality from Creutzfeldt-Jakob disease and related disorders in Europe, Australia, and Canada. Neurology 2005;64(9):1586-1591. 7.Kovacs GG, Puopolo M, Ladogana A et al. Genet ic prion disease: the EUROCJD experience. Hum Genet 2005;118(2):166-174. 8.Brown P, Brandel JP, Preece M et al. Iatrogenic Creutzfeldt-Jakob disease: The waning of an era. Neurology 2006;67(3):389-393. 9.Bradley R, Collee JG, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 1. Folia Neuropathol 2006;44(2):93-101. 10.Collee JG, Bradley R, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 2. Folia Neuropathol 2006;44(2):102-110. 11.Lefrere JJ, Hewitt P. From mad cows to sensible blood transfusion: the risk of prion transmission by labile blood components in the United Kingdom and in France. Transfusion 2009;49(4):797-812. 12.European Creutzfeldt-Jakob Disease Surveillance Network. vCJD cases worldwide. http://www.eurocjd.ed.ac.uk/surveillance%20data%204.htm. 13.de Marco MF, Linehan J, Gill ON et al. Large- scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain. J Pathol 2010;222(4):380-387. 14.Public Health Agency of Canada. Infection control guidelines: classic Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2002;28S5:1-110. 15.Canadian Food Inspection Agency. BSE in North America. http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml

http://www.phac-aspc.gc.ca/ccdrw-rmtch/2011/ccdrw-rmtcs1011r-eng.php

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Thursday 10th March 2011

At 930pm on Saturday 5^th March 2011 Jonathan Simms aged 26 from Belfast died of vCJD. Jonathan first became ill with vCJD when he was a talented young footballer in 2001.

His devoted family fought a protracted legal battle for Jonathan to be treated with Penstosan Polysulphate (PPS) a controversial drug that is administered into the brain. Jonathan was treated with this drug for over 7 years and it does appear that PPS can slow down the progression of the disease.

Due to the love, dedication of his affectionate family and their 24/7 care Jonathan remained alive for a further 7 years.

Jonathan was a handsome, healthy young man before the onset of the disease, yet another young life and future has been taken by vCJD. Another mother and father, siblings, cousins, aunts, uncles, grandparents, and friends are grieving over the unlawfully killing of another innocent member of the public…..

My thoughts and prayers are with Don his wife and family during this heartbreaking time.
___________

Belfast man with vCJD dies after long battle

Jonathan Simms, a talented footballer, first became unwell in May 2001.

Initially, doctors thought he had multiple sclerosis. But Jonathan's illness was later confirmed as vCJD. He was given just months to live.

After a court battle, the family won the right to use the experimental drug pentosan polysulphate in January 2003.

It had not previously been tested on human beings.

At that time, his father, Don Simms said the decision to give their son the drug was a "calculated risk based on 20 years of science".

The first symptoms that Jonathan suffered were that he became a little clumsy and had problems balancing - classic early signs of the prions that cause vCJD to damage the brain.

Jonathan required intensive care in the latter stages of his illness.

His family ran a campaign from their Highfield estate home for better treatment for victims.

He died at his home in the Highfield estate in west Belfast.

http://www.bbc.co.uk/news/uk-northern-ireland-12667709

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Monday 7th March 2011

Grant Goodwin aged 30 years old from Scotland died of vCJD on 16^th January 2009. Despite a death certificate stating this diagnosis, published papers in The Lancet regarding Grants death and dying of vCJD, the UK Government refuse to put Grant Goodwin down as a statistic on their official case list of definite/probable vCJD victims.

Grants death and dying have been deleted from UK official records and statistics.

Grant was the first officially recognised person to die of vCJD from the MV genotype( 52 percent of the UK population are this geneotype).

His death due to vCJD heralded a new wave of victims and meant that even more people exposed to BSE material could die of vCJD.

Below is a letter from Janet Sneddon Health Protection Team Edinburgh confirming the UK Department of Health and Whitehall’s stance that Grant will never ever be recorded on the official statistics for vCJD. This ‘ international criteria’ does not seem to extend to using and obtaining copious amounts of Grants blood for research into vCJD. This ‘international criteria’ I have found can be manipulated and used at will by various DOH medics to fit their scientific format and policy backed objectivity.

Grant is not the only victim of vCJD who has not appeared on the UK official CJD statistics …..So just how many people have really died of vCJD?

When are the UK public going to be told the real truth about BSE/Vcjd?

And the true numbers of people that have died of this UK man made manufactured disease? 

Dear Mr Goodwin,

Thank you for your further correspondence. I fully sympathise with your concerns, however the Scottish Government has clearly confirmed to you on a number of occasions that we are in no doubt that your son died as a result of vCJD infection. The fact that your son is not officially listed as a ‘probable’ case is because the internationally agreed criteria for this diagnosis has not been met.

I am very sorry I cannot give you the reply that you would like.

Kind regards

Janet Sneddon

Health Protection Team
3ES, St Andrew's House
Regent Road, Edinburgh, EH1 3DG

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Thursday 3rd March 2011

Printed below are two research papers and extracts from other scientists findings and published work.

The first paper discusses the fact that sporadic CJD may be caused by TSEs transmitted from animals. It significantly suggests that:

‘In particular, some data indicate that one of the new atypical BSE agents[5], the L-BSE or BASE agent, may have a similar or higher zoonotic potential than the Classical BSE agent’

This means other more deadly strains of the BSE agent have been and are in circulation which could have infected many more people. Are different strains of the disease responsible for the rising numbers of people developing sporadic CJD? Are many cases of sporadic CJD and vCJD the same disease but presenting differently in the elderly or older adults?

Many experts in prion disease/vCJD believe the tripling of cases of sporadic cjd in the UK and across the globe is not a coincidence and is to do with millions of individuals being exposed to BSE infected material in the food and medicine chain.

The Second paper from Switzerland below examines dramatically rising levels of sporadic cjd in Switzerland over a number of years. The increase in cases cannot be fully explained but many Swiss Scientists have told me that they believe environmental issues such as BSE is to blame.

BSE like any pathogen can and has mutated to other strains each one holding a potential death sentence to human health and life. Are these new strains responsible for young people still dying of vCJD in 2011 and/or responsible for the growing number of middle age and older people dying of sporadic CJD/dementia?. We face a worldwide epidemic of dementia and this expert’s assure me is not just age related.

Or does the development of the disease within humans depend on a specific route ..orally or intravenous through medicines? One expert from Erasmus University stated

‘Swiss CJD could have leapt to humans through the injection of
vaccines or medicines produced using serum made from cows, suggests Cornelia
van Duijn of the European collaborative group on CJD incidence at the
Erasmus University Medical School in Rotterdam, The Netherlands’.

Many other experts continue to discover links between the growing numbers of people with cjd and TSEs. The first paper urges the ongoing systematic monitoring and research into humans and animals regarding TSEs (transmissible spongiform encephalopathy) Yet the Conservative led Government are shutting down farms where animals were being tested/monitored for BSE, have raised the age when UK cattle are being tested for BSE and trying to reduce every piece of funding into areas such TSEs/ BSE and vCJD.

Scientists have told me that factors such as route of infection…either orally or intravenously plus age of individual victims all have an influence on how a patient presents with the disease both physically and within pathology at autopsy. There is a generalised pattern of symptoms for victims of vCJD but this can vary as I can testify having sat, talked filmed and interviewed numerous victims with differing genotypes of vCJD. This variety of ingestion and presentation also affects the pathology of brain material during autopsy. This has resulted in some patients with a dual diagnosis ‘ sporadic cjd with signs of vcjd’…….

I have a data base of clusters of cases of both sporadic and vCJD, and there are just too many of them in the same area to be co incidental. …environmental issues are playing a significant role in rising cases of scjd. ….many of these cases must have been influenced or caused by the same source of BSE infected material.

Before BSE sporadic cjd in the UK was just one in a million people in 2011 ‘one person in 33,000 will now develop sporadic cjd’.

‘Finding the source of the disease has "got to be priority number one for Europe", said Cornelia
van Duijn of the European collaborative group on CJD incidence at the
Erasmus University Medical School in Rotterdam.

Professor John Collinge told BBC1 ‘ Cases of sporadic cjd are rising and what is most worrying with much younger people developing the disease, is it because of better diagnosis? or as I suspect to do with BSE’.

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans

Webnachricht
19 January 2011

The European Food Safety Authority (EFSA) and the European Centre for Disease Prevention and Control (ECDC) have published a joint opinion reviewing the latest available scientific information on possible links between Transmissible Spongiform Encephalopathies (TSEs)[1] in animals and humans. Current epidemiological and laboratory tools and methods for the evaluation of possible association of animal and human TSEs were also critically evaluated.

In the opinion, EFSA and ECDC have undertaken the first comprehensive review of epidemiological and laboratory studies on possible links between TSEs in animals and humans at EU level. The opinion builds on previous work carried out by EFSA on the zoonotic potential of single TSE agents, as well as a considerable number of other scientific studies on prion diseases.

The findings in the opinion confirm that at present the only TSE proven to be zoonotic (i.e. transmissible from animals to humans), remains Classical Bovine Spongiform Encephalopathy (BSE), known in humans as variant Creutzfeldt-Jakob disease (vCJD)[2].

Epidemiological evidence shows that the most common form of TSE in humans is sporadic Creutzfeldt-Jakob disease (sCJD). The cause of sporadic CJD remains uncertain[3]. While scientific research to date has not identified an environmental source of infection[4], the Panel could not exclude the possibility that a small number of cases could be zoonotic.

Regarding Classical scrapie in goats and sheep, no epidemiological evidence suggests it is zoonotic; whereas for Atypical scrapie in sheep and goats, the scientific data currently available are too limited to conclude whether it has the potential to be zoonotic or not.

For other TSEs, a number of uncertainties make it impossible at present to draw definite conclusions on possible links between animals and humans. One of the reasons for this is that data on the monitoring of TSEs in animals are too recent to be compared to the respective human data. The opinion therefore recommends that systematic monitoring of TSE diseases be continued in both humans and animals.

In addition to epidemiological data, the scientists also evaluated evidence obtained from experimental transmission of TSEs in laboratory studies. The opinion states that the results of some of these studies suggest there might be a possibility of animal-to-human transfer for other TSEs, in addition to Classical BSE in cattle. In particular, some data indicate that one of the new atypical BSE agents[5], the L-BSE or BASE agent, may have a similar or higher zoonotic potential than the Classical BSE agent. The opinion however points out that at present it is not possible to define how informative these laboratory studies are for measuring the transfer of TSEs between animals and humans under real exposure conditions.

This joint opinion of EFSA and ECDC provides an overview of the situation in relation to the zoonotic potential of TSEs and may support risk managers in their work on those TSEs which are of major concern for human health.

For media enquiries, please contact:
Ian Palombi, Press Officer or
Steve Pagani, Head of Press Office
Tel: +39 0521 036 149 +39 0521 036 149
Email: Press@efsa.europa.eu

[1] TSEs or so-called prion diseases are a family of diseases that affect the brain and nervous system of humans and animals. These include Classical BSE and Atypical (L-type and H-type) BSE, Classical and Atypical scrapie, Chronic Wasting Disease and Transmissible Mink Encephalopathy.
[2] Creutzfeld-Jakob disease (CJD) is a transmissible spongiform encephalopathy in humans. Various forms of CJD are recognised: of these, sporadic CJD is the most common and its origin is uncertain; variant CJD was identified in the 1990s and is closely linked to exposure – probably through food – to the cattle disease bovine spongiform encephalopathy (BSE).
[3] See also World Health Organization
[4] For example, direct/indirect transmission of the infective agent from animals, micro-organisms, food, water, objects, body fluids or through air inhalation.
[5] Atypical H-type BSE (H-BSE) and Atypical L-type BSE (L-BSE or BASE) agents are two distinct Atypical BSE agents, discovered after 2004.

A case-control study of sporadic Creutzfeldt-Jakob disease in Switzerland:
analysis of potential risk factors with regard to an increased CJD incidence
in the years 2001-2004

Jessica Ruegger?1, Katharina Stoeck?2,3, Lorenz Amsler4,5, Thomas
Blaettler2,6,

Marcel Zwahlen7, Adriano Aguzzi2, Markus Glatzel2,8, Klaus Hess1 and

Tobias Eckert*4,9

Address: 1Department of Neurology, University Hospital Zurich, Zurich,
Switzerland, 2Institute of Neuropathology, University Hospital Zurich,

Zurich, Switzerland, 3Department of Neurology, University Hospital
Hamburg-Eppendorf, Hamburg-Eppendorf, Hamburg, Germany, 4Federal

Office of Public Health, Bern, Switzerland, 5CSL Behring, Bern, Switzerland,
6Bristol-Myers Squibb, Wallingford, CT, USA, 7Institute of Social and

Preventive Medicine, University of Bern, Bern, Switzerland, 8Institute of
Neuropathology, University Hospital Hamburg-Eppendorf, Hamburg-

Eppendorf, Hamburg, Germany and 9Swiss Tropical Institute, Basel,
Switzerland

* Corresponding author ?Equal contributors

Abstract

Background: In 2001, the observed annual mortality from Creutzfeldt-Jakob
disease (CJD) in Switzerland increased from less than 1.5 to 2.6 per million
inhabitants. An underlying cause could not be identified.

Methods: To analyse potential risk factors for sCJD in Switzerland, close
relatives of 69 sCJD-patients and 224 frequency age-matched controls were
interviewed in a case-control study using a standardised questionnaire. 135
potential risk factors including socio-demographics, medical history,
occupation and diet were analysed by logistic regression adjusting for age,
sex and education.

Results: sCJD patients were more likely to have travelled abroad, worked at
an animal laboratory, undergone invasive dental treatment, orthopaedic
surgery, ophthalmologic surgery after 1980, regular GP visits, taken
medication regularly, and consumed kidney. No differences between patients
and controls were found for residency, family history, and exposure to
environmental and other dietary factors.

Conclusion: Although some factors were significantly more frequent among
sCJD-cases, this study did not reveal specific explanations for the
increased incidence of deaths due to sporadic CJD observed in Switzerland
since 2001. Results have to be interpreted with caution due to multiple
testing and possible recall bias in association with a long incubation
period. The most plausible reason for the increase in Swiss sCJD cases after
2000 is an improved case ascertainment. Therefore, underreporting of cases
might well have occurred before the year 2001, and the "real" yearly
incidence of sCJD might not be lower than, but rather above 2 per million
inhabitants.

snip...

The third hypothesis to explain the increase in annual mortality rates from
sCJD in Switzerland between 2001 and 2004 is a better case ascertainment.
Over recent years in Europe, as a general tendency incidences have been
rising, however not to such extent as in Switzerland. Given that our results
do not support strong evidence for the hypotheses of a zoonotic or
iatrogenic cause, ascertainment bias due to a heightened perception and
awareness of the disease in physicians must be regarded as the most likely
cause for the observed increase. One factor that might be jointly
responsible for this increase might be altered reporting requirements in
1999. Since that year all suspected cases in Switzerland had to be reported.
In this respect, also the role of chance must be considered, as it is
possible that the observed increase of Swiss sCJD-deaths was due to random
fluctuation. The rise in annual mortality rate from the years before 2000 to
the period 2001- 2004, however, was statistically significant, and
therefore, chance must be considered a less likely explanation. In the most
recent years, the observed incidence in sCJD deaths (2005: 10; 2006: 13,
2007: 15) dropped to levels just slightly above those before 2000. When
recent incidence data until 2007 are included, however, the rise in the
annual mortality rate after 2001 was still significant. The sudden increase
in 2001 and the slow decrease afterwards are well in line with the media
coverage of the CJD topic in the respective years.

http://www.biomedcentral.com/1471-2458/9/18

Worst-case scenario If BSE is the cause of Swiss sporadic CJD - the
worst-case scenario - researchers have to work out how the cattle disease
can cause two different forms of the human disease: variant CJD in Britain
and elsewhere in Europe, and sporadic CJD in Switzerland.

This could be explained if British and Swiss cattle harboured different
strains of the infectious prion protein - but preliminary experiments
suggest that they are the same.

Alternatively, Swiss CJD could have leapt to humans through the injection of
vaccines or medicines produced using serum made from cows, suggests Cornelia
van Duijn of the European collaborative group on CJD incidence at the
Erasmus University Medical School in Rotterdam, The Netherlands. Finding the
source of the disease has "got to be priority number one for Europe", she
says.

Researchers now hope to establish whether sporadic CJD came from BSE. They
will use 'strain typing': infecting mice with the prions causing the two
diseases and seeing if the symptoms match up. "It's the best way to
establish or exclude any suspected link," says Moira Bruce of the Institute
for Animal Health Neuropathogenesis Unit in Edinburgh, UK. These experiments
will take at least a year.

Imperial College London

References 1.Glatzel, M. et al. Sharply increased Creutzfeld-Jakob disease
mortality in Switzerland. Lancet 360, 139 - 141 (2002). | Article | ISI |

---

Monday 28th February 2011

Here is a photo of me outside The Tower of London. During a recent stay in central London it brought back many lovely memories of laughing and having fun with my Andrew and Emma during happier times when my only son was healthy, handsome and with the beginnings of a wonderful career in the media. We spent many hours having coffee, walking along the Thames, sharing meals and talking about Andrews hopes for the future. During a windy and typical English February day as I watched other young men walk across Tower Bridge on their way to work or to meetings, designer dressed and looking forward to their future I remembered my son and how much he loved London life and all it had to offer.

I miss Andrew so much……

---

Wednesday 23rd February 2011

In October last year a study was published regarding tonsils tested for vCJD. All of these tonsils had been retrieved from people born between 1961-1985…many of those dying of vCJD in 2010 and 2011 were born after these dates. Why were tonsils not tested from younger patients? BSE infected material was in the food and medicine chain to at least 1997, cattle in the UK are still not free of BSE.  

Many world experts have told me that vCJD cannot be detected in tonsils in some people until they are very very ill almost at the point of death. A handful of victims of vCJD from France had tonsil biopsies that came back negative, despite all three being seriously ill with symptoms of the disease and eventually dying of vCJD. One Canadian Scientists told me ‘We know that primates used in experiments don’t show the rogue prions in their tonsils and that many humans are also the same.’

My Andrew had a tonsil biopsy just a few months before he died and it proved positive but I was told by experts that if Andrews tonsils had been tested just a short time previously they may well have been negative. So what is the point of this  study?

Finding one positive result is very worrying out of 9,160 tonsils tested but what is of greater concern is the continued manipulation of research and screening by the DOH and its scientists to undertake research that falsely reassures the public. Hundreds of thousands of pounds of funding is being poured into research that Whitehall knows are blind alleys or will reflect low incidences of vCJD. 

The DOH and Whitehall are using  UK scientists to look in areas where there will be least to find….One top Neurologist told me…’.Testing tonsils is not going to give us a clear idea, it gives the public the wrong reassurance. Rogue prions that cause vCJD don’t always show in this tissue, it’s the spleen and other places we should be testing. Every Spleen removed and every cadaver at post mortem should be tested for vCJD. Then the results would be alarmingly different’

I disagree with the numbers of victims of vCJD stated in the report below I have sat talked and interviewed victims who later died of vCJD and yet these individuals have never appeared on Uk Government statistics. In recorded interviews many families who have lost a loved one to sporadic CJD have also  told me of their grave doubts regarding diagnosis, convinced their loved one died because of BSE, these families have been intmidated and threatened. These families have given me information and evidence which support their concerns.  I believe many many more people have died of vCJD but these deaths are bering pushed under the umbrella of dementia, sCJD or some other less controversial neurological disease. 
'Possible' vCJD cases, and those with dual diagnosis ' possible vCJD/sCJD' are also not included in UK statistics for vCJD. Many 'unknown neuro degenerative? ' illnesses are affecting more and more people within the UK and globally.   More and more young people are also developing brain diseases which experts seem unable or reluctant to pinpoint or give an actual cause or clear diagnosis.

Why were UK Paediatric Consultants asked to monitor children under the age of 16 for vCJD? Many of these babies/ children were born years after the SBO ban and apparent exlusion of MRM in the food chain. Yet tonsils were only tested from much older individuals? This study of babies, infants and children below the age of 16 years was so secret and controversial that it was only carried out over a few years. During this study over 90 children died within a short time from illnesses that had similar symptoms to vCJD but these 90 plus children were given no clear diagnosis as to what killed them? Top paediatric nurses and other medical professionals involved in the care of children tell me they were not informed or aware of this study that was being conducted by the Consultants.Why were only Consultants involved in this research? Why were other members of staff  who had day to day contact with these children and their parents kept out of the loop?  How many children and indivduals have really died of vCJD?

As Anne Milton Secretary of Health in the UK replied in Parliament, July 2010 .' The Incubation periood of vCJD may vary due to factors such as route of transmission.'

One expert  in prion disease told me ‘ BSE material in the human food and medicine chain may well make certain individuals vulnerable to all sorts of brain problems and disease and our babies and children received the most toxic BSE material when they were most vulnerable, these illnesses would be a direct result of ingestion of toxic BSE material......in other words vCJD’…….

Once again the Whitehall and it corrupt officials are using their influence to manipulate and hide the ticking health time bomb that is vCJD.

'Large scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain'
Full study here - http://onlinelibrary.wiley.com/doi/10.1002/path.2767/full

http://www.medicalnewstoday.com/articles/203396.php

Study Results Are Consistent With Earlier Estimates Of VCJD Prion Prevalence In Britain

Main Category: CJD / vCJD / Mad Cow Disease
Article Date: 04 Oct 2010 - 4:00 PDT

The Health Protection Agency (HPA) and the UCL Institute of Neurology have conducted a sensitive examination of tonsil specimens to detect the presence of the variant Creutzfeldt-Jakob Disease (vCJD) related prion protein, and found results that are consistent with earlier estimates of vCJD prion prevalence in Britain. The findings are published today in The Journal of Pathology.

This study involved using immunohistochemistry to examine 9,160 anonymised tonsils for the presence of abnormal prions and found one sample showing evidence of prions associated with vCJD.

Study author Dr Jonathan Clewley, a HPA expert on vCJD, said: "We have used a sensitive test and the result is consistent with findings of earlier studies.

"The HPA will continue its research alongside the UCL Institute of Neurology and the Veterinary Laboratories Agency, to look at appendices by immunohistochemistry, in order to give greater confidence and accuracy to prevalence estimates of vCJD prions."

The anonymised tonsils used in this study were obtained from earlier studies - they had been removed from patients for clinical reasons and would otherwise have been discarded. Tonsils are one of a number of body tissues known to harbour abnormal prions in people who carry vCJD - other tissues where these prions can be found include the appendix.

Lead author Professor Sebastian Brandner, from the UCL Institute of Neurology, said: "Prevalence studies such as this are vitally important as they enable us to estimate the prevalence of vCJD in the population. However, it is important to understand that we do not know how good these tests are at picking up infected individuals and so the results may be an underestimate.

"They also give an indication as to the number of cases to expect in the future and the potential impact for the health service. Prion diseases can have long incubation periods, and an understanding of prevalence can help researchers devise measures to prevent further transmission of the disease."

There have been 220 clinically confirmed cases of vCJD worldwide, with the UK being most affected with 173 people having developed the disease, as a result of the epidemic of bovine spongiform encephalopathy in cattle in the 1980s. Large scale vCJD prion prevalence studies are challenging at present as there is no valid test available to screen for the vCJD prion in blood.

Notes

1) The findings were published in The Journal of Pathology, in a paper entitled 'Large scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain', Fernandez de Marco, Linehan J, Gill O, Clewley J, Brandner S. The Journal of Pathology 2010; 222: DOI: 10.1002/path.2767.

2) 'The Journal of Pathology, published by John Wiley & Sons Ltd on behalf of the Pathological Society, can be accessed online here. To access this article free of charge visit here.

3) The tonsil study used anonymised tonsils from patients in the 1961 to 1985 birth cohort.
4) Previous prevalence studies have included a 2004 study on appendices: Hilton DA, Ghani AC, Conyers L et al 'Prevalence of lymphoreticular prion protein accumulation in UK tissue samples'. The Journal of Pathology 2004; 203: 733-739, and a 2009 study by the Health Protection Agency which involved testing 63,007 tonsils - 'Prevalence of disease related prion protein in anonymous tonsil specimens in Britain: cross sectional opportunistic survey'. British Medical Journal; 338: 1442-1448

Source:
Health Protection Agency

---

Thursday 17th February 2011

BLOOD TEST FOR VCJD

(photo with blog of Peter Buckland who lost his son Mark aged 32 (2006)to vCJD through a contaminated blood transfusion, given by a blood donor that went on to die of vCJD)

Below is just one of the many articles that hit the headlines regarding the vCJD blood test developed by British scientist’s. I am glad this test is now out in the open but as

I have already stated on this blog/website, during several media interviews and in a letter to UK Prime Minister David Cameron on 12^th November 2010, this test is not new and has been used secretly by the DOH behind closed doors over a long period of time.

Scientists and experts in prion disease confirmed this to me during long recorded interviews many months ago that this ‘new’ blood test had and was being currently used on individuals over an extended period of months and years.

These world experts also informed me that the technology to screen our blood supply for vCJD is there, but various Ministers, committees, government departments and Whitehall cronies are doing their up-most to prevent this happening as its feared a ‘can of worms’ would be opened. This unforgivable delay is not about protecting the UK publics health and wellbeing but about protecting those responsible for this crisis in our blood supply.

Blood contaminated with vCJD has the potential for an epidemic of biblical proportions especially as we know of ‘carrier blood donors’ who remain well but can pass on vCJD through their donated blood. There are many ‘carrier blood donors’ some who have given blood for over 20 years who remain well but are implicated in giving blood to individuals who have died of vCJD. 2.4 million people give blood in the UK, they all need to be screened for vCJD. Each donation of blood can be used in a multiple manner and has the ability to infect tens possibly hundreds of people as components of blood donations can also be used in the process /preparation of vaccines.

Some reports stated that a blood screening test will be feasible within 18months, its now essential that the Department of Health stick to that and that we the UK public put pressure on for this test to be implemented ASAP.

There are arguments put forward by various government bodies see HPA (health protection agency’s statement below) that a screening test for vCJD may stop people donating blood, we already face a world shortage of blood because so many people are excluded because of exposure to BSE, so this test would open up the possibility for more people who are currently excluded to give blood safely.

See this email I received from Betty in the USA…

‘In Oregon, I was informed that I'm no longer a suitable blood donor - after 20 years of giving blood annually. Why - because I lived in the UK for two years in the nineties during the mad cow outbreak... I feel I'm "clean" but I prefer to have these strict standards to protect the public. We can't be too sure......i would recommend everybody with any association with CJD to refrain from donating blood.’ Betty USA

There are other challenges for example should blood donors be screened anonymously for vCJD? I would suggest from my discussion with experts that in many areas this is already happening…

There are other arguments that as vCJD is currently ‘terminal with no hope of survival’ that is would be wrong to give this death sentence to an individual, but when the first HIV/Aids test was developed and used the prognosis was very very poor. Because of the HIV test nowadays many many people with HIV live long and fulfilling lives due to treatments pushed forward because of the aids test. A blood screening test for vCJD would radically help potential victims/victims and would push forward new treatments. Research into cures and medication to treat vCJD would be prioritised once a screening test for our blood supply was assured.

Having seen my only son die horrifically from Vcjd, I don’t want any more people to die needlessly of vCJD and until our blood supply is screened for the rogue proins that cause vCJD……more innocent people will die.....

The clock is ticking and I wonder just how long it will be before a blood screening test for donated blood is implemented in the UK…..?.Even though we now have the technology …….. I fear for all the wrong reasons it could be years…….

Christine Lord 17^th February 2011 Portsmouth UK.

BBC NEWS

3 February 2011 Last updated at 01:22

Blood test for vCJD 'could identify carriers'

By Sonya McGilchrist BBC News health reporter

A blood test for variant CJD has been developed by British scientists.

Currently patients suspected of having the human form of BSE have to undergo a series of tests, including a brain biopsy, to confirm a diagnosis.

The new test, reported in The Lancet, offers the chance of earlier diagnosis and potentially the ability to screen donor blood.

But further studies are needed before it can be widely used to screen healthy people who may be silent carriers.

Variant CJD or vCJD is the human form of BSE - "mad cow" disease. It affects the brain and is believed to have passed from cattle to humans through infected food.

A previous study suggested one in 4,000 Britons could be incubating the incurable degenerative disorder without symptoms.

CJD causes the brain to develop a spongy texture known as spongiform encephalopathy.

Early symptoms include anxiety, depression and tingling pains. Doctors often do not realise that a patient has the brain condition until other features occur, such as difficulty with movement, or loss of mental abilities.

At present, there is no treatment for variant CJD and the diagnosis is often made when patients are terminally ill.

The new test was tried on 190 blood samples, of which 21 had variant CJD. The test picked up 15 of the samples with variant CJD - a 71% success rate.

It did not produce any "false positives" - showing that someone had CJD, when they did not.

Early diagnosis

Professor John Collinge of the Medical Research Council is one of the doctors involved in the research. He said that he would begin using the new test on patients in his clinic straight away.

He said: "An earlier diagnosis will give patients and their families more time to plan what they would like to do in the time left available to them."

Professor Collinge is currently working on research to treat the disease with antibodies.

He told the BBC that the first clinical studies involving patients could be carried out as early as next year.

A test that provides an early diagnosis will become even more significant if treatments for the disease become available.

The development was welcomed by Peter Mills, whose daughter Holly was diagnosed with variant CJD in 2003.

He described the test as milestone, saying: "This lifts us into the next stage and takes us to a position of hope. It gives us great confidence that therapies to treat the disease are a realistic prospect - but this test has to come first."

Silent carriers

The new test could provide more information on how many people have variant CJD and be used to screen for the disease.

However, further large scale studies on populations where the disease is not present would be needed before it could be used as a screening test.

The lead author of the research, Dr Graham Jackson of the Medical Research Council's Prion Unit, said: "This test could potentially go on to allow blood services to screen the population for vCJD infection, assess how many people in the UK are silent carriers and prevent onward transmission of the disease."

Patients and their families can find out more about the new development by looking at the National Prion Clinic website.

Chris James, from the Haemophilia Society said they would push for the test to be used as soon as it is clinically available: "The Haemophilia Society has long called for tests to be offered, in combination with pre and post-test counselling, to people with bleeding disorders who have been told they are at risk for public health purposes in relation to vCJD."

Health Protection Agency response to blood test for vCJD

Consultation on a new vCJD test for blood donors

The Health Protection Agency commissioned, on behalf of the Department of Health, a consultation to look at the social and ethical implications of a blood test for variant CJD. There is currently no blood test to detect vCJD infection in people who appear to be well. Such tests may soon be developed, and this consultation aimed to seek views about how these tests for vCJD could be used once they become available.

A vCJD test could be used to screen blood donors, allowing the blood services to prevent blood from people with positive tests from being given to patients. The consultation explored some questions and concerns about introducing a blood test, including:

1. Should a test for vCJD be introduced when it is not known whether people with positive test results would ever develop symptoms of vCJD, and if they would, how long this would take?

2. Should the UK blood services always tell donors if their vCJD tests are positive? And how should donors' GPs be involved?

                    3. If donors knew that they would be tested for vCJD, and that they would be told if they tested positive for vCJD, would they be put off giving blood?

---

Friday 11th February 2011

This blog is a forum for the truth, fact, justice and also for victims and family members who have lost loved ones to vCJD, as well as supporters to post their experiences.

Below is an open letter written by June Richer who lost her youngest daughter Kate aged 22 years to vCJD. Kate was a graduate at Glasgow University a talented musician and deeply religious. She was a beautiful bubbly girl who died horrifically aged 22 years old.

Her dad, Derek told me ‘Every day we remember our Kate and how she suffered, every day we wonder ‘what would our Kate be doing now?’ the loss will continue till we die and we can never forget Kate’s death was so avoidable, and those responsible have never been made accountable’. June Richer wrote a personal letter to the Prime Minister which was delivered to David Cameron on 12^th November 2010 as part of International CJD day, this heartbroken mother never ever received an acknowledgement or respectful reply.

Photos attached are of June and Derek Richer taken at their home this week. The other photo is of Kate taken in her first year at Glasgow University and the other photo just a short time later Kate (centre) already poorly with vCJD being held by her sister Mandy (right) and Liz.

‘TO OUR BEAUTIFUL DAUGHTER KATE ‘.

February 8th 1979- February 18^th 2001

‘Remembering the happy, joyful day you were born and the tragic, sad one when you were taken from us after 8 months of terrible suffering from vCJD.

How can we have lived 10 long years without you? ..Our sweetheart………

When we all miss and love you so much…..the family and your Dad and I would give everything to have you back alive and healthy with us again.

Your sisters and brother are all getting older and their little ones are all grown up, Kate you would have had such fun with them…our darling Kate.…..

We all send our love and kisses, always, forever safe in our hearts and minds and never far away…God Bless our precious one…..

Kate I hope you like this poem I wrote it for you ages ago, it comes with all my love Mum x

KATE’S PARTY

Now you are in heaven child,

We often sit and think,

Do you play your music there?

Like you always did.

And do they like your music?

Do they clap and cheer?

And when you make them laugh in heaven,

We wish that we were there.

And when you start to dance in heaven,

Do they all join in?

We like to think you’re happy there?

You loved to dance and sing.

And when the party’s over

And your friends all gather near.

Do they hug and hold you close?

Just like us, when you were here.

Precious memories not just of our Kate but all our young ones lost to vCJD who so loved their music……….June and Derek Richer, Gosport, Hampshire, UK. February 2011

---

Monday 7th February 2011

http://www.youtube.com/watch?v=4e1hHzQ7zdc&feature=player_profilepage

Here is the link to one of the many press interviews myself and other families and individuals who have been affected by vCJD gave to the media. This was in response to the fan fare of scientific back slapping from the Department of Health regarding the ‘new screening test for vCJD’ Below is the petition I sent to David Cameron on 12^th November 2010 in which I challenge the fact this test and blood screening tests have been used secretly by the department of health and its officials for some time. The UK Prime Minister and his government has failed to reply to this petition and personal letters sent to David Cameron urging for mass screening of blood to take place ASAP. The news released about the screening test for vCJD means little comfort for the health and safety of the UK population. The blood supply remains unsafe and not screened for vCJD and potentially thousands of ‘silent carriers’ donate blood every day across the UK .

All UK blood bags and components continue and will continue to carry the warning and disclaimer ‘RISK OF ADVERSE REACTION INFECTION INCLUDING VCJD’.

When are the Department of Health going to implement a blood screening test? They have the technology top scientists who work in this field have told me during recorded interviews that the technology is there to mass screen blood donors and donated blood.

Meanwhile the DOH and Whitehall delay and more innocent people will die of vCJD…via contaminated blood……….

http://www.youtube.com/watch?v=4e1hHzQ7zdc&feature=player_profilepage

______________

Ms Christine Lord, 2 Wilton Terrace, Southsea.
Portsmouth, Hampshire. P05 2BQ UK

Mschristinelord@aol.com     www.justiceforandy.com

12^TH November 2010

Dear Prime Minister,

JUSTICE ACCOUNTABILITY, RESPONSIBILITY FOR VICTIMS OF VCJD 
PREVENTION OF FUTURE AND FURTHER DEATHS OF VCJD THROUGH BLOOD SUPPLY/PRODUCTS
INTERNATIONAL CJD DAY

PETITION:

We want justice for all victims of vCJD here in the UK and across our global community. Today on International CJD day we represent not only people in the UK but our global family, whose representatives from the Jewish, Muslim, Christian, Buddhist, Sikh, Hindu and multi faith communities and cultures across the UK and globally have formed an alliance, all of these communities have been affected by vCJD. We demand accountability, responsibility and justice. We also want your help to prevent further and future deaths of vCJD through blood contamination.

The current Coalition Government must put clear blue water between the Conservative Party of the 1980s, 1990s, its policies and ministers which are culpable. .

We understand with your close connections to Margaret Thatcher, Kenneth Clarke and the fact that Peter Gummer head of Huntsworth (brother of John Gummer) is also a fund raiser for your political party and President of your constituency party, that independence may be difficult. We are asking you as Prime Minister to put these allegiances to one side and to let the truth shine through…..

We need answers, transparency and action:

Why is the true number of cases of vCJD not being recorded correctly on government statistics? Why have cases of sCJD (sporadic) tripled since BSE entered the food chain?

Why is the Phillips Inquiry allowed to be used by culpable officials and ministers as their ‘GET OUT OF JAIL FREE CARD’? How can the Phillips Inquiry be independent and true when it was staged by the very people it was supposed to investigate?

If the SBO Specified Bovine Offal ban in 1989 removed the threat of BSE from human consumption why do young people in their late teens early twenties continue to die of vCJD 2010?

Why are treatments that can prolong life and developments of treatments being stalled, blocked and withheld from victims of CJD? Why do the Government want victims to die rapidly without interventions?

Experts predict hundreds of deaths from vCJD in the coming years, especially from the most common genotype MV (52 per cent of population), most blood donors come from this group what is the Prime Minister doing about protecting our blood supply…..now??

One of the current victims of vCJD is dying due to a blood transfusion received in 2003

Their blood had been lecudepleted (filtered). Filtering does not work, its not a safe and costs millions. Yet blood screening tests are being repeatedly blocked by Whitehall… is it because the Government and DOH do not want to know prevalence of vCJD in the UK population? Top Scientists estimate’ One in a thousand of the population is probably carrying Vcjd’ John Collinge BBC1 May 2008

Currently a diagnostic and screening test is being used secretly by the DOH why isn’t this public and available to families who have been affected by vCJD and the wider population?

I hope as Prime Minister, as a parent and father, you can help the campaign and families who have been affected by vCJD to get the resolution they now seek, and to help us keep other families free from the heartbreak we live with every minute of the day, knowing our loved ones need not have died.

Yours sincerely,

Christine Lord (mother of Andrew)

Justice for all victims of vCJD, and on behalf of all families across the UK and globally.

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Thursday 3rd February 2011

It has been reported in the media and scientific world that there is now a screening test for vCJD. I have been involved in various interviews regarding this ‘breakthrough’.

This has been written during another sleepless night tormented by memories of my sons terrible death. These are my heartfelt feelings and personal experiences about this’ scientific discovery which I know is not that new as a screening and diagnostic blood test has been used secretly for a while by the Department of Health.. I petitioned David Cameron on 12^th November 2010 challenging him as why a test was available but was not being used to protect the publics health, so far I have received no acknowledgement or reply.

Medics instructed by Whitehall have been taking blood from victims of vCJD for a few years to measure levels of rogue prions in their blood. I was also told several months ago by a top research scientist that ‘ We already have a diagnostic and blood screening test for vCJD’

The real heroes behind this research are the victims and families who have allowed their loved ones to provide the much needed samples.

Donated blood could have been screened earlier, which means more innocent people will die needlessly…I just hope this fanfare of news and scientific back slapping results in a blood screening test this year and is not another case of delay, delay, block and delay.

Every day and week that passes where blood is not screened for vCJD means further unnecessary deaths. Since Andrew’s death myself and other bereaved families have been pushing for donated blood and organs to be screened for vCJD. We have been treated appallingly by Whitehall officials and department of health.

The cynic in me is watching and waiting to see when this test will be available to the public? , when will all donated blood screened?, who is in charge of collating the results and will they be revealed to the public and if given a choice individuals?

We face a lethal ticking health time bomb through secondary infection of vCJD via blood. Mad cows disease continues to kill people on a regular basis in 2011, I know because I sit, interview, film and photograph these ongoing UK victims some as young as 20 years old. Dozens of blood donors have died of vCJD

As a heartbroken mum, freelance journalist, I continue to investigate the corruption and lies that have exposed millions of us to mad cows disease.

My only son Andrew ‘Andy ‘Black died of vCJD. Handsome, talented, articulate, producer, researcher for Talk SPORT, BBC, ITV he had a wonderful life and career ahead of him. His death was horrific and unlawful, within months he was blind. deaf, quadriplegic and unable to recognise his family.

I welcome the developments of a screening tests for vCJD., and am in contact with microbiologist Atarashi from Nagasaki University, Japan. Since Andrews’s death I have pushed for all blood donors to be screened for vCJD, currently our blood is not safe or free of the horrific brain wasting disease.

I continue to battle the establishment and those responsible for BSE/vCJD asking for transparency and truth, I have been threatened, bullied, intimidated by Whitehall officials and Ministers.. …

Everyone over 13 has eaten at least 50 BSE infected meals and been exposed to its lethal man made pathogen vCJD, even strict veggies have died of the horrific brain wasting disease.

Everyone who has lived worked or traveled to this country since 1980 for more than a few months is unable to donate blood abroad as we are all considered ‘ at risk of developing vCJD’. All blood bags and components since July 2007 carry the warning ‘RISK OF ADVERSE REACTION INFECTION INCLUDING VCJD’

2.5 million People in the UK donate blood; experts believe ‘One in a thousand of the UK population could be carrying vCJD’(Professor John Collinge May 2008 BBC1)

People can silently carry the human form of BSE never fall ill but have the ability to pass on vCJD through blood. Several companies have developed tests over the years but the Department of Health continue to block their implementation in the UK and the advancements of treatments. Whitehall do not want to the public to know the true prevalence of vCJD in the population or for the exact source of the infectious material to be traced.

The UK Department of Health are aware of these ‘ asymptomatic individuals, and have collated data and details, one ‘asymptomatic donor’ who gave blood for over 20 years remains healthy but two of their recipients have died of vCJD.

Another group of victims highlights the terrifying scenarios that we face regarding blood safety. Stephen Lunt victim of vCJD received blood after a car accident; he then became a blood donor . One of his donations infected a young guy aged 32 who also died of Vcjd through Stephens contaminated blood. . What happened to Manchester resident Stephen Lunt’s original donor? Has that donor ever been traced? been prevented from donating more blood? Is this original blood donor still alive and well? How many other people received blood from the initial donor?

During a lifetime of giving blood donors have the ability to save hundreds of lives but without screening for vCJD they could also put hundreds of lives at risk. vCJD can have an incubation period of decades. Donated blood is used in many medicinal products including vaccines. Two victims of vCJD from Southampton died within months of each other after receiving polio vaccines from the same batch, at the same time.

One of the current victims of vCJD is dying due to a blood transfusion she received for a back operation in 2003, from a hospital in Southern England. Apparently this victims blood donor remains healthy and has not developed the disease.

When my Andrew was dying he asked me ‘Find out out who did this to me mum’ and always thinking of others said ‘This must never happen again’. I continue to honour the promises I made to my dying son and despite threats and the most appalling treatment by Whitehall officials continue to uncover the truth.

If you want to see the true horror of my sons last days check out the home page on www.justice4andy.com, click the link at the bottom of the page to watch the BBC1 documentary I helped to produce and film about my Andy. I am currently writing a book about the cover-ups and lies that led to Andrews’s untimely death

Giving blood or donated organs is a wonderful gift but we must be sure that it preserves life and that all blood donors are screened for vCJD.

.Help me to keep your families safe to get to the truth and in doing so protect the health and well being of you the public….it wont bring my Andrew back but would be a fitting tribute to my beautiful boy… Thank you Christine Lord Portsmouth UK.

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