In 2007 my beloved son Andrew Black was unlawfully killed by
VCJD/Human BSE, know as the human form of mad cow disease.
He was just 24 years old. Since his untimely and avloidable
death I created a campaign to find out why my Andrew died
and who is responsible. Food and medicines should be safe and never kill.
This is my blog containing the history of my investigations, facts and information the UK
government have tried to supress. It is the history of my ongoing investigations, and how
millions of us remain at risk of developing Human BSE. The disease has not gone away
and continues to kill people and animals globally in 2017.
CHRISTINE’S DIARY AND BLOG
Tuesday 9th October 2018
Pioneering new treatment for Sporadic cjd what about Human BSE vairant CJD? 1 in 2,000 of the UK population now ‘ carry or incubate the human form of mad cows disease’.
This is a huge breakthrough but, how many cases of sporadic cjd are really vcjd HUman BSE anyway?
Pioneering treatment for CJD to be given to a UCLH patient
CJD is a rare but devastating disease that causes brain damage and for which there is currently no treatment. It is always fatal and most patients sadly die within six weeks of diagnosis.
Researchers at the Medical Research Council (MRC) Prion Unit at University College London (UCL) have developed an antibody, called PRN100, for treating CJD. Laboratory testing of the antibody has been encouraging but it has not yet been used in patients.
UCLH is set to give the antibody to a patient for the first time in the world after a judge in the Court of Protection today confirmed that it is lawful and in the patient’s best interests to receive the unlicensed treatment.
UCLH’s chief executive Professor Marcel Levi said: “Creutzfeldt-Jakob disease (CJD) is a rare and cruel disease which rapidly destroys the brain, affecting memory, thinking, speech, balance, movement and behaviour.
“There is currently no cure or treatment for CJD. At present, caring for patients with CJD involves trying to use medicines to alleviate symptoms only but sadly, the disease always results in the rapid death of the patient.
“The court’s confirmation today is an important step forward in tackling this devastating illness.”
Professor Levi added: “UCLH is an innovative healthcare institution committed to ensuring our patients have access to the most cutting edge treatments available.”
Sporadic CJD, the most common form of the disease in humans, is caused when healthy proteins which exist normally in the human body become spontaneously misshapen and build up in the brain. These misshapen proteins, which are called prions, stick to other healthy proteins causing them to become misshapen too and the disease spreads through the brain.
Our immune system produces antibodies to fight infections which invade the body. However, as abnormal prions are made of one of the body’s own proteins, our immune system does not make antibodies to fight them.
Professor John Collinge, director of the MRC Prion Unit at UCL, who led the development of the PRN100 treatment, said: “The treatment is an artificially manufactured antibody which has been created in the laboratory.
“The antibody has been designed to bind tightly to normal proteins in the brain. The aim is to prevent abnormal prions from being able to attach themselves to healthy proteins, meaning that they cannot grow and cause devastation throughout the brain.
“As this is the first time this treatment has been used in humans we cannot predict what the outcome will be but laboratory testing has shown the potential to treat prion infection. A key issue will be whether a sufficient quantity of the drug is able to cross the blood brain barrier to reach the brain tissue where it needs to work.
“We will proceed with extreme caution in very tightly controlled conditions. A team of experts from a range of disciplines will make collective decisions in the best interests of the patient.”
The patient and their family expressed their wish to receive this treatment and supported UCLH’s court application.
The patient will initially receive the treatment by a drip into a vein in the arm. They will be monitored around the clock by a team of experts from UCLH.
We are preparing for a range of possible outcomes including the treatment having no measurable effect and the treatment slowing or halting the progression of the disease. The treatment is not expected to reverse any brain damage that has already occurred.
The patient may also experience side effects which could lead the clinical team to limit or halt the doses of the treatment given.
In order to provide this treatment to a patient, UCLH created an oversight group, independent of the MRC Prion Unit and treating clinicians. The group comprises world-leading experts from a range of disciplines and it has met regularly with lawyers and patient advocates from the charity Cure CJD Campaign. The group considered the numerous and complex clinical, safety, legal and ethical issues arising from the potential use of this unlicensed treatment for CJD.
We will await the response of the first patient to this treatment before we consider a second patient.
A Q&A about this treatment
For further information please visit our frequently asked questions section on Prion diseases and Creutzfeldt-Jakob disease (CJD) on our website.
Patient advocate: Colin Beatty, Cure CJD Campaign charity
Colin Beatty lost his wife, Annie (pictured right), to sporadic CJD in 2010. Annie was 70-years-old and the couple had been married for 40 years.
“The diagnosis was devastating. It was like a bomb had gone off in our family,” said Colin.
“Annie was a former nurse so she knew what CJD meant and she was very frightened.
“It was a very difficult time. We cried many tears but I felt like it was my job to keep the family strong.”
Colin, 75, from Dorset, said the illness made Annie vacant in the beginning. Then her speech became muddled and she would wander off without warning, which he said was terrifying.
“It was heartbreaking to watch Annie deteriorate.
“I nursed her at home initially but she became very difficult to care for so we had to admit her to a nursing home.”
Colin said if the PRN100 antibody had been available at the time, he would have wanted Annie to have had the opportunity to be treated with it.
“It’s true that the treatment carries potential risks, and the benefits are not yet certain, but without it, there is no hope. The only certainty with CJD is death.
“For us, the decision about whether or not to have the treatment would’ve been a no brainer.”
Following Annie’s death, Colin became involved with the Cure CJD Campaign charity. He has represented the charity on UCLH’s PRN100 oversight committee.
“I got to know the team at UCLH’s National Prion Clinic very well when Annie was ill.
“Since we lost Annie, I have been committed to helping the team find a cure for this terrible disease.
“I don’t want other people to experience what we went through.”
Colin and Annie met in 1967 while they were working on a cruise ship which travelled between New York and Bermuda. Annie was the ship’s nursing sister and Colin was an electrical engineer.
“I was besotted with Annie. She later told me that as soon as she saw me, she knew I was the man she wanted to marry.
“She was a bubbly, popular person who was always laughing.
“She was a wonderful and supportive wife. We did everything together – we were so close as a couple and as a family.”
Colin and Annie have two sons, Chris and Nick, and four granddaughters.
FRIDAY 21st September 2018
Mad cow disease/BSE found in USA, Florida herd. The USA has dropped its budget for BSE testing its 94 million cattle to just 20k a year.
Yet this animal with such minimal testing was found with BSE? See details of press release below 29th August 2018.
How many thousands of other cattle have BSE and are being allowed into the human food chain? As this particular infected animal was bought and sold several times, its impossible for the authorities to check its parents, siblings and other members of the herd that are probably also carrying/incubating the deadly brain wasting disease BSE. Those animals will already have gone to slaughter and entered the human food chain and will now be sitting on supermarkets/shops shelves across the US and abroad.
How many more innocent people will die at the altar of greed and corruption that is big business, government and the food and pharmaceutical industries?
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection
USDA Animal and Plant Health Inspection Service sent this bulletin at 08/29/2018 10:00 AM EDT
Sunday 2nd September 2018
Today would have been my son Andrew’s birthday.
I will never again buy Andrew a birthday card declaring:
‘Happy Birthday Son!’
i will never be able to wish my son a ‘Happy Birthday’ ever again. I walk past the cards in gift shops with the words ‘ SON’ splashed all over their covers featuring cars, champagne, flowers. Multiple gifts arrayed depicting the wonders of a precious son’s ‘Birth Date’.
Inside I cry for all those seconds, minutes, days, weeks, months and years my son has lost. All the
‘Happy Birthday Son!’ cards I will never buy, give or share with my Andrew ever again.
The cakes I will not bake, buy and the gifts I will never choose.
There are no ‘birthday celebrations’ today, instead I will walk with Emma my daugher and Andrew’s younger sister to his graveside and put two bunches of flowers on top of the earth where he now lies.
This is the reality of loosing a child and loved one to Human BSE a needless, avoidable and unlawul death. So many lives lost and continue to be taken by Human BSE, a UK man made manufactured disease.
In the last week of August another cow has be reported with BSE in Florida, USA, how many other cows, domestic animals continue to get into the food chain, how many more people like my Andrew will die?
Andrew (first left) with friends celebrating 2006
he was already starting to show symtoms of human BSE
Wednesday 22nd August 2018
The NEW SCIENTIST DISCUSSES A victim aged 36 years old, who became ill with vcjd in 2014 and how this unidentifed man was from the MV genetype. Its dismisses the death of Grant Goodwin in 2009 who was also MV and died of vcjd. Despite the UK govenment scientists and Professor John Collinge and the Tax payer funded CJD unit writing to the Goodwin family declaring that their son Grant had died aged 30 years old of vcjd and was from the MV gene group.
The Goodwins were warned by govenrment agencies not to speak to me as a member of the press and not to speak out about their son Grant’s diagnosis.
Grant Goodwin from Glasgow Scotland died of vcjd aged 30 MV genegroup
FRIDAY 17TH AUGUST 2018
My article about on-going grief was published online and in print in the Daily Mail.
Friends who cross the road to avoid you because you’ve lost a child: Grieving mother tells of her pain when sympathy ran out as people decided she should ‘move on’
Christine Lord’s son Andrew, died from Variant CJD ten years ago at age 24
She says people feel awkward and cringe when she talks about him
She says it seems there is a time limit on grief and people choose to avoid her
Christine experienced crushing isolation when she most needed unity
Father-of-five John, experienced odd reactions after his daughter Felicity died
He claims the atmosphere changed if he mentioned her even in passing
One counselor says bereaved parents feel expected to forget their child
By CHRISTINE LORD and KATHRYN KNIGHT FOR THE DAILY MAIL
On a recent holiday, a friendly couple sitting at the next breakfast table regaled me with stories of their grandchildren.
‘Do you have children?’ one asked. It’s a natural question, and one I expected — and, as always, I gave the only answer I could.
I told them I have a 28-year-old daughter and a son, who would have been 34. ‘Sadly, he died ten years ago,’ I added.
Then the conversation ground to an uncomfortable halt — and it wasn’t long before the couple left.
Andrew at School aged 6 years old
I should be used to it by now; since my beloved son Andrew passed away, I have learned just how deeply our society struggles to confront the reality of parental loss. Andrew was just 24 when, in 2007, his life was claimed by Variant CJD, the human form of what is colloquially known as mad cow disease.
Christine Lord (pictured right) revealed the struggles of coping with grief after the death of her son Andrew (pictured left) who died from Variant CJD at age 24 +4
Christine Lord (pictured right) revealed the struggles of coping with grief after the death of her son Andrew (pictured left) who died from Variant CJD at age 24
Watching my brave, beautiful first-born battle with this degenerative condition was the hardest thing I and his sister Emma have ever had to endure.
Andrew knew he was dying and, in his last week, asked: ‘Will you remember me?’
I sobbed as I promised that the pride I had in him was eternal and would endure until I took my last breath.
Yet I totally underestimated how difficult and off-putting others would find my attempts to keep that promise.
Christine and Andrew family holiday New York, Central Park, 2002
I don’t chatter on about Andrew needlessly, but when others talk about their children or parenting, I want to share my stories, too — to recall his smile, his jokes, his work successes. Yet, all too often, reactions to a mere mention of his name range from awkward silence to cringeing embarrassment.
While we have learned to openly discuss other uncomfortable realities — from cancer to mental illness — we still struggle to find the right way to handle the loss of a child, perhaps because it’s such an awful and terrifying event.
Christine Emma and Andrew in happier times
Yet many have suffered it. Official figures show that from 2010-16, between 8,600 and 9,800 people under 30 died each year. That means tens of thousands of newly bereaved mothers, fathers and siblings.
All of us will deal with our grief differently, but many find that the devastating ripples from their loss reach other areas, with marriage breakdown, depression and suicide bids all too common.
Andy Langford, a counsellor and chief operating officer for bereavement charity Cruse, says: ‘The death of a child is particularly devastating because both our future and part of our ancestry are severed at once. It feels entirely unnatural — we expect to bury our parents, and we feel we should die before our children.’
As a society, we’re not universally good at talking about grief anyway, but the death of a child compounds this as it is so difficult to accept. Sadly, bereaved parents often feel like they are expected to forget that child to avoid forcing other people to confront their own fears.’
Yet how could we possibly forget? Andrew will always be a part of my family, and a part of me.
Christine recalls her son Andrew (pictured age four) dying in her arms. She says the sympathy of others seemed to have an expiry date and many bereaved parents also feel an expectation to ¿move forward¿, to ¿forget¿, or to find ¿closure¿ after a year or two +4
Christine recalls her son Andrew (pictured age four) dying in her arms. She says the sympathy of others seemed to have an expiry date and many bereaved parents also feel an expectation to ‘move forward’, to ‘forget’, or to find ‘closure’ after a year or two
Andrew aged 21 years old San Diego USA
I raised him and his younger sister Emma as a single parent for most of his life. Until he fell ill my vibrant, kind son had everything going for him: a career he loved in the media and a great group of friends.
Then, towards the end of 2006, he started to suffer from weak muscles, anxiety and pain. Endless visits to the doctor proved inconclusive.
Desperate, I researched condition after condition and came to my own conclusions. I found seven young people in my area, Portsmouth, had died of Variant CJD, which is contracted by humans exposed to bovine spongiform encephalopathy (BSE) — mad cow disease. I was perplexed, as our family hadn’t eaten meat for many years due to health concerns. Yet the horrific catalogue of symptoms rang true for Andrew.
So, with trepidation, I raised my fears with doctors. Ten days later they were confirmed: Andrew had Variant CJD — we will likely never know how he contracted it — and was given six months to live.
It is impossible to fully describe the horror of watching my beautiful, physically fit son deteriorate before my eyes. vCJD punches hole after hole in the brain, robbing the body of its primary functions one by one. Andrew lost his sight, his hearing and his ability to move before finally, on a chilly December night, he died in my arms in his bed.
Andrew first day at school aged 4 years old
Both Emma — just 17 at the time — and I descended into the dark tunnel of extreme grief, compounded by the unbelievably cruel nature of Andrew’s death. It was senseless to me that something so simple as a meal had cut him off in his prime.
In the immediate aftermath there were times when I felt I might not physically survive. The mere act of taking another breath felt like a Herculean task.
And as ill-equipped as I felt to continue living while my child did not, I soon discovered that society was ill-equipped to deal with me, too.
Of course, in the early days, I received no end of welcome sympathy, practical help and listening ears. People did their best.
Quickly, though, I realised that often — not always but often — their sympathy came with an expiry date, in some cases soon after the funeral. It seemed there was a time limit on grief.
I’ve met many people who believe that after one year, or two, a bereaved parent should be able to ‘move forward’, to ‘forget’, or to find ‘closure’ — terms which make me shudder.
At the very least, they felt we should be able to neatly package our grief and give it a clear beginning, a middle and a final, accepting end.
Christine (pictured today) says each passing birthday and Christmas reminds her of a life missed out on. She lives in constant awareness of the experiences her son didn’t get to have +4
Christine (pictured today) says each passing birthday and Christmas reminds her of a life missed out on. She lives in constant awareness of the experiences her son didn’t get to have
It’s a message reinforced by endless television dramas: a death is quickly played out and followed by a weepy, emotional funeral, but then the plotlines quickly move on.
Yet, as grief counsellor Andy Langford makes clear, grief is timeless. ‘It’s not a case of moving on and the grief ending because we will always have a relationship with the person who has died.
‘What bereaved parents want more than anything is acknowledgement of that, for others to acknowledge their child’s identity, that he or she existed.’
Because, as I know all too horribly well, when you lose a child you deal with it for the rest of your life. My pain may not be as raw as it was, but my heart is still broken.
Contrary to common expectation, grief can expand with the years, instead of diminish — with each passing birthday and Christmas, each summer holiday crossed off on the calendar a reminder of a life missed out on.
When I most needed unity and proximity, my grief, and people’s inability to deal with it, led to crushing isolation – Christine Lord
Since my son’s death I have lived with a constant awareness of all he didn’t get to experience. To me, his memory is ever-present.
Yet with the passing of time others have become dismissive, less able to engage. Eager to forget the whole, horrible tragedy.
I have watched people I once called friends go out of their way to avoid me, crossing the road while walking their dog or, in the case of one ex-neighbour, turning his back on me in the local coffee shop where we once swapped pleasantries. While it makes me sad, I can understand it a little: I hold up a mirror to their worst fears, making them think about things they would rather not.
But the fact is that when I most needed unity and proximity, my grief, and people’s inability to deal with it, led to crushing isolation.
One close friend with children the same age refused even to visit once Andrew had been diagnosed. She said she ‘couldn’t face’ seeing him — as if I or anyone else wanted to see him like that. And aside from a bereavement card, she has not been in contact since. It was another aching loss to add to the one that had redefined my life.
Christine (pictured with Andrew as a child) says not telling the truth about her son when people ask about her children would feel like a betrayal of his memory +4
Christine (pictured with Andrew as a child) says not telling the truth about her son when people ask about her children would feel like a betrayal of his memory
Strangers bring their own troubling dynamic: it is only when you lose a child that you realise just how much adults bond by chatting about their offspring. Whether it is at the café counter, at a drinks party, or over that breakfast table on holiday, I brace myself as I await the inevitable question: ‘Do you have children?’
Not telling the truth would feel like a betrayal of Andrew’s memory, yet the truth brings responses from cliche to downright cruel.
I have lost count of the occasions I’ve been told ‘time is a great healer’, while in the latter category I’d put the mother of three healthy children and a grandmother six times over, who told me my son was ‘in a better place’, along with the neighbour who suggested I ‘get a dog’ to keep me company.
None, I am sure, intended to cause distress. I understand how difficult it is to know what to say in the face of profound grief.
I have often wondered if I should sanitise my feelings and choose, if not to lie, then to tell half-truths about Andrew
The irony is that so little is required to make us feel a little better: a simple touch on the arm and ‘I’m sorry’. Anything that acknowledges what we, the unenviable group united by losing a child, are feeling — even years after the initial loss.
Another member of this miserable group of bereaved parents is John, a father of five and successful businessman. He lost his youngest daughter Felicity, aged 21, following a car accident on a gap-year holiday.
Grief drove this confident, articulate man to profound despair and, as he resurfaced, he encountered another challenge that endures to this day.
‘I found that if I mentioned Felicity, even in passing, the atmosphere changed and became stilted and odd,’ he recalls.
‘Customers in my engineering business and even friends at social events would get embarrassed and didn’t know how to react. I’d start to feel guilty that somehow I had upset them, ruined their day or evening.’
It’s a guilt I recognise: I have often wondered if I should sanitise my feelings and choose, if not to lie, then to tell half-truths about Andrew.
That was John’s solution. He has found that the only way he can cope is to pretend his devastating loss hasn’t happened.
These days, when he meets new clients, he tells them he has four children, not five.
‘It made it easier,’ he tells me, head in hands. ‘I even took down a family photo of us all from my office wall. It became just too awkward. It’s as if Felicity has been wiped out.’
By denying her existence in order to spare other people’s discomfort, he feels he is losing her all over again.
IT consultant Nicholas, meanwhile, lost his 28-year-old son Will several years ago to cancer. His eyes fill with tears as he recalls attending a work conference and striking up a conversation with a stranger about their sons.
‘It was great to share, laugh and compare notes with this other father — it was a lovely relaxed evening,’ he recalls.
But when the stranger said how much he would love to meet Nicholas’s son, he was blindsided. ‘I drank my pint quickly and left as I couldn’t bear to say Will died three years ago. Bereaved parents are not supposed to laugh and chat about their late children.’
Yet how can we not? The fact is that talking about loss is essential for mental health — it certainly has been for mine. Andrew may be gone, but he remains a big part of my life and Emma’s and we talk about him a lot to one another.
If only others would, too. There is not even a word to sum up our plight — no ‘widow’ or ‘widower’ label to lend us dignity.
And yet, loss is an inevitable part of life, and one we will all suffer. So the next time a bereaved parent talks about their child, please don’t walk away. Instead, be brave. Listen, laugh and reminisce with them. They will be more grateful than you can know.
Who Killed My Son? by Christine Lord, is available from Amazon. Paperback £7.99, Kindle version £2.39.
THURSDAY 16th August 2018
The Independant newspaper reports that Australia will be flooding the market post Brexit with meat products currently banned by the EU!
How Australia’s meat industry plans to flood post-Brexit Britain with products banned in EU
Exclusive: Campaigners and farmers concerned by removal of ‘technical barriers’ to trade with Australia that could cause influx of lower quality products August 5th 2018
Australian meat industry leaders are heavily lobbying their government to put pressure on Britain to accept products currently banned under EU law after Brexit.
Among the meat products suggested for export to the UK are hormone-treated beef and “burnt goat heads”.
Ministers from both countries met last week to discuss the future of their trading relationship, amid concerns that the Australian government could force the UK to lower food standards.
Trade minister Liam Fox has long mooted Australia as a key trading partner for the UK when it ceases to be part of the EU.
The Department for International Trade has stated it “will not lower food, animal welfare or environmental standards as part of any free trade agreement”.
“Maintaining them is the right thing to do for our consumers and maintains the UK’s world-renowned reputation for high-quality products,” a spokesperson told The Independent.
But Kierra Box, Brexit campaign lead at Friends of the Earth(FoE), said the government is “saying one thing but doing something completely different”.
“The government can continue to claim they are protecting our environment and health but in reality these promises are flimsy and unconvincing.”
Wednesday 15th August 2018
MONGOLIA REPORTS MORE CASES OF MAD COW DISEASE
TWO CASES IN AUGUST AND 15 CASE OF MAD COW DISEASE IN
Must soum of Khovd Province in the west in mid-May.
Source: Xinhua| 2018-08-09 13:28:38|Editor: Chengcheng
ULAN BATOR, Aug. 9 (Xinhua) — Two cases of mad cow disease were found in Mongolia, local media reported on Thursday, citing the country’s Ministry of Food, Agriculture and Light Industry.
With more than 66 million livestock animals, Mongolia aims to raise meat exports tenfold in the coming years and to diversify its heavily mining-dependent economy.
But frequent outbreaks of livestock animal diseases such as mad cow disease and the foot-and-mouth disease have taken a toll on its meat exports. Most recently, 15 cases of mad cow disease were reported in Must soum of Khovd Province in the west in mid-May.
FRIDAY 20th July 2018
The research article below was published during a lot of other ‘media stories’. A great day to bury bad news. Brexit, World Cup Football, Trump. All of these stories were covered to excess whilst this health story that affects us all was virtually ignored. BSE CWD, human form of mad cow disease, is a pandemic in waiting!
As myself and others have suspected Chronic Wasting Disease in Elk/Moose/Reindeer/deer which is the equivalent of BSE in cattle can now convert human prions to related disease, ie Human BSE or the human form of mad cow disease.
It has been known for a long time that people who hunt and regularly eat deer or related animals across the USA and other countries have a higher rate of dementia or cjd type illness or disease. How many more people will die of the equivalent of BSE before safety measures are put in place? The cull all of the animals concerned including cattle that continue to die of BSE should be a priority, Not just a few random cattle, deer or herds. The disease both BSE and CWD is endemic in these types of domestic animals and animals that are eaten and are also used for medicinal purposes.
When Avian flu was diagnosed in Hong Kong every chicken and fowl was destoryed this stopped the disease in its tracks. Unfortuantely the west is motivated by money, greed and profit, with human and animal health at the bottom of the list. My son Andrew who died of vcjd aged 24 paid the ultimate price of that greed and corruption, corporate manslaughter by those named and shamed on www.justice4andy.com.
Chronic wasting disease prions can convert human prions into disease-associated form
Jul 2018: A team of CCBS researchers led by Marcelo Barria have published findings that prions that cause chronic wasting disease in deer and elk can convert human prions in a test tube to the disease-associated form.
Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. It might also be a public health issue. The recent discovery of CWD among free-ranging reindeer and moose in Europe prompted a group of CCBS researchers at the National CJD Research and Surveillance Unit to revisit the unresolved issue of whether CWD can spread from animals to humans, as can bovine spongiform encephalopathy (so-called mad cow disease).
Both diseases are caused by prions, misfolded protein particles that are detected in the neural tissue of infected animals. The researchers, funded by the Department of Health and Social Care and the Scottish Government, found that CWD prions from cervids (e.g., elk, white-tailed deer, and reindeer) in North America can convert the human brain prion protein in a test tube into the disease-associated form but that the efficiency of conversion is affected by variation in the cervid and human prion protein genes.
Given the similarity of North American cervids to those in Europe, the researchers underscore the need for a more comprehensive and thorough assessment of whether CWD can cross the species barrier and infect humans.
The findings have been published today in the journal Emerging Infectious Diseases. “Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions” by Marcelo A. Barria, Adriana Libori, Gordon Mitchell & Mark W. Head.
Emerging Infectious Diseases journal
Prion disease research at the Centre for Clinical Brain Sciences
National CJD Research and Surveillance Unit
This article was published on Jul 11, 2018
Friday 22nd June 2018
My interview with Mark Mardell for BBC, Radio4 World and One was broadcast today. The full interview as part of the 12 part series Brexit: A love story? is now avialable via the BBC podcast. My interview will be embedded on this website within the next week.
Below is a photo of me and Mark Mardell, talking about my son Andrew and the impact of BSE on my family and of course the UK public past, present. What will happen when we leave the EU and the de-regulation of food standards and safety measures?
Christine with Mark Mardell
FRIDAY 20th July 2018
Wednesday 30th May 2018
Large scale intensive beef farming in the UK, means cattle no longer eat pasture grass and are hemmed in a small area. This intensive farming in the 1980s and 1990s, created BSE and human BSE.
Greed and profit always comes before human and animal health. Read the investigation in the Guardian below. I wonder who is in charge and profits from the privately owned intensive farms? Supermarkets such as Waitrose, Lidl and the Co-Op buy meat from these beef farms.
The Guardian May 30th 2018
Revealed: industrial-scale beef farming comes to the UK
Investigation uncovers about a dozen intensive beef units, despite assurances that US-style practices would not happen here
Animals farmed is supported by
Animals farmedAbout this content
Andrew Wasley and Heather Kroeker
Tue 29 May 2018 15.00 BST Last modified on Wed 30 May 2018 08.59 BST
Some of the UK’s intensive units can hold up to 3000 cattle at a time. Photograph: Bureau of Investigative Journalism/Guardian
Thousands of British cattle reared for supermarket beef are being fattened in industrial-scale units where livestock have little or no access to pasture.
Research by the Guardian and the Bureau of Investigative Journalism has established that the UK is now home to a number of industrial-scale fattening units with herds of up to 3,000 cattle at a time being held in grassless pens for extended periods rather than being grazed or barn-reared.
Intensive beef farms, known as Concentrated Animal Feeding Operations (CAFOs) are commonplace in the US. But the practice of intensive beef farming in the UK has not previously been widely acknowledged – and the findings have sparked the latest clash over the future of British farming
The beef industry says that the scale of operations involved enables farmers to rear cattle efficiently and profitably, and ensure high welfare standards. But critics say there are welfare and environmental concerns around this style of farming, and believe that the farms are evidence of a wider intensification of the UK’s livestock sector which is not being sufficiently debated, and which may have an impact on small farmers.
In contrast to large intensive pig and poultry farms, industrial beef units do not require a government permit, and there are no official records held by DEFRA on how many intensive beef units are in operation.
But the Guardian and the Bureau has identified nearly a dozen operating across England, including at sites in Kent, Northamptonshire, Suffolk, Norfolk, Lincolnshire, Nottinghamshire and Derbyshire. The largest farms fatten up to 6,000 cattle a year.
A number of British supermarkets are among those found to be sourcing beef from UK intensive farms.
Drone footage and satellite images reveal how thousands of cattle are being kept at some sites in outdoor pens, known as corrals, sometimes surrounded by walls, fences or straw bales. Although the cattle will have spent time grazing in fields prior to fattening, some will be confined in pens for around a quarter of their lives, until they are slaughtered.
Supermarket demand is believed to be, at least in part, driving the trend. In addition, some smaller and medium-scale beef producers have struggled to farm profitably in recent years, with sometimes tight margins and fluctuating costs. Most of the units identified are believed to have grown incrementally, rather than setting up from scratch.
A number of retailers, including the Co-op, Lidl and Waitrose, are among those found to be sourcing beef from UK intensive industrial scale farms, most of which are privately owned but sell to beef processing companies, which in turn supply retailers.
Chris Mallon, director of the National Beef Association (NBA), the industry trade body, said the reason the largest units have come about was purely down to “efficiency”.
“What we’re talking about here is commercial production, for feeding people. It’s not niche market. A lot of this will be on supermarket shelves – that’s where it’s coming into its own. In the catering side as well, they’ll be doing it,” he said.
“One of the things we’ve seen over the years is supermarket domination of the beef trade. What they want is specification, size of cuts, size to fit certain packaging, size of roasts – this has all become incredibly important.”
But he cautioned that farms dedicated to fattening cattle had always been bigger than those rearing them, “so actually having higher concentration of feeding cattle on units [isn’t new].
“The difference is we’re getting some larger units now and that will be because of economies of scale … if you can give the people you’re supplying a constant supply of cattle that are in the right specification, that makes you more valuable. And that’s one of the reasons we’ve seen a move towards it.”
Dr Jude Capper, a livestock expert who has studied intensive beef units in the US and elsewhere said that due to economies of scale “it’s almost inevitable that a larger farm can produce a greater quantity of a more affordable product – we see this in almost all agricultural sectors globally, just as we do in other industries”.
“Cows belong on pasture,” according to Compassion in World Farming.
The Guardian and Bureau last year revealed that 800 poultry and pig “mega farms” or CAFOs have appeared in the British countryside in recent years, some housing more than a million chickens or about 20,000 pigs.
Following the revelations, the environment secretary, Michael Gove, pledged that Brexit would not be allowed to result in the spread of US-style agribusiness: “I do not want to see, and we will not have, US-style farming in this country,” he said in a parliamentary statement.
Although the number of beef units is tiny in comparison with intensive poultry or pig farms, the latest findings have further fuelled fears that the UK could be embracing industrial-scale practices.
Caroline Lucas, MP for Brighton Pavillion, said the farms were “gravely concerning” and that “with Britain hurtling towards Brexit, and with our animal and environmental protections facing an uncertain future, I’m worried that we could end up adopting more of this US-style agricultural practice”.
Richard Young, Policy Director at the Sustainable Food Trust, said: “Keeping large number of cattle together in intensive conditions removes all justification for rearing them and for consumers to eat red meat… More than two-thirds of UK farmland is under grass for sound environmental reasons and the major justifications for keeping cattle and eating red meat are that they produce high quality protein and healthy fats from land that is not suitable for growing crops.”
Young added that that smaller scale beef farmers might feel the impact, as larger farms were likely to be “more efficient in purely economic terms”, allowing the supermarkets “to drive down the retail price of beef below the price at which more traditional farmers can produce it. As a result they go out of business.”
Beef production in the UK typically involves three distinct stages – calf rearing, growing and fattening – with many farms specialising in one part of the rearing process. Cattle may move between a number of different farms during their lifecycle. (A smaller number of farms rear cattle from birth and keep them on the same farm until being sent to the abattoir.)
After spending time on pasture many cattle are moved to dedicated “finishing units” and are typically housed in barns or grazed whilst being fattened ahead of slaughter, often for around 6 months. Many are fed specialist diets designed to encourage weight gain.
But in the US, much beef fattening takes place in “feedlots” with cattle held in vast outdoor pens where the largest facilities confine up to 85,000 livestock. Such “feedlots” have proved controversial in the past, both because of their size and because many cattle were given hormones and antibiotics, sometimes to encourage rapid growth. (Such practices are not permitted in the UK).
Despite acknowledging the arrival of intensive beef farming in the UK, experts reject the notion that the British beef sector will see a wholesale shift towards farming on a US-scale.
In the US the rise of the CAFO has been paralleled by a fall in the number of small farmers.
“Are we likely to see huge – 100,000 head – feedlots? No. We don’t have the market, infrastructure or public demand for them,” said Capper. “However, could we make better use of male calves from dairy farms by rearing them for beef in feedlot-style operations, using feeds that we cannot [or] will not eat, such as by-products from human food crop production? Absolutely – some beef producers are already doing this.”
Caroline Lucas called for the system of permits to be tightened up, and said “the Government should be officially recording the number of feedlots rather than letting reporting slip through a loophole … we need a proper debate in this country over what kind of agriculture we want in the future.”
A spokesperson for DEFRA said that “beef farms are regulated in exactly the same way as any other farms”. But it later acknowledged that “Defra does not have a database of feedlot style units…The Cattle Tracing System can provide figures on the number of holdings split by premised type e.g. Agricultural Holding, Slaughterhouse, Market etc. and the number of animals registered to each. However, it does not hold any data in respect of the feeding practices on the holdings.”
Waitrose said of its own supplier: “Animal welfare is of the highest importance to us and a large farm does not equal poor animal welfare standards. The farm is run under a bespoke environmental management plan in conjunction with Natural England. All the cattle graze the marshes during the summer season then during the winter months, when the grass is dormant the cattle are bought back to the yard when the finishing/fattening cattle are housed in covered sheds. For clarification the length of grazing season is weather dependent, once the grass stops growing the cattle need to be yarded and fed a forage based ration in accordance with animal welfare and best practice.”
A spokesperson for the British Retail Consortium said: “Our members take their responsibilities to animal welfare very seriously and work closely with trusted suppliers so that high welfare standards are upheld. They have strict processes in place and will thoroughly investigate any evidence of non-conformity to ensure that any problems are immediately addressed.”
The reason that larger units have come about is down to efficiency, according to Chris Mallon, director of the National Beef Association.
The reason that larger units have come about is down to efficiency, according to Chris Mallon, director of the National Beef Association. Photograph: Bureau/Guardian
The Guardian approached several of the largest units but all declined to comment.
Some in the beef industry itself have expressed unease about the intensive farming system. Russ Carrington, of the Pasture Fed Livestock Association, said: “It is sad that the travel towards cheap, de-valued food has led to the removal of livestock from fields. There is a very different, more sustainable way of producing high quality beef which is also considerably healthier for humans to eat – 100% grass-fed and grain-free, which has lower total and saturated fat content, a better ratio of omega 3 to omega 6 fatty acids and more vitamins and minerals, which comes from the diverse pasture they eat.”
Pressure group Compassion In World Farming (CIWF) have raised concerns that some cattle held at in “feedlots” are kept in “high stocking densities” with little or no shelter or shade and “no dry ground to rest on.” The group says it believes “cows belong on pasture”.
Christine and Andrew aged 18months 1985, just a few years before the first UK cow was officially recognised as dying of BSE. Though that was kept secret from the public by the UK Government and its ministers for a few more years.
In response Dr Jude Capper said: “In my experience at feedlots all over the world, I’ve yet to see any welfare issues that are inherent to the system. If we are to assume that cattle must be able to graze to lead a ‘happy’ life, then confinement may be regarded as an issue. However, I’ve yet to see this being backed by [any evidence-base].”
“It’s almost inevitable that a larger farm can produce more a greater quantity of a more affordable product,” says Dr Jude Capper.
“It’s almost inevitable that a larger farm can produce more a greater quantity of a more affordable product,” says Dr Jude Capper. Photograph: Bureau/Guardian
Evidence compiled by the Bureau and Guardian suggests that most intensive beef farms appear to operate to high welfare standards.
Chris Mallon said: “Cattle actually will be very happy in [these systems]. Cattle in the wild don’t build nests for themselves or hide in caves, they’re an outdoor animal and I think we’ve got to remember that.”
Thursday 27th April 2018
THURSDAY 27th April
Christine’s BBC INTERVIEW AND FEATURE PUBLISHED ‘ The silencing of bereaved parents!’
Lost For Words? The Silencing of Bereaved Parents
Portsmouth journalist and campaigner for justice for victims of vCJD (the human variant of ‘Mad Cows Disease’) Christine Lord recounts her experiences of losing a child and asks why society still struggles to acknowledge and address grieving parents.
Stage and TV actor Kim Cattrall – known for her role in ‘Sex in the City’ – told Radio 4’s Woman’s Hour in 2015 that she objected to terms like ‘childless’ to refer to women who have not had children.
“It’s the ‘less’ that is offensive: childless – it sounds like you’re less because you haven’t had a child,” she said.
Her objection got me thinking about my own situation and how language and wider society treat people like me. Like Kim, I don’t feel represented in the lexicon of parenthood because there are no words, titles or labels in the English language to describe my circumstances.
I am the mother of a dead child.
There. I have written those dreaded words. The worst nightmare of every loving parent/guardian, or caregiver. Stark prose from which most adults recoil, whether they are ‘child free’ or a parent.
My son Andrew was killed aged 24 years old in 2007. His sister Emma was just 17 when she lost her only sibling.
Yet Emma remains Andrew’s sister and I remain a mother of two.
We belong to a growing club whose membership runs into the tens of thousands in the UK. According to the Office of National Statistics, between 2010-16, between 8,600 and 9,800 young people under the age of 30 died annually in the UK (an average of 9,000 per year). This means tens of thousands of newly bereaved mothers and fathers every year. Hundreds of thousands across Europe and millions across the globe.
As a bereaved mother, qualified counsellor and journalist, I wanted to write about how it feels to be a parent of a dead child: how people’s sympathy often comes with an expiry date, and how we have a problem in our society if we cannot acknowledge and understand grief.
Bereaved parents are expected to neatly package our grief: to give it a clear beginning, middle and a final, accepting end, tears no longer shed, pain ceased and the dead child deleted as quickly as an unwanted email. At the same time, the catastrophic event of losing a child creates divisions within relationships – from close friends to work colleagues. In the media, parents of dead children are often written about as tragic humans, broken by tragedy.
How we treat grieving parents is important because it shows us how as a society we deal with – or hide from – our deepest fears, and the isolation this causes to those of us who have lived through those fears becoming real.
I buried my only son just a few days before Christmas on 21st December 2007. In the last week of his life Andrew asked me, ‘Will you remember me?’ I sobbed and assured him that I would always be so proud of him and would talk about him and his achievements until the day I died. Why wouldn’t I?
But in the months and years that followed, I learned that our society would often find my attempts to keep that promise difficult, embarassing, and off-putting. I still, proudly, declare that I am a mother of two children. In my experience, what to me is a simple fact has for others the power to perplex and shock.
I have discovered that many people view the death of a child as ‘taboo’; a subject that shouldn’t be talked about too often once the funeral has taken place. Part of this seems to be based on a perception that there is – or should be – a time limit on grief.
I’ve met many people who believe that after one year, or two has passed, a bereaved parent should be able to ‘move forward’, to ‘forget’,or to find some form of ‘closure’. All these terms have come to make me shudder, and to understand that our society does not like to address what life is like when you lose a child.
Contrary to this common expectation, the grief of bereaved parents is more likely to expand with the passing years, with each birthday, each Christmas and holiday. The life that should have been lived is ever present for us. Blinded by disbelief, we try and make sense of this unknown landscape, where we continue to live when our children are dead.
I still want to keep Andrew and his memory alive in my ongoing relationships. I want to talk about his job, his smile, his funny jokes. I don’t chatter on needlessly about Andrew, but when others talk about their children or parenting, I want to share stories about both of mine, too. This is not maudlin but a celebration. Andrew existed and he contributed to so many people’s lives and experiences. He will always be a part of my family, and a part of me.
In the early days after Andrew had died, I witnessed an array of responses. Sympathy, practical help and listening ears were welcome. But as time passed, people became dismissive, less able to engage.
‘He’s in a better place,’ I was told by a mum with three healthy kids and six grandchildren.
A neighbour suggested I ‘get a dog.’
Countless times I was told, ‘time heals.’
I’m not saying people mean to cause distress, I understand how difficult it is to know what to say in the face of tragedy and profound grief. But at the same time, to hear these remarks feels at worst, cruel, at best, thoughtless.
I spoke to John and Nicholas, two fathers who have also lost a child, and found similar experiences to my own.
John is 54, from Wimbledon, and a father of five. His youngest daughter, Felicity, died aged 21 after a car accident during a gap year holiday. He told me how he has to adjust his conversation in everyday life, so that he doesn’t upset other people.
‘After Felicity’s accident, I was totally numb for many years. I worked non-stop to try and ease the depression and shock. Meeting clients was and still is difficult.’
‘I am confident, articulate, I like socialising. But I found after Felicity’s death, if I mentioned my daughter even in passing, the atmosphere changed and became stilted and odd. Customers and even friends at social events would get embarrassed and didn’t know how to react. I then feel guilty that somehow I had upset them, ruined their day or evening.’
John put his head in his hands as he told me, ‘I don’t talk about Felicity at work anymore. I tell new clients I only have four kids, it made it easier. I even took down a family photo of us all from my office wall. It became just too awkward. It’s as if Felicity never existed, as if she has been wiped out.’
Nicholas, 48, is an IT consultant on the south coast. He raised Will as his own from the time Will was a toddler. Will died from cancer, aged 28. He excelled at sports and had just got engaged when he was diagnosed.
Nicholas told me. ‘Will was the centre of my world and I miss him so much. I would probably be a grandfather now if he was still alive.’
‘One night after a work conference in Scotland. I got chatting to a stranger in a bar. We both started to talk about our sons. It was great to share, laugh and compare notes with this other father. Of course we talked of other things and topics, it was a lovely relaxed evening. At the end of the evening the stranger said, ‘I’d really like to meet your boy, he sounds a great young man.’
With tears in his eyes, Nicholas told me, ‘I drank my pint quickly and left as I couldn’t bear to tell the stranger that Will had died three years ago. Bereaved parents are not supposed to laugh and chat away about their late children.’
I know exactly what John and Nicholas were talking about, it’s other people’s attitudes to our loss that can be shockingly painful.
It has been over ten years since Andrew was killed and no, the pain is not as raw as it was, but my heart is broken. It will remain shattered. There will never be a quick fix. Because my son is never coming home.
Losing a child is horrendous and terrifying, but it’s also something that as a society, we should try to learn from.
If a person has lost a husband or wife, the terms widow or widower lend a sense of dignity and significance. Would giving bereaved parents a definitive title offer the same respect and empathy?
In the decade since my Andrew died I still ache with longing, still get angry, still shed a tear. Yet people ask, astonished, ‘aren’t you over it yet?’ or tell me, ‘you need to move on’ as if I have failed in some way, or have just mis-laid a favourite handbag on a train.
Talking about my son has been essential for my mental health. All of us will suffer loss, death is an inevitable part of life. So the next time a bereaved mother, father, guardian, care giver talks about their lost child, please don’t walk away from difficult emotions and leave them alone with their grief.
Instead, be brave. Listen, comment, share, laugh and reminisce with them. It will be good for your mental health too.
Christine Lord’s book Who Killed My Son? is available from Amazon, with profits from the paperback/kindle versions going to her campaignwww.justice4andy.com, supporting families affected by BSE.
Her latest documentary about the food industry, Cows, Cash and Cover-ups? will be broadcast this year, and you can view the trailer below.
Friday 20TH April 2018
‘We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria.’
BSE, mad cow disease continues to spread its toxicity across the globe. People continue to die, develop or are disabled by human BSE/Prion Disease/vCJD. The disease has not gone away and continues to spread amongst the animal kingdom. The equivalent of BSE has recently been found in Camels in Algeria.
Camel meat and milk are everyday foods for many people across the globe.
Dolphins, cats, dogs, horses, deer, zoo animals,mink, have all been killed or are developing the equivalent of BSE. Which has spread to domestic animals as well as cattle including pigs.
With incubation periods upwards of 50 years in humans and many decades in animals, we continue to face a global ticking health time-bomb. One that continues to be ignored, hidden or dismissed by the very people, ministers and governments who are condoning and allowing BSE infected material to still feed humans and animals.
See below the latest research into the Camels in Algeria found to be infected with prion disease which is the equivalent of BSE.
Just last month March 2018, here in the UK, in Salisbury Hampshire, three people were nearly killed by the deadly use of a ‘nerve/ chemical agent’. There was rightly world wide disgust of the use of unlawful ‘chemical agents’. The UK government will now spend millions of pounds clearing and cleansing the areas affected.
Yet the UK and global governments continue to hide its head in the sand regarding the toxic and lethal BSE and its continual spread within animals and humans. UK and global blood donation supply is not tested for human BSE, people have died of vcjd/prion disease from receiving tainted blood. BSE and its human equivalent can take decades to develop and for humans or animals to become ill.
From camel meat to beef, animals in the UK and globally continue to die/develop BSE or its equivalent. The disease cannot be killed by cooking, boiling or searing, the disease can then can be passed on-wards to people by the food they eat, or vaccines, blood.
photo of Andrew aged 24 with his friend Becky. Just a few months before he died of human BSE.
The BSE toxic agent cannot be destroyed! It remains active for generations. BSE and its equivalent continues to be re-cycled within the human and animals population.
People in the UK and across the globe continue to die of vcjd the human form of mad cow disease. Yet these victims and families are kept away from the media, told to ‘ keep quiet’ and intimidated by government officials.
It appears the beef, pharmaceutical, and agriculture industries and corporations hold governments to ransom with their funding, and overflowing coffers and offers of cash.
Once again ‘profit always before human and animal health’.
‘Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE).
After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions.
We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria.
Cows, Cash & Cover-ups? – Official Trailer on Vimeo
Cows, Cash & Cover-ups? Investigating vCJD – Official Trailer A documentary exploring Variant Creutzfeldt-Jakob Disease (vCJD), the human form of BSE (Mad
Cows, Cash & Cover-ups? – Official Trailer on Vimeo
Cows, Cash & Cover-ups? Investigating vCJD – Official Trailer A documentary exploring Variant Creutzfeldt-Jakob Disease (vCJD), the human form of BSE (Mad
Saturday 24th February 2018
Over 16 health and safety breaches in meat production every week in the UK. When will UK and global governments put human health before shareholders profits?
My son Andrew was unlawfully killed by the human form of BSE and UK man made deadly infection in cattle that then transferred to humans. Now one in 2,000 of the UK public carry or incubate human BSE, and with incubation periods upwards of 50 years many more could die or pass on this deadly brain disease via blood, operations and medical proceedures.
Se this Guardian Article which highlights the on-going risk to the public, meanwhile food corporations continue to profit at the expense of human and animal health.
Monday 12th February 2018
Read this article from the Star and Crescent online newspaper about my new documentary and the how much higher the stakes are regarding food and medicine safety post Brexit.
Thursday 11th January 2018
President Trump continues to de-regulate the food industry in the USA, this means globally and especially post-Brexit the UK will be importing meat that is not thoroughly tested for BSE and also food and medicines imported from the US will not have strict regulations to eliminate mad cow disease. For Trump ‘profit it paramount’.
In Dec. 14 2017 press conference, Trump said the US government had taken 67 such deregulatory actions through Sept. 30 — with an annual savings to society of $570 million — and had imposed just three new regulations. Instead of two for one, the ratio was 22 to one, he said..
The photo below was taken during my trip to South Korea. In 2008/9 after many years of South Korea banning US beef due to ‘mad cow disease’, a ‘cheap deal’ was done between the USA and South Korea. This deal made millions for the USA coffers and also big business in South Korea.
The ‘knock-down cheap’ US beef came and still comes from ageing US cattle, deemed ‘unfit for US public consumption’. These old herds of US cattle, very few tested for BSE continue to be sent to South Korea to feed its citizens and children. In South Korea school meals and national service is mandatory and the most infectious parts of these old, knackered US cows go to make meals for the South Korean school children/students and also South Korean military personnel.
This photo below was taken during the many peaceful demonstrations that the South Korean people including the elderly, students, children and families took part. These protests were to try to prevent the beef contract between the USA and South Korea. Unfortunately the US/South Korean beef contract was agreed and since then children, families, service personnel and hospital patients across South Korea have had to ingest ageing US beef in their daily meals.
I attended several of these peaceful demonstrations in Seoul, many led by Catholic priests and people of faith in 2008. The governments answer to ‘free speech’ was often brutal with unnecessary violence aimed at peaceful demonstrators. Many young students were blinded by water-cannon and elderly people thrown into prison, just because they attended these protests.
Many of those imprisoned talked about my Andrew, this website and my campaign.
Upwards of 50,000 people attended these demonstrations but their voices remained unheard. Unfortunately the deal was struck and USA cheap, ageing beef most at risk of BSE continues to flood into the South Korean food and medicine chain.
Big business and profit always comes before public and animal health.
Post Brexit and with President Trump shutting down agencies once funded to test US cattle for BSE and research into ‘human mad cow disease’ means the human food and medicine chain continues to process cattle and animals incubating or infectious with ‘mad cow disease’
It also means our blood supplies, vaccines and medicines continue to be exposed to humans carrying or infected with vcjd/prion disease/ human BSE.
The ticking health time-bomb that is human and animal BSE will continue to kill individuals and animals and with these de-regulation of health and safety rules another epidemic with human and animal victims becomes more and more of future possibility.
South Korean peaceful demonstrators attacked by Police/Government Security forces
Saturday December 16th 2017
Ten years ago today at 9.25pm my only beautiful beloved son Andrew Black aged just 24 years old, was unlawfully killed by Human BSE/ Human mad cow disease. Now often quoted as vCJD or prion disease
Times does not heal, when a dearly loved child is killed needlessly through greed, corruption and cover-ups. When those responsible for his manslaughter have so far not faced criminal action or punishment.
I miss Andrew every day of my life, I miss what he is missing, the future he would and should have lived.
To quote Maya Angelou
‘People will forget what you said, people will forget what you did. But, people will never forget how you made them feel.’
My son Andrew made me feel sunshine, rainbows and the wonders of life through his eyes as a child and then as a young guy on the cusp of so much life, love and adventure. I miss his optimism, his laughter, his kindness and clarity. My Andrew was an old soul with much wisdom and compassion. He made me feel so happy.
I never forget or stop loving you Andrew, I will never stop fighting and searching for the truth. So that you and all victims of human BSE past, present and those unfortunately to come will get the justice you deserve and families the answers they need.
Andrew I send you hugs and love. I am still and always will be holding your hand……till we meet again…….
Tuesday 28th November 2017
Latest research highlights the deadly consequences of BSE and how generations of our UK/global families remain at risk of human mad cow disease. This research shows how human BSE can be transmitted via skin.
Monday 27th November 2017
I have just met with my Labour MP Stephen Morgan and am pleased that justice4andy has the backing of the Labour Party.
During our meeting Stephen Morgan and I discussed many of the deadly and on-going public health issues regarding human mad cow disease. Post BREXIT the stakes are even higher.
My new documentary ‘Cows cash and cover-ups?’ was discussed and I presented Stephen with a copy of my book, ‘Who killed my son?
i am currently finishing the final chapters of my new book, and with my feature film, Cows, cash and cover-ups? due for release in 2018, WATCH THIS SPACE!
Thursday 26th October 2017
I have just returned from visiting five countries across Europe. I like to say thank you to all the people and friends I made in Germany, Austria, Denmark, Sweden and Slovakia.
I conducted a lot of research for my latest book and the campaign.
Sky news and various media see below are covering the ‘Contaminated blood scandal’ in which thousands of people including many children across the UK were given lethal blood products condoned by government ministers. This sub standard blood were sourced from blood donors who were ill with a variety of transmissible diseases. These blood products/medicines were also sourced from blood donors who were either carrying or went on to develop vcjd, human mad cow disease.
Many of those implicated in the ‘Contaminated Blood Scandal’ are also named and shamed on this website and implicated in my Andrew’s unlawful death and all those affected by Human BSE. JOHN MAJOR, KENNETH CLARKE are in the frame …at the moment Kenneth Clarke has refused to comment to SKY news or other media questions.
A secret memo written in 1987 by John Moore clearly shows the dis-regard Thatchers government and her Ministers and officials showed for public health. The memo clearly states the scale of the problem with contaminated blood, and how many people were suffering and dying and also ways the government and its ministers could remove themselves from implication or responsibility.
These government memos were being written the same time that BSE and its lethal dangers to humans were also being kept secret from the UK and global community by the same ministers and officials in the Department of Health. Including Minister of Health Kenneth Clarke.
I wish all my colleagues and friends at ‘Contaminated Blood’ campaign the best with their fight for justice and I know that many of the same people/ministers/ officials culpable in the deaths of thousands due to ‘contaminated blood’ are also implicated in the BSE scandal and my Andrews unlawful death at 24 years old.
Snip from SKY NEWS BROADCAST 26th October 2017
The document was unearthed by campaigner Jason Evans, whose father Jonathan was infected with both HIV and Hepatitis C and died in 1993, when his son was four.
The memo is a note of a proposal put to the Cabinet Home and Social Affairs Committee sub-committee on AIDS, a body that included some of the most high-profile ministers of the Margaret Thatcher Government including Willie Whitelaw, Norman Fowler, Douglas Hurd, Kenneth Clarke and future Prime Minister John Major.
QUOTE FROM MEMO ‘ IT WOULD BE CONSISTENT WITH THE POLICY OF NOT ACCEPTING ANY DIRECT RESPONSIBILITY FOR DAMAGE CAUSED IN THIS WAY’.
The meeting was convened to discuss the fall-out from the unfolding contaminated blood scandal on November 4, 1987, a day before the Haemophilia society was due to lobby MPs in Parliament.
By 1987 it was clear that thousands of people had been infected and were dying, and in the memo Mr Moore acknowledged the scale of the problem.
Saturday 2nd September 2017
Today would have been my only son Andrew’s 34th birthday.
I can’t imagine how he would look or be as a mature man. The life he should have led, the relationships he would have forged, the wonderful career he would have had in the media, the friends he would have made, the children and grandchildren with whom he may have been blessed. All those days, nights, months and years he has lost. All those holidays, family celebrations, he has missed.
The empty seat at the dinner table will never be filled, there is void in our family that grows bigger with the passing years.
Andrew (centre holdiing a bottle) celebrating his 23rd Birthday.
Forever Andrew will be a young guy in his early twenties, dying far too soon and young.
Today I will walk to the cemetery and place flowers on his grave. A journey I have made every week for ten years. The cemetery is a harsh and uncompromising place for parents who tend their children’s graves.
Time does not heal and until those responsible ( many named and shamed on this website) are punished for stealing my son’s life and future, there is no healing for me or any of those victims and families who have been affected by human BSE/ vcjd/cjd/ prion disease, the human form of mad cow disease.
Andrew aged 22 on his way to a shift at TalkSPORT National Radio, London
WEDNESDAY 23rd August 2017
TUESDAY 1st August 2017
The research below highlights how people suffering from vCJD the Human form of BSE have passed the diseased on-wards through blood and medical procedures. This research found that many other tissues and parts of the body contain the rogue prions that cause human mad cow disease which are infectious and could have be a danger during surgery.
As this research states we need a individual blood test for vcjd so that all patients before hospital procedures are screened and all blood donors are screened for the human form of mad cow disease.
The consequences of BSE remains a lethal threat for millions of people across the globe and generations to come. A blood screening test for vcjd would stop the re cycling of this deadly disease within our global blood supply and during hospital procedures.
The UK Department of Health continues to with hold the facilities to implement a blood test for vcjd as it knows the legal implications when 1 in 2,000 people could be carrying of incubating the human form of mad cow disease.
All those named and shamed on this website would face criminal proceedings and the ‘establishment’ would be rocked to its core. This is why a blood test for vcjd will continued to be blocked by the UK DOH.
Volume 23, Number 6—June 2017 Synopsis
Distribution and Quantitative Estimates of Variant Creutzfeldt-Jakob Disease Prions in Tissues of Clinical and Asymptomatic Patients
Jean Y. Douet, Caroline Lacroux, Naima Aron, Mark W. Head, Séverine Lugan, Cécile Tillier, Alvina Huor, Hervé Cassard, Mark Arnold, Vincent Beringue, James W. Ironside, and Olivier Andréoletti
Comments to Author Author affiliations: Institut National de la Recherche Agronomique, Toulouse, France (J.Y. Douet, C. Lacroux, N. Aron, S. Lugan, C. Tillier, A. Huor, H. Cassard, O. Andréoletti); University of Edinburgh, Edinburgh, Scotland, UK (M.W. Head, J.W. Ironside); Animal and Plant Health Agency, Loughborough, UK (M. Arnold); Institut National de la Recherche Agronomique, Jouy-en-Josas, France (V. Beringue) Suggested citation for this article
In the United-Kingdom, ?1 of 2,000 persons could be infected with variant Creutzfeldt-Jakob disease (vCJD). Therefore, risk of transmission of vCJD by medical procedures remains a major concern for public health authorities. In this study, we used in vitro amplification of prions by protein misfolding cyclic amplification (PMCA) to estimate distribution and level of the vCJD agent in 21 tissues from 4 patients who died of clinical vCJD and from 1 asymptomatic person with vCJD. PMCA identified major levels of vCJD prions in a range of tissues, including liver, salivary gland, kidney, lung, and bone marrow. Bioassays confirmed that the quantitative estimate of levels of vCJD prion accumulation provided by PMCA are indicative of vCJD infectivity levels in tissues. Findings provide critical data for the design of measures to minimize risk for iatrogenic transmission of vCJD
Most previous studies with tissue from vCJD patients have failed to identify consistent accumulation of the vCJD agent outside the nervous and lymphoreticular systems. However, data obtained in this study clearly demonstrate the presence of vCJD prions in a wide and unexpected variety of peripheral tissues.
Natural scrapie and experimental BSE in sheep are 2 models of orally transmitted prion diseases (24,25). In both diseases, the agent accumulates in the lymphoreticular system and the enteric nervous system during the early preclinical phase of the incubation period. Moreover, an early and persistent prionemia is observed in asymptomatic infected animals (26,27). These features were also observed in vCJD in humans and in view of the likely origin of vCJD (oral exposure to BSE agent), these similarities have led to a consensus that BSE and scrapie in sheep and vCJD in human have a common pathogenesis (28).
Although vCJD prions in a variety tissues, such as bone marrow, kidney, salivary gland, skeletal muscle, pancreas, liver, or heart, might be surprising, each of these tissue has already been demonstrated to accumulate prion infectivity or abnormal prion protein in TSE-infected sheep (29–33). Because low levels of infectivity have been reported in blood fractions from a vCJD-affected patient, such widespread tissue positivity might be derived from residual blood, rather than from the solid tissue in these samples (16). However, this proposal seems unlikely because in whole blood PMCA amplification inhibitors preclude detection of endogenous vCJD agent by this method (11,34–36).
The patient in our study who was infected with a prion containing PRNP gene codon 129 Met/Val is 1 of only 2 identified vCJD agent–infected persons known to have died of other causes before onset clinical symptoms of vCJD, and the only person who provided consent to sample autopsy tissues for research. For this patient, all previous investigations did not detect abnormal prion protein or infectivity in the brain (12,37). The negative PMCA results we obtained for cerebral cortex, dorsal root ganglia, and trigeminal ganglia tissue from this patient are consistent with a lack of central nervous system involvement at the time of death. However, PMCA seeding activity in the pituitary gland was surprising in this instance.
The presence of abnormal prion protein accumulation in the pituitary gland and other circumventricular organs before deposition of PrPres in surrounding brain has been reported in TSE-infected sheep (38). However, this phenomenon in animals does not represent the main route for neuroinvasion and is a probable consequence of hematogenous dissemination of the TSE agent through the fenestrated capillary system of the circumventricular organs, which is substantially more permeable than the other capillaries in the brain (blood–brain barrier). Therefore, this finding might be a consequence of the hematogenous route of secondary vCJD in this person (by transfusion of packed erythrocytes from a vCJD-infected donor), in contrast to the oral route of infection in primary clinical vCJD cases (12).
Andrew (centre sitting down) aged 23 one year before he died of vcjd
vCJD prions were detected in certain peripheral tissues from the patients infected with a prion containing the PRNP gene codon 129 Met/Val. Although distribution of vCJD seeding activity in lymphoreticular tissues was similar to that observed for symptomatic vCJD patients, several tissues that were positive in clinically affected patients were negative in this heterozygous asymptomatic person. These findings suggest that involvement of some peripheral tissues might occur at a later stage in the incubation period than others, or that they could involve recirculation of the agent from the central nervous system (i.e., centrifugal spread in a late state). However, we cannot discount the possibility that that these differences in tissue distribution are caused by the hematogenous route of infection in this person (as opposed to the probable oral route in patients with clinical vCJD) or the difference between the PRNP gene codon 129 genotype of the asymptomatic vCJD–affected person (PRNP gene codon 129 Met/Val) and persons with clinical vCJD (PRNP gene codon 129 Met/Met).
Irrespective of the actual explanation for these differences, the presence of vCJD agent in peripheral tissues of patients during preclinical and clinical stage of the disease indicates the potential for iatrogenic transmission of this fatal neurologic condition by surgical procedures. Furthermore, this finding shows that, for certain peripheral tissues, a level of infectivity equivalent to an end stage titer (and attendant risk) is reached at a preclinical stage.
Several hundred cases of iatrogenic CJD have been reported worldwide. These cases appear to result from transmission of sporadic CJD, and most cases have occurred in recipients of human dura mater grafts or after administration of human growth hormone extracted from cadaveric pituitaries (39). Although in sporadic CJD the distribution of the agent is largely restricted to the nervous system (central and peripheral), the wide distribution of the vCJD agent in the asymptomatic infected patient we report might serve to increase the range of medical procedures, including dentistry, organ transplant, and surgery involving nondisposable equipment, that might result in iatrogenic transmission of vCJD (40–43).
Nevertheless, >20 years after identification of the first vCJD patients, only 5 cases that are a probable consequence of iatrogenic vCJD transmission are known, all in the United Kingdom and associated with blood and blood products. These cases were caused by transfusion of non–leukocyte-depleted erythrocyte concentrates or by treatment involving large amounts of pooled plasma from the United Kingdom that were known to include donations from persons who later showed development of vCJD (12,44–46).
None of the 220 other vCJD cases identified worldwide have been linked to any other medical or dental procedure. Whereas this fact is reassuring, it would be unwise to disregard the threat that vCJD still poses for public health. Despite the relatively low number (n = 178) of vCJD clinical cases observed in the United Kingdom, the most recent epidemiologic studies indicate that ?1 of 2,000 persons in the United Kingdom could be infected with the vCJD agent (as indicated by the presence of abnormal prion protein detected by immunohistochemical analysis of lymphoid follicles in the appendix). Each asymptomatic vCJD-infected person represents a potential source of secondary infection. The data in our report offer an opportunity for refining measures that were implemented in many countries to limit the risk for vCJD iatrogenic transmission. The apparent concordance between PMCA biochemical and infectivity bioassay data, and the higher analytical sensitivity of PMCA, suggest that future research need not rely exclusively on time-consuming and costly animal bioassay.
Our results indicate the need for vCJD screening assays. After more than a decade of effort, several vCJD blood detection tests have reached a stage in their development that could enable their evaluation as screening or confirmatory assays (11,47,48). In particular, there is now a strong case for use of PMCA in a highly sensitive and specific blood test for vCJD, as indicated by our previous studies (11,16) and studies by Bougard et al. (35) and Concha-Marambio et al. (36). The relationship shown here between PrPres amplification by PMCA and detection of infectivity by bioassay indicates that PMCA seeding activity is a good surrogate marker of infectivity and could provide a sound basis for a vCJD blood test for use with blood or tissue donors.
Dr. Douet is a research scientist and assistant lecturer in ophthalmology at the National Veterinary School of Toulouse, Toulouse, France. His primary research interests are the pathogenesis of the prion disease with special emphasis on the iatrogenic risk of transmission.
Andrew as a baby just after having vaccines which I didn’t know were made from BSE infected cattle
This study was supported in part by the Department of Health Policy Research Programme and the Scottish Government. The National CJD Research and Surveillance Unit is supported by the Policy Research Program of the Department of Health and the Scottish Government (DH121/5061). The Edinburgh Brain Bank is supported by the Medical Research Council (MRC grant G0900580). The Unité Mixte de Recherche 1225, Ecole Nationale Vétérinaire de Toulouse was supported by the European Union FEDER/INTERREG (EFA282/13 TRANSPRION), the Institut National de la Recherche Agronomique Institut Carnot en Santé Animale, and an Agence Nationale Recherche grant (Unmasking Blood Prions; ANR-15-CE18-0028).
WEDNESDAY 7th JUNE 2017
Chronic wasting disease or CWD is the equivalent of BSE in cattle and human mad cow disease/vCJD in people. CWD is killing deer, elk and animals that are hunted and are eaten by individuals and groups across the USA and Canada.
CWD in deer herds is the equivalent of BSE in cattle, and has the same lethal consequences to the animals and also to humans that eat or ingest infected meat from deer/animals suffering from CWD.
There have been many cases in the USA/Canada of people who hunt or have eaten deer developing CJD or dementia type disease. These cases have been dismissed by the authorities as being spontaneous and nothing to do with the individuals close proximity or having ingested meat from deer. The families of those killed by CJD/dementia type disease, who have been active hunters for many years insist that the symptoms suffered by their loved ones are exactly the same as my Andrew’s symptoms and other victims of vCJD. Both BSE and CWD are prion diseases and can have long incubation periods. All of these bereaved families concerns have been dismissed by the authorities.
Hunting of deer across the USA and Canada is a huge sporting activity with deer meat prized in many communities. There would be huge financial and legal implications if links were made between CWD in Canadian and USA deer herds and vCJD within the deer hunting community.
In the White Paper below experts highlight the ticking health time-bomb that CWD poses for deer/elk herds across the USA/Canada and also its deadly risk to humans. As many deer in the USA and Canada and across the globe are wild this also has huge implications for other wildlife and of course agriculture.
Most recently in the USA a deer herd was found to have CWD, the animals who were chronically diseased were destroyed and meat from the rest of the herd was distributed to ‘deprived people in the area’. As experts know, animals can be infectious with the lethal prions that cause vCJD in humans but be symptom free.
This is appalling as it means those poorer people are being allowed to eat meat from a herd infected with CWD, meat that is not deemed fit/safe enough to feed richer and more prosperous people in society.
So are these poorer folks being experimented upon to see how many of them develop vCJD in the next decades? In the same way that Margaret Thatcher and her government allowed BSE infected material to feed UK children in their free school meals and also vaccines made from BSE infected herds? Is this why so many younger people then died of vCJD in the UK and continue to die?
THE COVER UP CONTINUES.
CHRONIC WASTING DISEASE CWD TSE PRION ZOONOSIS ZOONOTIC INSIDIOUS AND DIRE CONSEQUENCES AHEAD
Alliance for Public Wildlife Living Legacy White Paper
The Challenge of CWD: Insidious and Dire Only immediate action will avoid catastrophic outcomes
Valerius Geist, Professor Emeritus, University of Calgary David Clausen, (former) Chair, Wisconsin Natural Resources Board Vince Crichton, (former) Co-Chair, Canada’s National Wildlife Disease Strategy Darrel Rowledge, Director, Alliance for Public Wildlife
Download this White Paper Download this white paper and other related publications at www.apwildlife.org/publications For more information To order copies of this white paper or receive information about other related publications, please contact Alliance for Public Wildlife at email@example.com
CWD is now deemed to be the largest-ever mass of infectious prions in global history, and experts sum up the threat (to wildlife, agriculture, our economies, and potentially to human health) in two words: “insidious and dire.” Current policy and apathy toward the levels of CWD consumption by people has been described as “one of the most outrageous human susceptibility experiments in history.
We have a problem. A big problem. Chronic Wasting Disease (CWD), a sister to BSE or ‘mad cow,’ is threatening our deer and elk. Unfortunately, CWD has broad implications. Without immediate action, we are heading for worst cases outcomes that include severe population impacts, extinctions, crashing economies, and, although unlikely, potential transfers of CWD to people.
Chronic Wasting Disease is an incurable, always fatal degeneration of the brain. Technically, it’s a Transmissible Spongiform Encephalopathy (TSE), but there are a number of quite different versions, depending on species. They include in humans kuru and fatal familial insomnia, as well as some with even more unpronounceable names, such as the dreadful human Creutzfeldt-Jakob Disease (CJD) and Gerstmann–Sträussler–Scheinker Disease (GSS). The largest TSE epidemics have been in domestic or captive animals: such as Scrapie in domestic sheep, Bovine Spongiform Encephalopathy (BSE), or so-called ‘mad cow’ disease, Transmissible Mink Encephalopathy (TME) on mink farms, and CWD in captive deer and elk.
CWD emerged as a particular nasty variant, because it can be transmitted by body fluids of infected animals (urine, feces, and saliva). Unlike BSE, CWD is highly contagious and can spread to and through wild ungulate herds. The infective agents are mis-folded proteins called prions; they are virtually indestructible, can persist in the environment, and tiny quantities can transmit the disease. Prion diseases have repeatedly jumped species barriers—most alarmingly in the United Kingdom, when BSE-infected beef killed 229 people.
As CWD spread, naturally and through trade, the U.S. in 2001 officially declared a “State of Emergency.” Every factor has since gotten worse. It has now been confirmed in 24 US states, 3 Canadian provinces, South Korea, and recently in Norway. Field studies are confirming potentially severe impacts on wildlife populations. So far no transmission to humans has been documented, but the risk is not zero. Non-human primates and transgenic (humanized) mice have been infected. In many jurisdictions, a lack of awareness and availability of free, rapid, and convenient testing of harvested deer has led to significant level of human exposure. Estimates show 7,000 to 15,000 CWD-infected animals are being consumed by hunter families every year, and this number continuing to rise by as much as 20% per year. The combination of threats is sobering. CWD has been shown to persist and remain infectious in the environment, including in clay-based soils that can dramatically increase infectivity (up to 680 times). Decomposing carcasses create contaminated “super-sites.” Prions are extremely resilient, known to resist disinfectants, alcohol, formaldehyde, detergents, protein enzymes, desiccation, radiation, freezing, and incineration >1100°F. Facilities infected with CWD have resisted all efforts at removing the infective agent. Canadian officials report that even on premises thought to be very low risk, restocking with healthy animals led to a 50% re-occurrence of CWD.
Transmission occurs animal to animal, soil to animal, mother-to-offspring, and from exposed plants or other surfaces including tools or surgical instruments (even autoclaving is ineffective). Now there is evidence the infective agent is taken up via the root systems of plants growing in contaminated soils, with transfer to stems and leaves. These were shown to be infective via inter-cerebral injection (oral tests are ongoing).
Left unchecked, the prospects for wildlife are bleak. CWD has clear population impacts; some models suggest extinction. Disproportionate impact on mature males carries implications for hunters and wildlife economies let alone populations. Still more bad news: Efforts for vaccines have failed, and evolutionary or adaptive salvation is unlikely and would be too late in any case. CWD is now deemed to be the largest-ever mass of infectious prions in global history, and experts sum up the threat (to wildlife, agriculture, our economies, and potentially to human health) in two words: “insidious and dire.” Current policy and apathy toward the levels of CWD consumption by people has been described as “one of the most outrageous human susceptibility experiments in history.”
The good news
There is, of course, much more—but we need to get to the good news: There is hope, beginning with the fact that CWD is relatively new—not a long-standing or indigenous disease of our wildlife. The vast majority of our herds are still disease-free. We have considerable expertise, leading-edge technologies, and the benefit of experience. We faced a crisis on this scale once before, almost exactly a century ago, when the very existence of wildlife on this continent was threatened by the severest of over-exploitation. Hunters and conservation organizations led the efforts to avert disaster. With the courage and foresight of presidents and prime ministers enlisting the best and ablest on both sides of the US/Canada border to enact science-based policies, they turned our greatest tragedy into a ‘triumph of the commons.’ Anchored in the public trust doctrine, and now recognized as the North American Model of Wildlife Conservation, it replenished an entire continent with wildlife.
We need, today, nothing less than a similar effort to manage the Chronic Wasting Disease crisis. We have the benefit of experience and principles for success. Following the Roosevelt Doctrine, the same concerned hunter and conservation organizations must once again be the standard-bearers of principled, science-and evidence-based leadership in wildlife conservation. We must be relentless in following the leading science and scholarship, tracking the evidence, and engaging in comprehensive analysis to foresee the implications. We understand how policies affect the spread of diseases, as documented in the scientific and historical record summarized below. This threat is dire, and immediate action is warranted.
While details and methods must be guided by science and evidence, there is significant agreement on critical needs; and we have assurances from leading experts and labs that we have the capacity to meet this challenge. We must secure mandate and funding to:
- Contain the geographic spread of CWD by enacting and enforcing an immediate ban on the movement of all live cervids, all potentially CWD-infected carcasses, animal parts, products, exposed equipment, trailers, or other sources of infectious materials.
- Mandate and implement for hunters, convenient, cost-free, rapid testing of all animals harvested from CWD-affected areas.
- Ensure that no CWD-infected material reaches the food or feed chains, and that it is instead properly disposed of.
- Establish and fund accountable research and science-based policy to protect public interest (health, wildlife and related industries, agriculture, our economies and communities).
The issues are numerous, serious, and complex, but complacency is not an option. The sooner we act, the greater the prospects to protect our greatest living legacy. Further details, discussion, citations, and scientific references follow.
Potential Risk of Transfer to People There are few considerations which require greater foundational context than questions of zoonotic risk of infectious diseases. Combining public policy and science is very much a matter of addressing uncertain risks that are dynamic, evolving, and with complex, even profound consequences.
The reality is that most (~70%) emerging zoonotic diseases have come from animals.150, 151 Each presented uncertain risks, and in every instance there was a point in history where the animal to human transfer of that particular pathogen had not yet occurred. Such absence of evidence or ‘proof’ can often elicit false inferences that dismiss or underestimate the risk. The UK example of BSE (unexpectedly) transferring to people as vCJD, is but one recent example.152 The impacts were complex, extending far beyond immediate victims, bringing serious and prolonged socioeconomic and health consequences that included suicides tied to the severe economic impacts of BSE on the agricultural economy.153 There are persisting uncertain zoonotic risks related to the BSE that remain to this day. For example, findings in lymphoreticular tissue (archived through appendix samples) indicate that 1 in 2,000 of the UK population are asymptomatic carriers infected with abnormal PrP.154 The long term implications are unknown.
Zoonotic risks are neither static nor merely historic phenomena: “it is estimated that approximately 75 per cent of ‘new’ human pathogens reported in the past 25 years have originated in animals and the risk of zoonoses is predicted to continue to increase.”155 As status quo matters of public policy they require consideration of known and potential consequences. “The Global Burden of Disease Study estimates that, in the year 2000, infectious diseases were responsible for 22% of all deaths and 27% of disability-adjusted life years worldwide.”156
Such risk profiles can only be considered as snapshots in dynamic, evolving landscapes, where observation and evidence of variability—indicating change or evolution—is a vital consideration. This underscores the very essence of the precautionary principle, and nowhere is it more requisite than with respect to infectious pathogens. Inadequate policy or regulatory failures can result in pandemics that kill thousands or even millions of people or other animals, causing enormous damage on economies and ecosystems.
The Precautionary Principle
Where there is a potential for severe or irreversible harm, especially to public wellbeing and interest, an absence of scientific consensus or proof of harm cannot be used to allow or maintain policies or actions underlying the risk. In such cases, the burden to ‘prove safety’ falls on those advocating the potentially harmful policy or action.157
The standard of “severe or irreversible harm” is a very high bar; yet one CWD has long surpassed regarding public wildlife. It is only against that backdrop that the potential transference of CWD to people can be reasonably considered. We must consider risk, consequences, and even worst case scenarios. The fact is that prion diseases are described by physicians and victim’s families as aggressive, horrific, and dreadful.
Faced, in his medical practice, with the reality of human prion and neurodegenerative diseases, a leading scientists like Dr. Neil Cashman, (former) Scientific Director, PrioNet Canada, have long warned that CWD is “an emergency in slow motion.” At the “On The Horizon” PrioNet Research Conference Dr. Cashman summarized the background and urgency as follows:
“CWD is spreading like wildfire. From a few foci in Saskatchewan, it has now come to involve deer and elk in Alberta and Saskatchewan and there are no geographical barriers. It will spread until it infects the entire continent. It also spreads across species. …It can persist in water; it can persist in soil. It’s spreading without check. It’s arguably the most contagious prion disease, and the human health impact is unknown. We just frankly do not know if humans are susceptible to chronic wasting disease. It’s an emergency in slow motion.”158
This combination of growth, spread, changing risk, and extreme consequence explains the near unanimity of caution in available zoonotic analyses: “Although the zoonotic potential of CWD is considered low, identification of multiple CWD strains and the potential for agent evolution upon serial passage hinders a definitive conclusion.”159
Assessing zoonotic risk of new, emerging, and especially fatal diseases, is challenged by the inability to experimentally test susceptibility in people. Indeed, the ethical challenges are formidable enough regarding potential treatments. Yet questions of susceptibility require new approaches combining epidemiological and laboratory analyses (both in vitro and in vivo), as well as considerations of known and probable human exposure. Questions of appropriate policy and regulatory responses must be weighed against all implied consequences (biological, social, and economic), and the entire range of outcomes. This must include potential worst case scenarios even if they are thought extremely unlikely, not just because of evolving risk, but because market, media, and societal responses are often based more on perception than on science or reality.
Experts weigh in
Given their own and the risk analyses of others, leading scientists are expressing concern: “The increasing levels of CWD exposure are highly concerning.” “As a matter of policy, I believe all animals taken from CWD-infected areas should be tested before consumption and people should definitely not be consuming any infected material.”181
Qingzhong Kong, PhD, Case Western Reserve University
“The CWD situation and increasing levels of CWD exposure is a concern for cervid and human public health.” “CWD-testing should be conducted on animals harvested from CWD-infected areas prior to consumption.”182
Candace Mathiason, PhD, Colorado State University
“ … The more opportunity to expose humans to this stuff, the more we’re potentially playing with fire, in terms of these strain adaptations. It wouldn’t take very many cases of human prion disease that were linked back to chronic wasting disease, to where this whole conversation could change, fairly dramatically, and pretty much overnight. So I think while we have the opportunity, to get out in front of this … where we can as best we can, we should probably take advantage of that.”183
Michael Miller, PhD, CO Division of Wildlife
The full spectrum
The scope of human exposure to CWD is broader than is generally appreciated. It includes some direct exposures that have been largely ignored, lessons from history notwithstanding. When early suspicions of BSE being spread through consumption of blood, bone, and nerve tissues were confirmed in 1988,184 it led to bans on feeding meat and bone meal (MBM) supplements.185 Yet the potential risk of CWD in velvet antlers (i.e., blood, bone, and nerve tissue) sold for human consumption continued to be ignored long after both the confirmation of BSE being transferred to people as vCJD,186 and the repeated findings of CWD on game farms.187
A Risk Assessment of TSE products (dated June 2000) undertaken for Health Canada identified “pharmaceutical products containing high risk tissues and elk antler velvet food supplement” as the highest ranking risks.188 Under public pressure the Canadian Food Inspection Agency pledged in October 2000 to destroy velvet antler from CWD-infected animals. However, no recalls nor warnings to potential consumers have ever been issued.189 The difficulty of recalling product widely distributed throughout Asia is accepted; but it also illustrates the challenge and the consequences of failing to detecting potential zoonotic transfer. Furthermore, this passive approach regarding velvet antler continues even after confirmation of PrPd in velvet antler in 2009.190
As evident from challenges in achieving a CWD vaccine for cervids, there is little hope that breakthrough treatments would soon emerge. CWD has been in the shadows; but the toll of other protein misfolding diseases in people (Alzheimer’s, Parkinson’s, Huntington’s, ALS, CreutzfeldtJakob, etc.) affects tens of millions of Americans and cost hundreds of $billions per year. Yet the scale of complexity and level of difficulty is such, that, even after decades of research, there are no cures, and few effective treatments for any of them.191 Moreover, and as with any disease, containing and managing risk of CWD will demand an understanding and acceptance of the relentless capacity of this disease, as it continues to grow, spread, persist, and evolve. “Prions are distinguished from other amyloid diseases both by their infectious character and the observed exponential growth of infectious material.”192
With its growth and spread, human exposure from all sources has been increasing exponentially, and we would do well to consider the implications of both known and unknown factors. For example, prion load has been shown to be relevant, but note the title of McLean and Fryer’s 2011 work “There is No Safe Dose of Prions.” Analysis of 4,338 mice showed “that infection is possible at the very low dose of a 1000-fold dilution of the dose that infects half the challenged animals (ID50).” 193
After pointing out that bank voles (which are circumpolar) are described as the ‘universal acceptor for prions,’ Sigurdson asks if the sequence in the human ?2-?2 loop creates a permissive host PrPC sequence that is converted by prions from other species, despite sequence mismatches.194 With multiple avenues of direct and indirect human exposure, potential bioaccumulation, the potential role of co-factors, stressors, and potentially consequential passage to or through intermediate species, caution remains prudent. Moreover, it’s becoming clear that our understanding will be well served by looking beyond mammals. Quite apart from the work documenting mammalian prions taken up or adhering to plants, Susan Lindquist’s team has recently shown the “first protein from the plant kingdom with bona fide prion attributes.”195
Science, our greatest ally
These analyses outline more than risk: they offer hope. Lindquist has long been at the front of breakthrough prion research with yeast, and has not only documented many collaborative interactions, but key evolutionary and epigenetic analyses to help explain the phenotypic benefits that have conserved prion existence for 800 million years. These and other insights 196 into prion function may well open opportunities to prevent, limit, or potentially even reverse prion disease.197
However hopeful those breakthroughs might be, they are distant, and the levels of human exposure to CWD are already into the UK’s range of 1,000—10,000 BSEinfected carcasses sufficient to result in BSE transferring to a person.198 North American hunter families are consuming some 7,000—15,000 CWD-infected animals per year, and the number is growing exponentially.199 Though deer are much smaller in mass than cattle, this is more than offset by the fact that CWD prions are spread far more broadly than BSE prions in tissues most likely to be consumed.200 Prion load per animal may thus be higher in deer, despite the difference in mass. And while retail markets for beef reach more genetically susceptible consumers, that is less comforting when considering that the entire deer is often consumed by one hunter family.
Overall, the zoonotic risk profile of CWD is complex, uncertain and evolving. Without exception, dozens of experts consulted for this work concur with the current Director, Prion Diseases Program for the Public Health Agency of Canada, Dr. Michael Coulthart, who describes the risk of CWD transferring to people as “far from negligible.”201
Implications are broad, deep, and longterm
What is clear to policy analysts is that even a single transfer of CWD to a person will carry catastrophic implications in reactions of the public, in markets, and in public policy and international trade, regardless of how the disease manifests. And we cannot ignore the reality that CWD is highly contagious in deer.202
It is not inconceivable that a possible transfer to people could result in similar prion shedding in urine, feces, and saliva. Such an occurrence is beyond any known, practical means of containment or treatment, or avenues to curtail the economic fallout. If less dramatic, the risk profile is broad, complex, and with potentially dire outcomes at every turn. As to one minor example: consider the risk of CWD transfer through pet food. That was included in the UK’s updated, March 2016 Qualitative Risk Assessment regarding chronic wasting disease being introduced into Great Britain.203 The assessment asks: What is the risk of CWD being introduced into Great Britain (GB) from North America and causing infection in deer?
The analysis focuses on three routes of potential CWD introduction:
- importation of animal feed
- importation of deer urine lures
- importation of CWD prion on contaminated equipment and clothing/footwear of hunters or other tourists and British servicemen
The assessment cites the European Union Trade Control and Expert System (TRACES), which confirmed that “in November and December 2015, for example, GB imported 13.6112 tonnes of processed cat and dog food (including dog chews) containing products of ungulate origin from Canada and USA.”
The UK Assessment points out that while the U.S. Food and Drug Administration (FDA) recommends that CWD positive deer or elk, or even such considered at risk, may not enter the animal feed system, it is only a recommendation. They therefore conclude that CWD risk material “may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins imported from the U.S. into GB.” therefore considers that “there is a greater than negligible risk that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.” (Emphasis in the original.)
As more information becomes known, and major market players get involved, that status quo is unlikely to stay. Pet food regularly includes a variety of rendered animals and animal parts, including road kills. Sept. 15, 2003 the FDA issued guidance that “Material from CWD positive deer and elk may not be used in any animal feed.” That may have seemed a solid precautionary measure, however, Dr. Dave Clausen (from the CWD positive state of Wisconsin) explained that the results soon turned perverse: “Since results of CWD tests would typically take a few days or weeks, renderers in the CWD areas cite this section as the reason to not accept any deer carcasses that have been tested for CWD. Fear was that a positive test would compromise their interest and/or shut down operation. Thus renderers will take untested carcasses just not tested ones.”204
Then, with CWD continuing to extend its range to 24 states and 2 provinces, the FDA recently took further steps, adding a section to cover: “deer and elk considered at high risk for CWD”205 But as the UK Assessment pointed out, this is mere guidance, and does not establish legally enforceable responsibilities.206 Moreover, FDA rules and guidelines for ensuring composition requirements, compliance, monitoring and enforcement are weak, and interstate and international transport of pet foods is widespread and poorly regulated.207
Given their experience with BSE, the UK assessment of risk via pet food is somewhat surprising. Their experience included the world’s first documented instance of interspecies transfer of prion diseases in 1990, when a house cat developed scrapie-like skin irritation so fierce he licked himself bare. Dubbed “Mad Max” by the British press, the cat died from Feline Spongiform Encephalopathy (FSE), a toll eventually reaching 89 domestic cats in UK, one in Northern Ireland, one in Norway, one in Switzerland, and one in Liechtenstein.
Virtually all species of large cats in zoos were similarly infected, including: five cheetahs, three pumas, three ocelots, three tigers, five lions, and one Asian Leopard Cat.208 All were instances of simple oral ingestion of BSEcontaminated feed. The news of transfer across species barriers immediately rocked public confidence and affected markets, which were damaged further with the subsequent admission that people were dying of vCJD from consuming infected beef.209
The UK assessment outlines a similarly “greater than negligible” risk of importation of CWD prion on contaminated equipment and clothing/footwear of hunters, and that “the annual risk of at least one infection of deer in the UK with CWD from deer urine lures imported from the USA is medium.” But whereas official assessments of CWD threats to European wildlife have been measured, largely unseen, and potentially understated, concerns raised by NGOs and the media have been blunt, as in an article in The Times headlined: “Disease from the U.S. could wipe out all the deer in Britain.”210
Any news of international transfer of CWD by any means, to any species whether deer, rodents, pets, or livestock (such as domestic sheep), would almost certainly have severe consequences. The economic implications would be felt most acutely in North American CWD affected areas.
The UK experience with vCJD is instructive, but key differences are noteworthy. Despite recent confirmation of PrPd in saliva of BSE cattle,211 the absence of (efficient) lateral transfer of BSE between living animals limited growth and spread of the disease,212 and it allowed the ruminant feed ban to eventually halt both the epidemic and the subsequent trade embargo. This underscores a contrast of some significance: CWD with its prolific prion shedding in saliva, feces and urine, is a highly contagious, extremely persistent disease, which has established unprecedented reservoirs in public wildlife and the environment. Compared to BSE, CWD offers no apparent ‘off switch.’
Lessons from BSE
From a public policy perspective, the experience with BSE offers vital lessons—from the foundational frame to the conclusions and recommendations by the official inquiry (paraphrased for brevity):
- “At the heart of the BSE story lie questions of how to handle hazard — a known hazard to cattle and an unknown hazard to humans.”
- “BSE developed into an epidemic as a consequence of intensive farming practice(s) … unchallenged over decades, (that) proved a recipe for disaster.”
- “Government was preoccupied with preventing an alarmist over-reaction … (they) believed that the risk was remote. It is now clear that this campaign of reassurance was a mistake.”
- “Public was repeatedly reassured that it was safe to eat beef.” 213
- “Repeated statements that ‘there is no evidence that BSE is transmissible to humans’ does not explain that such evidence would take many years to emerge.”214
- “Even when risk to humans seems remote, all reasonable precautions must be taken.”
- “There should be more checks on possible pathways of transmission, and on occupational risks.”215
- “Where there is uncertainty, government must not shrink from saying “we are not sure.”216
The analyses and recommendations of the UK experience with BSE are founded on failures of governments to uphold public trust and the precautionary principle. The lessons are directly applicable to CWD: Without immediate, science-based intervention by North American governments to contain and limit the spread, growth, evolution, and exposure of CWD, the likelihood of ‘worstcase’ outcomes will continue to increase, and wildlife is in the cross hairs in every scenario.
Monday 15th May 2017
CATTLE IN SPAIN WITH MAD COW DISEASE
On the 28th April 2017 it was confirmed in that cow from Cantabria, Spain born in 2002 (aged 15 years old) was diagnosed with BSE. See report below from the Spanish Government.
Over 50 other animals in the same herd are at risk. The Spanish authorities state that it ‘poses no risk to human health?’ I am afraid that cattle do not develop BSE in isolation, what about the fields these animals have been grazing on? What about the milk and butter that has already gone into the human food chain? Also what about the meat from other animals in the herd which is now in supermarkets and shops?
This diseased cow was 15 years old how long had it been ill?
Human BSE remains a deadly risk for us all and this new case of BSE in Spain, highlights that the disease has not gone away and continues to affect cattle globally and Human BSE continues to kill people.
As the report says below the origins are unknown, so how many other cattle in the area may be suffering from BSE but not showing symptoms when they enter the slaughterhouses?
The report below ends ;THIS EVENT IS RESOLVED’ ??? HOW CAN IT BE RESOLVED BY THE DESTRUCTION OF ONE COW, WHEN 50 PLUS ARE AT RISK AND THE REST OF HERD MAY ALSO BEEN INFECTED.
— SPAIN OIE Bovine Spongiform Encephalopathy atypical L-type Camargo, CANTABRIA
Subject: SPAIN OIE Bovine Spongiform Encephalopathy atypical L-type Camargo, CANTABRIA
|Bovine spongiform encephalopathy , Spain|
Information received on 12/05/2017 from Dr Valentín Almansa, Director General, Sanidad de la Produccion Agraria, Ministerio de Agricultura, Alimentación y Medio Ambiente, Madrid, Spain
|Source of the outbreak(s) or origin of infection||
|Epidemiological comments||On April 28th, 2017, the Central Veterinary Laboratory at Algete (National Reference Laboratory for transmissible spongiform encephalopathies accredited under UNE-EN ISO/IEC 17025:2005) received a brainstem sample suspected to be BSE-positive from the regional accredited animal health laboratory of Cantabria (official regional laboratory) after a positive result was obtained through the Bio-Rad TeSeE SAP rapid test.
The National Reference Laboratory undertook the confirmatory tests authorized according to Regulation (EU) No. 1148/2014. The selected assays associated were Western blot (Prionics) and ELISA (TeSeE SAP Bio-Rad). Following positive results to both assays, the National Reference Laboratory performed assays to discriminate the BSE strains by immunoblotting with results for atypical BSE type L on May 5th, 2017.
The sample was taken within the national TSE surveillance program (sampling of dead or non-slaughtered animals for human consumption over 48 months old). The animal was a crossbred (conjunto mestizo) female born on 25 February 2002.
|Measures to be applied||
Diagnostic test results
|Laboratory name and type||Central Veterinary Laboratory, Algete ( National laboratory )|
|Tests and results||
|The event is resolved. No more reports will be submitted.|
WEDNESDAY 19th April 2017
BRAZIL FACES 63 INDICTMENTS FOR YEARS OF UNSAFE TOXIC MEAT FLOODING GLOBAL MARKETS
Huge corruption within Brazils Ministry of Agriculture has meant toxic lethal meat has flooded the global food market for years. Federal Auditors for the Brazilian Government and Ministry of Agriculture at meat processing plants took bribes for years in exchange for false health and safety permits for beef and poultry and domestic animals for human consumption.
63 indictments are being prepared by Brazil’s Federal Police force.
Across Brazil people continue to die of vcjd. These cases of human BSE are all pushed under the carpet by the South American authorities.
Brazil is one of the biggest exporters of meat globally and this corruption means that even more animals w infected with BSE would have also flooded the human food chain for years. JBS the biggest meat packer in the world had one of its staff in Brazil suspended over his involvement with members of the Ministry of Agriculture.
MOY PARK. EUROPES LARGEST POULTRY PROCESSOR WITH 12,000 STAFF ACROSS UK, FRANCE AND NETHERLANDS WAS BOUGHT BY JBS FOR £944 MILLION IN JUNE 2015.
POULTRY GO TO SLAUGHTER BEFORE THEY CAN SHOW SYMPTOMS OF ANY DISEASE INCLUDING THE EQUIVALENT OF BSE.
Mad cow continues to kill people. Food corporations and governments globally profits grow to billions of pounds whilst, thousands of people, young men and women, mums, dads, sisters, grandparents, brothers and children continue to die or suffer the long term lethal effects of the human form of mad cow disease.
Brazil Meat Scandal: 63 Indictments
By Greg Henderson April 17, 2017 | 3:07 pm
Federal Police in Brazil has indicted 63 people for their role in a vast corruption scheme within the Ministry of Agriculture. The charges allege federal auditors at meat processing facilities took bribes for years in exchange for fraudulent sanitary permits.
The probe into Brazil’s meat corruption was launched March 17, 2017, by Brazil’s Federal Police. Brazil, the world’s largest beef and poultry, and the fourth largest exporter of pork, saw its exports drop to near zero within a week of the scandal’s announcement, though most export sales have resumed.
The suspects in the case are charged with falsifying medical records and certificates, tampering with food products, conspiracy and corruption. One employee at a JBS processing plant in Brazil was included in the investigation, allegedly due to his relationship with federal inspectors. The employee was suspended.
Allegations also include selling spoiled meat and injecting water to sell poultry at higher prices. Police also reported that the producers under investigation used ascorbic acid and other chemical ingredients, in quantities far above the legally permitted amount, in order to “disguise the physical aspect or smell of rotten meat.”
No JBS brands or products are associated with product tampering nor has JBS been accused of selling tainted or rotten meat. The majority of this investigation, particularly the food quality issues, focused on the actions of smaller companies in Brazil that supply the domestic market, not JBS.
JBS is the largest meat packer in the world, with subsidiary JBS USA the second largest beef packer in the U.S., with nine beef plants and estimated 2016 sales of $14 billion. JBS USA is not involved in the Brazilian scandal. JBS USA is a “leading processor of beef, pork and lamb in the U.S., a leading processor of beef in Canada and the largest cattle feeder in the world.”
Monday 13th March 2017
A cow born in 2003, over 14 years old has been diagnosed with BSE in Spain March 2017, ( see news links below) this cow produced many calves all of which would have entered either the human food or medicine chain for over a decade.These calves would have been used for milk, butter, meat and in some cases their cells/tissue used for vaccines and blood products. The cow with BSE milk would also have been sold to supermarkets and shops.
There is now a so called ATYPICAL BSE WHICH AUTHORITIES ACROSS THE GLOBE ARE USING TO FUDGE THE TRUE NUMBER OF CATTLE DYING OF MAD COW DISEASE. The authorities falsely reassure the public that ATYPICAL BSE is almost a natural disease in the same way that SPORADIC CJD IS IN HUMANS. Both are falsehoods, dodgy accounting by governments to keep the true numbers of BSE cases in cattle lower and deaths of vcjd the human form of mad cow disease lower in humans.
Before BSE there was no such thing as ATYPICAL BSE IN COWS. This new title for BSE is used to protect the global food and pharmaceutical industries and the farmer in Spain who for over a decade had been selling milk from a cow with BSE, selling the cows offspring for meat and medical use. All of these animal products would have entered the human food and medicine chain.
Its a crude ‘damage limitation’ by the authorities in Spain saying the cow had Atypical BSE. (which means it was an odd case and old before BSE was diagnosed) hoping that the public will believe that ATYPICAL means ‘safe’. Unproven science to falsely reassure the public that beef from this BSE cow from this farm in Spain was and is ‘safe for human consumption’. BSE is lethal to humans and animals, sometimes animals or humans have long incubation periods before they become ill, but they are still toxic to other animals or humans.
This cow which was 14 years old in Spain was found to have BSE and that is a lethal risk to human health. This cow also developed BSE in the same region where a few years ago a mother aged 60 and her son in his 40’s died of vcjd. There have also been other human cases of vcjd in the area of Spain where this cow was recorded as having BSE.
The global cover-up regarding animal BSE and human mad cow disease continues!
ABC NEWS AND OTHER MEDIA REPORTS.
Wednesday 1st March 2017
Had two brilliant radio interviews this week, one with presenter Cheryl Fergus-Ferrell at Croydon Radio, London and another with Pippa Jones at TalkRadio Europe which was broadcast across Spain. Both were extended items, talking about my Andrew the campaign and documentary ‘Cash. cows and cover-ups’. See link below to the podcast Croydon Radio.
Monday 13th February 2017
We have released a trailer of our shocking new one hour indpendent documentary,
’ Cash, cows and cover-ups’
Please share the link below. I will let you know when the documentary in full is being broadcast. I have worked for over 18 months researching and filming the documentary and have uncovered some shocking new facts and information that the UK government and other establishments wanted to keep secret. Partickular Films are the great production company which has filmed, edited, and directed this great film. It has been produced with passion, professionalism and facts, with many world exclusive revealed. Director Joseph Andrew Mclean, cameramen Martin Heron, Dale McEwan and a great crew in the USA.
We have filmed across the UK and in the USA and the documentary is for release to a national and international audience.
This campaign and film is not just about the unlawful death of my son Andrew and all victims of human BSE but about you and your families. I want to know that the food that children and families in 2017 are eating and the medicines they are ingesting are safe and not a poisoned chalice. Sadly our governments and the global food companies care little for animal or human health with profits the driving force.
If you care about the food you eat, the scientists you put your trust in and the politicians you vote for please watch the trailer and support the documentary when its broadcast.
This concerns everyone, I want to make sure your children are safe, your friends, family and you do not become infected with BSE, do not become disabled or die through human mad cow disease.
‘cash, cows and cover-ups’ and justice4andy campaign is about keeping your family safe too!
The trailer is also on YouTube
The link is now on Vimeo: https://vimeo.com/203115042
Monday 6th February 2017
This evening I am appearing on BBC1 ‘INSIDE OUT’ at 7.30pm its a shocking investigation into diseases that can be transmitted from domestic animals to humans. How the UK government in 2017 continue to cut funding regarding testing farm animals for disease and its on-going effect on food safety.
Below is latest research which highlights the on going ticking time-bomb which is human BSE and how millions remain at risk of dying of the human form of mad cow disease.
With this blog is photo of me filming in snowy countryside on a farm. I talk about BSE and my fight to protect the UK and global public from the government/ corporate greed and corruption that unlawfully killed my son Andrew and how BSE will continue to kill people for generations. I also discuss other zoonotic diseases which will flourish all the time government policy condones profit before human health.
Many more people could still die from mad cow disease in the UK
Wednesday 1st February 2017
Roger Hiorns Turner nominated artist has an exhibition of his work at the world famous IKON gallery in Birmingham, UK.
The show is on for 3 months December 2016- March 2017 and includes items from www.justice4andy.com campaign and also Roger’s art expressing the tragedy and corruption surrounding the BSE epidemic and its fatal human consequences. Please go along if you are in the area.
Photo with this blog is of Christine and Roger at his show. My book ‘Who killed my son?’ is also available at the IKONs book store and their catalogue. See link below.
Monday January 30th 2017
This footage on Youtube (see below) of a cow staggering and dying of BSE in Belgium , highlights the ticking health-time bomb that is mad cow disease. It has not gone away and is endemic in cattle. With the closing of animal autopsy facilities in England and the UK no longer testing for BSE. How many hundreds of cattle here in the UK and globally are still entering the human food chain that are infected with mad cow disease?
The footage of the cow unable to walk due to deadly mad cow disease and the Belgium officials off-hand response that:
‘Only one cow has BSE’ and that it’s therefore safe and ok for Belgium families and their children to consume bovine material is false. Totally appalling that profit before lives always dominates governments agendas.
BSE in cattle is never isolated to just one case. What about the cows that had already gone to slaughter and not showing symptoms? they would be toxic and infectious too!
How many cows in the Belgium herd were incubating or carrying mad cow disease and entered the human food and medicine chain?
Of course people who consume this toxic material will not show symptoms for many years, by then the farm may well be owned by another farmer and the officials who say eating beef is safe moved on to another post.
All of the cattle in the affected herd should have been immediately destroyed including calves and parents of the cows.
Also all meat and milk that had been sent from the farm should have beentraced and consumers informed.
The culture of global ministerial and official secrecy which killed my son Andrew and hundreds innocent victims, disabled thousands and put millions at risk continues to condone and hide the truth/ facts about BSE and its human on-going deadly consequence vcjd
Photos with this blog of me and my son Andrew aged 24 at Southampton Hospital the day he was diagnosed with human mad cow disease, and 6 months before he died of human BSE. The other photo taken just a short while before of Andrew healthy and well in San Francisco USA.