Revelations in Britain during 1996 have brought a new dimension to the incurable Brain infections - Creutzfeldt-Jakob disease [CJD] in humans and bovine spongiform encephalopathy [BSE] in cattle.
Before then, science and health experts had maintained that humans could not catch CJD from eating BSE-infected beef. An announcement from the House of Commons on March 20 (1) turned that assurance on its head with an admission that meat products from BSE-infected cattle had probably spread a novel form of CJD to humans.
Attracting less international attention, a landmark High Court ruling on July 21 (2), deemed that the Dept of Health had been negligent in permitting the human pituitary growth hormone treatment of short-statured children up until 1985, following warnings back in 1977 that the hormone was possibly contaminated with the agent of CJD.
Disingenuously, the High Court passed no judgement on the clinical use of another hormone, human pituitary gonadotrophin, that was produced under the umbrella of the absolute same program that manufactured the paediatric growth hormone, and which, with identical clues to its CJD contamination, had been injected into infertile women during exactly the same time frame.
Formerly a rare disease that affected less than one per million in most countries, one worst case scenario predicts that the incidence of CJD in the UK will escalate from, on average, fifty annually to claim ten thousand Britons by the year 2000, and a further ten million by the year 2010. Another predicts that half the British people, some 30 million, will be left Brain-dead by CJD.
While a CJD epidemic of this proportion largely defies contemplation, it has also raised the question of whether nature or human error was responsible for what amounts to an unprecedented assault on human and animal life.
As the history behind both announcements unfolds, it becomes increasingly obvious that the BSE/CJD tragedies were born out of a Brain-dead culture that arose from the overlapping agricultural and medical impropriety of this century.
Plainly, the legacy of the Brain-dead culture is a public health and economic scandal of unequaled proportions.
Responsible management of the disastrous situation is largely dependent on overturning the Brain-dead notions which over time have established the dire 1996 BSE/CJD positions.
Faced with a worldwide boycott of British beef, and with millions of cattle destined for cremation, authorities have disenchantingly persisted with face-saving reassurances, the majority of which have been disproven with almost monotonous regularity.
In keeping with the medical imperialism that turned infertile women and short-statured children into human incubators of pituitary hormone-related CJD, mad cow imperialists have suggested that the Third World can rescue Europe from the impending BSE-related financial disaster, and intensely preoccupied with another incurable Brain illness, kuru, which had reached epidemic (3).
Already India, Cambodia and Afghanistan have, very unofficially, been touted as dumping grounds for BSE-infected cattle in a last ditch attempt to salvage something from the chaos.
Malignant twists of nature, by way of bubonic plague through to potato blight, have killed masses throughout the ages, but the present story of spongiform encephalopathies is unique in that the epidemic was largely manmade. Scrapie, the sheep equivalent of BSE/CJD, has been around for more than two centuries.
Somewhat in contrast, human spongiform encephalopathy was unheard of before two German physicians, Creutzfeldt and Jakob, independently reported the initial cases in the 1920s.
There had been no concerted effort to find a diagnostic screening test to identify CJD/BSE infection until the financial undertones of the 1996 BSE straits stimulated a re-interest in the CerebroSpinal Fluid test (4) which Michael Harrington had already developed in California a decade earlier (5), but there is no known medication that can cure or allay the cruelty of human or animal death from the diseases.
In humans, outward warning symptoms only emerge after a prolonged incubation period that, in iatrogenic cases, has ranged from as few as two to as many as thirty five years.
By that stage, the agent of CJD has already turned the Brain into the sponge-like mass that led this group of diseases to be classified as spongiform slow virus disorders in the first instance.
Death may be a welcomed escape from the myoclonic jerks of CJD which, while silently eating away at the Brain over years, robs humans of their every means communication; the ability to hear, see, and speak.
Gone too is the understanding of written and spoken native language, and with it every scrap of dignity. Similarly, BSE has no respect for cattle decorum, and a furnace is the fate of confused and trembling animals that the disease has deprived of their own feet to stand on.
The original lesson about the infectious nature of these Brain diseases came from a 1934 vaccine catastrophe in the UK which brought scrapie to almost five thousand out of eighteen thousand lambs within two years of their immunization against louping-ill virus infection.
Scientists tracing back discovered that the vaccine Serum was prepared from a number of lambs whose dams had subsequently developed scrapie or "mad sheep disease".
The significance of scrapie passing vertically from ewes to their lambs, and horizontally from lamb to lamb by virtue of the vaccine injections, was kept from international eyes when a series of egotistical carry-ons prevented the data from reaching the pages of the scientific literature for a further fifteen years.
By then, as the 1950s dawned, "mad sheep disease" jumped the species barrier when a scrapie-infected food supplement brought a similar Brain illness to farm mink in 1947 (6).
This news scarcely interested the medico-scientific community who, by this stage, had become proportions among the Fore people living in the highlands of New Guinea.
Anthropologists from the Univ of Adelaide unravelled a chain of events to trace kuru back to the reverent consumption of deceased tribal member's bodies, with the Brain almost certainly being the vital infectious denominator.
Kuru was essentially eradicated when New Guinea authorities acted on the anthropological clue in 1959 to outlaw the eating of human flesh, but the 1976 Nobel Prize was instead awarded to American Carlton Gajdusek whose experiments had demonstrated that injections of kuru Brain in 1967, and CJD Brain in 1969, reproduced similar illnesses in chimpanzees (7).
Currently out on bail while awaiting trial for multiple charges of child molestation laid against him by one the New Guinea youths he has sponsored into the United States over the past 30 years, Gajdusek's research did however put an end to ideas that species barriers were an impediment to the spread of this type of disease.
Two neuroscientists from Yale Univin the United States, Laura and the late Eli Manuelides, went on to illustrate by 1975 that injections of human blood, like injections of Brain taken from kuru and CJD victims, transmitted the disease across the species barrier to laboratory animals (8a,7b).
Their prophetic, but unheeded, message implied that blood was the vehicle that carried the agent of CJD around the body until it chanced upon a hospitable residence like the Brain.
In other words, the blood route was identified as a key element in the transmission of CJD from a primary host to secondary one.
As distinct from infections such as influenza which is caused by an air-borne virus, but in parallel with AIDS and hepatitis B which are caused by blood-borne viruses, this meant that recipients exposed to human pituitary gland hormone injections, or to blood or organ transplants from a donor with CJD, risked becoming secondary CJD hosts once contagious material entered their blood stream.
Even as the understanding of spongiform encephalopathy increased, various human pituitary hormones programs in countries such as Australia, France, Great Britain, New Zealand, and the United States were attracting hefty government sponsorships.
Few of the program's stalwarts caught onto the implications of the Manuelides' experiments, and attempts between the years of 1978 and 1982 (9) to filter the CJD agent out of the pituitary hormones being injected into unsuspecting short-statured children and infertile women were left to British scientist and scrapie expert, Alan Dickinson.
At about the same time, a British Royal Commission on Environmental Pollution in 1979 raised the possibility that the unregulated cycling of protein-rich sheep remains back into animal feed might spread scrapie to cattle, as it had done to farm mink three decades beforehand, via the oral route.
At the same time too, in the push to meet the insatiable demand for more and more growth hormone, India, the world's second most populous country, became a Mecca for pituitary gland harvests.
Literally millions of pituitaries were harvested from cadavers in the subcontinent and sent to government laboratories back in Europe and North America.
The promised repayment in kind, namely with a supply of extracted growth hormone to treat short-statured children in India, became an unpaid debt.
Ironically, that broken imperialist promise may account for India's enviable present day position of discounting the presence of CJD anywhere in the country (10).
By 1985, the first of the fatal legacies from the medical imperialism emerged with four cases of CJD in human pituitary growth hormone-treated children.
Programs were immediately halted in most countries, the notable exception being France where the growth hormone treatment of children continued, based on the haughty assumption that the purity of the French hormone-extraction process accounted for the absence of a single case of CJD to that point in time.
Four years later, in 1989, during which time the number of French children at risk of growth-hormone-related CJD had practically doubled, the first French children fulfilled that tragic legacy (11).
In 1993, France's medical imperialists contended with possible manslaughter charges (12), and by 1996 France owned half of the world's 90 cases of pituitary hormone-related CJD (13).
From the earliest stages of the human pituitary hormone programmes, the wheels had been set in motion to conceal the fate of infertile women exposed to CJD-contaminated gonadotrophin (14).
Unlike growth hormone-treated children, whose years of biweekly to daily injections made it impossible for paediatricians to avoid the clerical red-tape that came with government sponsorship, women's gonadotrophin injections usually lasted for less than six months.
As a result, there was frequently left-over gonadotrophin that infertility specialists could inject into new candidates without going through the bureaucratic application process to renew hormone supplies.
This also meant that government records of women exposed to pituitary gonadotrophin were less than complete.
Additionally, just three years after the first cases of pituitary growth hormone-related CJD, the National Institutes of Health in the United States prematurely assumed in 1988 that the short-term nature of the gonadotrophin treatment precluded any risk of contracting CJD, and set about shredding the records of infertile women treated by some 250 US gynecologists over the previous 15 years.
A year later, in 1989, the pituitary infertility hormone snared its first CJD victim, a forty year-old woman in Australia (15). By 1993, the CJD of another three Australian women, all aged within a year or two of forty, had been traced back to injections of pituitary gonadotrophin.
By the time news of pituitary gonadotrophin-related CJD hit the headlines in Britain in 1993, authorities were in no position to answer consumer inquiries, one of which came from a 32 year old woman whose mother had died of CJD when aged 55 in 1975.
After having received five pituitary gonadotrophin injections in 1960, because whatever records had once existed had by then also been shredded (16).
Officially, 300 infertile British women were exposed to pituitary gonadotrophin, but medical literature (17a, 16b, 16,c, 16d, 16e, 16f) from UK infertility circles, dating back to the 1960s, indicates that the number was probably much larger.
While the risk of gonadotrophin-related CJD to Australian and, to a lesser extent, British women has reached the general media, the entire issue for American, German and Scandinavian women (18a, 17b, 17c, 7) has scarcely been touched.
Although the general elitism of human pituitary programmes restricted the medical imperialism to North America, Europe and Australasia, Third World children and women did not altogether escape the insanity of applying Frankenstein medicine to social conditions.
A medical report in 1991 (19) linked the CJD death of a young Brazilian man, like those of five youthful New Zealand men and women (20), with a childhood treatment involving pituitary growth hormone obtained from the US.
It goes without saying that the fate of women in Mexico City whose breasts were injected with US pituitary hormones, in an appalling experiment (21) to increase the volume of milk in lactating mothers, some already pregnant again, will never be known.
The opportunity to contain the CJD legacy of pituitary gonadotrophin injections has probably been lost as women unwittingly risk spreading their legacy via blood donation.
Similarly, the possibility that women treated with pituitary gonadotrophin may have transmitted their CJD legacy to their children has been totally cast aside, and there is an overwhelming medical disinterest.
Or perhaps ignorance, to investigate whether pituitary hormone treatments in the 1960s, 1970s and 1980s may account for the CJD deaths of women, aged a decade younger than the average age of sporadic CJD victims, which frequent the pages of medical journals in the 1990s (22a,21b).
Oddly, although the entire concept of blood-transfusion-related CJD was frankly dismissed by health authorities, by 1987, all US and New Zealand registered recipients of pituitary growth hormone had been advised not to donate blood and organs.
It took until 1992 for Australian and British blood banks and transplant programmes to follow suit, with the result that the Australian and UK general communities were exposed to the risk of secondary CJD transmission for five years longer than their American and New Zealand counterparts.
Somewhat inexplicably too, despite the theory of blood-transmitted CJD remaining largely unproven in humans, actions in the past two years indicate that authorities have finally opened their minds to the public health implications of the Manuelides' experiments.
Canadian authorities spent $15 million in 1995 to withdraw pooled plasma, already in the process of being transfused to thousands across the country, on the grounds that it contained a donation from a man who had subsequently died of CJD (23).
Similarly, in 1996, New Zealand authorities bit the bullet, albeit under weight of public pressure, to quarantine blood products that had been contaminated by a donation from a CJD infected donor (24).
And British blood banks also increased their precautionary measures with an extended questioning routine designed to screen out donations from parents, siblings, and children of CJD victims (25).
British microbiologist Steven Dealler, estimates CJD-infected blood may reach as many as 60,000 recipients each year (26), but the years-long incubation time preceding CJD symptoms increases the difficulty to link a blood transfusion recipient's CJD with a donor source.
It falls within the realms of possibility that secondary CJD in a transfusion recipient may appear years in advance of the primary CJD in a blood donor, and direct evidence of blood transfusion-transmitted CJD remained largely anecdotal until 1996 when the case of CJD in a liver transplant recipient was, after the liver donor had been cleared, traced back to a CJD-like illness in one of the blood donors (27a,26b).
One year after the first cases of pituitary growth hormone related CJD in 1985, the first of the protein-fed cattle came down with BSE (28). Advisory committees were set up around the world.
Apparently none had the foresight to include public health experts trained to weigh policy in terms of both best and worst predictions. Instead, for the next ten years authorities seized every chance to preserve the reputations and careers of eminent politicians, physicians and scientists, and managed to allay public anxiety by keeping news of their bungles out of the media.
Public and animal health ran a very poor second to the market pressures (29) that had transformed cattle from BSE-free herbivores into BSE-infected carnivores with a nonregulated protein diet.
In fact, even as BSE emerged in protein-fed British cattle in 1986, scientific advice that the epidemic could best be contained by compensating farmers for the immediate destruction of the ten thousand-odd infected cattle was dismissed solely on the basis of the financial outlay.
Following the ban placed on scrapie contaminated animal feed in 1988 the epidemic of BSE in cattle was supposed to be under control.
According to authorities, the peak 1992 weekly average of 700 new cases of BSE has fallen to 70 cases per week in 1996. At the same time, the notion of control was practically contradicted by the BSE in some 27,000 cattle born after the 1988 ban.
Rather, these figures, together with the 60 per cent of 1996 cases occurring in cattle born post-1988, indicated that pre-feed regulated cattle had passed BSE onto their calves.
Like the theory of blood-borne CJD in humans, earlier suggestions (30a,29b) that the BSE epidemic in cattle was maintained by maternal transmission were dismissed, and at times ridiculed, until a 1996 study proved otherwise (31).
Erring on the side of caution has invariably fallen foul of the Brain-dead culture underpinning the BSE/CJD fiasco.
As an example, the British Ministry of Agriculture, Fisheries and Food, known as MAFF, sabotaged a 1990 Brussels ruling designed to prevent the spread of BSE across to the European mainland (32).
MAFF instead issued civil servants with secret orders to skip the computer vetting of calves set for the lucrative sale yards of member countries of the European Union.
As a result, there were no checks to determine whether about two million veal calves sold to the European Union between 1990 and 1995 were born to BSE-infected cows or not.
Even the computer tracing of the BSE parentage of some two thousand cattle sold for foreign breeding after 1990 may be untrustworthy, partly because of MAFF's skulduggery, and partly because the calculated mean incubation periodof BSE is five years.
In the absence of a diagnostic screening test for BSE, the years-long period between infection and symptoms meant that it was impossible to determine which cattle were infected and which remained free of BSE.
But, an estimated 700,000 BSE-infected cattle entered the human food chain; chiefly because the animal's slaughter age, usually three years, predated the age at which they would show signs of BSE infection (33).
For the same reason, there is simply no way of knowing the number of breeding stock that were exported to the four corners of the globe before their sire or dam's BSE was subsequently uncovered.
Britain was not alone in the cover-up of the BSE scandal. In September, 1996, the French newspaper Liberation (34) revealed that a memorandum from French official Gilbert Castille had suggested back in 1990 that Britain ought to be asked not to publish its research results, saying it would be better to minimize BSE by practicing disinformation.
In fact, rather than ganging up on Britain, Brussels via Guy Legras, head of the European Commission's agricultural directorate, warned of the financial repercussions from a beef panic and hushed news of the BSE situation.
Additionally, cattle may not be the only species within the meat industry that are harboring the BSE/CJD agent in readiness for the food chain. Until March of 1996, no restrictions were placed on feeding cattle offal to pigs and hens (35).
Together with a common practice whereby animal-feed manufacturers share the same equipment to mix both cattle and pig-feed, this approach reflects a glaring ignorance within the agricultural industry about the dangerously infectious nature of diseases such as BSE and CJD.
This background, together with the extreme resistance of BSE and CJD to high temperatures and caustic chemicals that customarily rid instruments and tools of infectious materials, may explain the disproportional excess of CJD infection occurring in the farming community.
It also brings the focus back to blood-route transmitted CJD, and raises the prospect of simple kitchen injuries introducing BSE from meat products into the bloodstream of an unsuspecting public (36).
Some argue that the BSE panic is thinly supported by firm scientific evidence. Mad cows, mad scientists, and mad politicians feature prominently in the insults that flow back and forth.
History will be the ultimate judge, but in the absence of a plausible alternative to BSE-infected beef that would account for the recent spate of unconventional CJD in youthful victims - aged two to five decades younger than the majority of sporadic CJD cases - both animals and humans have earned a policy that errs on the side of caution.
Medical impropriety rather than nature has already destroyed the lives of 90 pituitary hormone recipients and their families; young lives have been snuffed out by an atypical, but equally cruel, form of CJD that appears to have come from herds infected by agricultural impropriety; and innocent British cattle are at threat of extinction because of BSE inflicted on them during a period of financial megalomania.
Sixty years of underestimating and mistaking the gravity of CJD/BSE issues for both humans and animals are enough.
Notions (37) that culling half of Britain's cattle population could make early inroads into global greenhouse targets, like those that propose restocking the sacred herds of India, and detonating Cambodia and Afghanistan's land mines with BSE-infected cattle are barbarous extensions of a Brain-dead culture which fostered its own breeding ground by convincing the public that "there was no evidence" of a dire outcome.
More truthfully, there was "no way of telling", and it remains to be seen whether the final consequences of the CJD/BSE mismanagememt will match or outscore the ramifications of the AIDS epidemic.
A worst case scenario-sized CJD epidemic will smash rather than stretch every available human resource. European imperialists, joined in this century by those from the United States, and to a lesser extent Canada and Australia, have widened the gap between developed and developing regions with modern discrimination (38a, 37b, 37c, 37d, 37e) that transgresses the boundaries of animal and human rights, development, environment, nuclear weapons, population, trade and wealth.
Similarly, the bigotry of medical expansionists has exploited the vulnerability of infertile women and short-statured children with human pituitary hormone cures that, in the end, have clouded their futures with a life-long threat of CJD.
Infertile women are the invisible victims within the scandalous human pituitary hormone equation of the medical imperialists.
Mad cow imperialists may be intent on turning Third World countries into storage yards for manmade BSE, but their would-be victims, wary of their abuse as virtual dumping grounds for nuclear waste, toxic chemicals and perilous medications, are highly unlikely to fall for that caper.
Rather, like the absurd reassurances from government authorities, and the invisibility accorded infertile women by CJD imperialists, these racist proposals are proof that a collective Braindead culture has learned little, or perhaps nothing, from sixty years of its own mindless economics, science and politics.
Articles for publication should be sent to me at: The Pathology Laboratory, Burnley General Hospital, Burnley, UK BB10 2PQ
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