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"Mad Cows and Englishmen"

Why the Current BSE epidemic in England Raises Questions About the Safety of Foodstuffs and Glandulars

 by Lily Giambarba Casura

    Vegetarian cookbooks are undoubtedly enjoying brisk sales in England these days,as concerns over the safety of British beef make headlines again in the European Economic Community. For the second time in the last ten years, an unusual virus is infecting herds of British cattle in record numbers and causing widespread concern among beef-eaters both in England and abroad. While the British government has come out soundly in favor of its now twice-hit beef industry by proclaiming that beef is "perfectly safe," not every scientist is so convinced. A growing body of evidence points to a connection between the disease affecting cattle, and a rare, degenerative and fatal brain disease in human beings.

    The virus in question causes bovine spongiform encephelopathy (BSE), a disease that has been nicknamed "mad cow disease" by the British press, a tag taken up elsewhere because it so aptly describes the stumbling gait, aggressive behavior, and degenerative brain disease that ultimately claims the afflicted cows' lives. Although no one seems to be exactly clear on what causes BSE whether it is a slow virus, or a rogue protein called a "prion" that can multiply without benefit of genetic material or even fully how it is transmitted, the current fear is that it is somehow linked to an equally tragic and fatal brain disease in human beings, Creutzfeldt-Jakob disease - the same disease that claimed choreographer George Ballanchine's life in 1983.

    Although both diseases were extremely rare in years past (BSE was unknown before 1986, when it first showed up in British cattle, and Creutzfeldt-Jakob disease is known to afflict fewer than one in one million people, generally the elderly), today both are on the increase, and the experts who see the diseases as linked (the suspicion that BSE in humans is Creutzfeldt-Jakob) are concerned that we may in fact be at the beginning of a human epidemic.(1)

    What complicates matters most, for the scientist and the layman alike, is that both diseases have extraordinarily long incubation periods from one to as many as fifty years making it that much harder to discern when and if exposure has become a risk. So long are the incubation periods, says one British public health expert, that "It will be many years before we know if human health has been compromised."(2)

An Accidental Experiment in Dietary Transmissibility

    The first evidence of BSE came to light in 1986, when British medical officials surmised that infected cattle may have contracted the disease from sheep who were infected with "scrapie."(1) ("Scrapie" is so named because of the afflicted animals' tendency to scrape themselves on fences, rocks, walls, etc.) Apparently, it had been the practice to grind up the carcasses of dead sheep and cattle and feed them to other animals, particularly cattle, as a "protein supplement"(3) - an unusual practice, considering that cows are herbivores. Although typically "soybeans and fish meal provide the protein in the best-quality British feeds, animal matter is used in cheaper ones," according to one source. The BSE epidemic this practice is reported to have caused is what one British health expert calls "an accidental experiment in dietary transmissibility between sheep and cows."(3) As a result of the original outbreak, the government in 1988 imposed a ban on the sale of cattle and sheep offal, excepting that of calves under six months old, "to prevent its resale."(4) [Offal in general is waste products, such as organs, from the slaughtering process. In this case, specified offal is defined as brain, spinal cord, tonsils, thymus, spleen and intestines (from duodenum to rectum inclusive), taken from cattle over six months old.](5) The British have always been known to be fond of such dietary items as meat pies, which can contain "ground-up brains or other organs" - in short, parts of the affected cattle carcass that may harbor the BSE virus.(2)

Thrown Off Their Feed

    In the wake of the current crisis, the British government has stepped up its public relations efforts to help the ailing British beef industry (a $7.5 billion business), attributing the BSE scare to sensationalist journalism ("Death in a Burger!" crowed the headline of one British tabloid, the Daily Star); nevertheless, despite the admen's best efforts, reports a recent New York Times article, "the public is voting with its fork." The last time around, then-minister of agriculture, John Gummer, ate a hamburger on television with his four year old daughter, Cordelia, defending beef as "perfectly safe," in a gesture intended to quell public fears about safety. Now, the current health secretary, John Dorrell, says publicly that eaters of British beef run "no conceivable risk of contracting Creutzfeldt-Jakob Disease," but the public appears less than convinced. British beef consumption, which had fallen off by 19% after the 1986 epidemic, fell an additional 5% this November, with the second round of BSE-reported deaths. Almost 1/4 of British adults have stopped eating beef or are eating less.4 Despite Gummer's best efforts, most affected have been the sales of hamburger, which are off 40%.(1)

    The scare has broadened to other countries as well. Other Common Market countries, led by Germany, have banned the sale of British beef, although it seems that the Russians have - or had - been willing to purchase it. Farmers in the United States, where herds are apparently currently free of BSE, are watching the epidemic carefully.

Realitively New on the Horizon

    Neither BSE nor CJD have been around for very long, relatively speaking. CJD's existence has been known for decades only, and BSE first came to light a mere 10 years ago, when British beef herds began to be infected by a strange new pathogen, giving rise to the nickname "Mad Cow" disease. At the height of the epidemic, in mid-1993, more than 100,000 cows (out of a total British cattle population of 11.8 million) had been affected by the ultimately fatal brain disease.(1) The resurgence in BSE cases noted again this past fall in England, while measuring only a third of the rate of the earlier epidemic, raises new and troubling questions about the health of British beef because of several other factors that have come to the fore.

    One is the death of four British dairy farmers from the relatively rare, but pathogenically similar, CJD (a fatal disease of the central nervous system, marked by motion disorders, aphasia and ultimately death), an event which is a "statistical improbability," according to Sheila Gore of the Medical Research Council's biostatistics unit. From Gore's point of view, the chance of four such deaths occurring by chance over the last three years is less than one in 10,000.(2) Second is the death of several British teenagers from CJD - a disease previously thought to strike only tiny numbers of the middle-aged and elderly. In fact, the number of British cases of CJD have doubled over the same time period that BSE has been known and now stand at 55 cases. The third is the fear that, even though the number of recorded cases of BSE is down, relatively speaking, compared to the last epidemic, the cases represent the failure of the scientific community to understand how BSE is transmitted, and government regulations to fully control its spread.

Historical Background

    BSE was completely unknown until 1986, when British domestic beef cattle began to be infected with a previously unknown pathogen. Apparently, cattle with the disease can appear quite normal for several years after infection. Then, they begin to walk unsteadily or to stagger, and become aggressive and dangerous - hence the nickname for the disease ("mad" is British slang for crazy). The scientific name for the disease, bovine spongiform encephelopathy, points out more clearly what is going on. At autopsy, according to the Harvard Health Letter, the cow's brain "looks spongy and full of holes under the microscope."(6) Also noticeable at autopsy are protein fibrils - fine, hairlike structures that seem to accumulate in the infected animal's central nervous system.

L-o-n-g Incubation Periods

    Creutzfeldt-Jakob disease, in addition to being rare, is progressive and fatal, with an extraordinarily long incubation period between exposure and onset. While a few cases in the scientific literature seem to be hereditary, there are a number of gruesome iatrogenically-induced examples of the disease as well. Most worrisome of all, however, are the extraordinarily long incubation periods of both BSE and CJD. According to one British medical journal, the incubation period of BSE is approximately one to eight years, with a mean of four to five years.(3) The Economist quotes a scientist suggesting a "15- to 40-year" incubation period for CJD, after initial exposure; England's Dr. Lacey mentions a "10- to 50-year" span wherein contracting the disease is possible, and the aptly-named Morbidity and Mortality Weekly, in an article on CJD cites shorter - eight years - but still disturbingly long incubation periods as well.

The Epidemiological Argument

    One argument that is raised is that the apparent rise in deaths from CJD are really the evidence of "better reporting." This is a common epidemiological argument that is raised, but one which is hard to prove conclusively. Ironically, the incidence of CJD in England is, apparently, similar to that of other European countries where BSE is either minimal or non-existent. However, in the absence of conclusive evidence that BSE and CJD are wildly dissimilar, or one is unable to be contracted from the other, caution prevails.

Scientists Dispute Cause of BSE and CJD

    The World Health Organization reported on the BSE and CJD purported connection in a 1993 memorandum. In the memorandum, they acknowledged - based on the research being done to date in England and throughout Europe and the U.S. that transmissible spongiform encephalopathies were on the rise. According to WHO's findings, until 1985, six total transmissible spongiform encephalopathies (TSE) were known, three in man and three in animals. From 1985 to May, 1993, nine further species have developed naturally-occurring TSE, (besides BSE in cattle).(7) WHO noted the high incidence in the U.K. - 92,000 cases at the time, a figure which has continued to grow - as opposed to other countries in Europe: Ireland (69); Switzerland (34) and France (5).(7) They also noted that spongiform encephelopathy has been successfully transmitted to mice, cattle, sheep, goats, pigs, marmosets and mink (data not published) after parenteral administration of brain from cattle confirmed to have BSE.(7) They added to this that "oral or feeding exposure to infected material from BSE-confirmed cattle was attempted and successful in mice, sheep and goats," but qualified that "infectivity has been detected so far only in brain and spinal cord from cattle with BSE."(7) And despite the low figures being reported elsewhere in the press [perhaps they have not read the WHO report?], the health organization mentions that in England, between May, 1990 and April 30, 1993, 250 cases of suspected CJD were notified to the surveillance unit; 117 of them have been classified as definite or probably CJD.(7) No doubt trusting in the conventional wisdom of the time, that the government's ban of sale and reuse of sheep and cattle offal would control the problem, the report's conclusion inspired what now seems to have been a false hope. "These events," it states, "are considered to represent a negligible risk to human health."(7)

To Jump - or Not to Jump - the Species Barrier

    Much has been made in the press, and in the scientific journals, of whether the transmissible spongiform encephelopathy, BSE, has the wherewithal to "jump" the so-called "species barrier" between cows and man. In some ways, this argument seems specious indeed, considering that virtually everyone involved in the controversy has acknowledged for the last several years that how BSE came about in the first place was vaulting the same barrier from sheep to cows - perhaps without so much as a backward glance.

    While authors in the British Medical Journal and Lancet argued about the specific mechanism of BSE's transmissibility - whether it was a "slow" virus or prion involvement - by 1994, an article in the Lancet stated that CJD belonged to a group of "transmissible spongiform encephalopathies," including BSE. Further, the authors remarked that in a study they had done, "Virus-like particles (10-12 nm diameter) have been observed in the experimental model of scrapie in hamsters. We report identical particles in brains of CJD patients but not in the brain of a patient with Alzheimer's disease or in controls without neurological disorders."(8) So scrapie in sheep could become BSE in cattle, which could conceivably become (or had already become) CJD in humans.

Leaping Lizards

    Other evidence of BSE's and CJD's transmissibility abounds. An excellent article in the November, 1990 issue of Harvard Health Letter reveals the following: "In the U.S., rates of scrapie infection are reported to be increasing, and the disease is now identified in goats, as well as in captive mule deer and Rocky Mountain elk... During the mid-1980s in Wisconsin, some cows that died before slaughter were fed to a population of mink, which subsequently developed the mink version of spongiform brain disease. Does this mean that the cattle were the source? Again, only speculation is possible."(6) In addition to the finding cited above that between the years 1985 and 1993, the number of TSEs worldwide increased from six to nine, "confirmation that prion diseases can be conveyed from one animal species to another originally came from the work of Clarence Gibbs, at the National Institutes of Health. He showed that scrapie, kuru and CJD can be transmitted to monkeys, which respond in all three cases by developing spongiform brain disease."(6) The same Harvard Health Letter mentions Britain's first case of a five year old Siamese cat diagnosed with CJD, apparently from a pet food source. Today, 50 such cases have been found. So much evidence seems to stack up on the side of transmissibility, whether as a virus or with prion involvement, that leaping the species barrier seems like not such an obstacle as once thought. In fact, as one microbiologist who has been following the controversy since the beginning, Robert Lacey of Leeds University says, "We know in general that most infectious agents can go from one animal to another...the exception is when they don't."(1)

Revising the Definition of "Life Form"

    The protein fibrils known as prions have been the subject of much controversy among scientists interested in tracking the spread of the disease, as well as other spongiform encephalopathies. According to work done by Bruno Oesch and his colleagues at the University of Zurich, these fibrils are highly infectious - so much so that their infectiousness increased 10,000-fold when they were concentrated in laboratory conditions. Strangely enough, however, when the fibrils were analyzed individually, nothing unusual was found. Each appeared to be a normal host protein modified by the disease, but not an actual foreign entity. In fact, the protein itself is apparently not infectious - only in concentration does it seem to be so. But how these protein fibrils manage to replicate - as they appear to in host organisms' central nervous systems - without benefit of genetic material is one of the epidemic's largest, and strangest, unanswered questions. In the words of one scientist, "If an infectious protein is the cause of these diseases, the definition of life itself may have to be reconsidered."(6)

Heat-Proof Prions

    One of the most frightening aspects of the research into prions, as these protein fibrils have been termed by the University of California's Stanley Prusiner, is that they can survive intact many of the methods that break down organic material like RNA and DNA, leading one scientist to conclude that either there is no genetic material, or that it is present in "a virtually undetectable form."(6) The inability to "kill off" the prions has particularly significant implications for cattle products in the human food supply. If the particles cannot be killed by heating or cooking, there's no safe way to justify ingesting the parts of cattle most commonly infected with the disease - the same offal that was banned by the British government for sale as a result of the BSE outbreak, beginning in 1988.

Spotty Government Regulations

    Unfortunately, the ban restricting sale of offal has not worked completely; and ironically, such a ban is not in effect elsewhere, including in the United States. The fact that 300 cases a week of BSE in cattle are being confirmed, six years after the ban took effect, many of these cases in cows who were born after the ban was instituted, means that either there are other ways of transmitting the disease from cow to calf, or that the ban in allowing the sale of offal from calves under six months old is not restrictive enough.

    In addition to the destruction of cattle offal except for calves' of a certain age, any cow exhibiting signs of BSE is supposed to be killed. The system does not always work very well, however. Apparently, only a quick, visual inspection is done; the British government has so far refused to do sample testing; and inspections show that regulations are not always scrupulously being followed.(1)

Guess What's Coming with Dinner

    If you follow the prion theory, as many British scientists do, any lack of thoroughness in inspecting and/or destroying infected foodstuffs is particularly frightening. Given the prions' ability to concentrate and/or replicate in infected tissue, Richard Barlow, of the Royal Veterinary College in Hertfordshire, [the main British center for BSE research] has shown that "the infectious agent of mad-cow disease can be transmitted to mice by feeding them infected brain tissue."(6) According to one report, "The infectious agent, whatever it is, appears to multiply in nervous tissue and the lymphatic system. Thus, the brain and spinal cord, spleen, thymus (sweetbread), and tonsils are considered to be high-risk tissues the most likely to be infectious if eaten."(6) As the New York Times reported recently, these proteins, which seem to propagate in organs and brains, "are not deactivated by cooking."(1)

    While the British public, thanks to the help of the government, has sworn off organ meat at least temporarily, unfortunately such organ meat is likely to be present elsewhere, especially products made from such organ meat. Given the extraordinarily long incubation periods of both BSE and CJD, the problem may remain in the planet's food supply for many years to come. Especially at risk is pet food, where ground-up organ meat has been used in the past as a cheap form of protein. In England, the CJD Surveillance Unit has determined that at least fifty cats have contracted CJD and pet food is likely to be the culprit.(6)

Mucking with Milk

    Another bizarre twist to the whole BSE story brings in a seemingly unrelated, but also controversial health matter that of treating dairy cows with recombinant bovine growth hormone (rBGH), a practice that seems deservedly to have come under fire in the United States. rBGH, manufactured by Monsanto Corporation, is a genetically-engineered growth hormone given to dairy cattle to artificially increase their milk production, for what seem to be inscrutable business-driven reasons. Scientific data indicates that rBGH-treated cows develop mastitis more readily, which then is treated with antibiotics, which eventually end up in our food supply. In 1992, the FDA went forward with the sale of rBGH, against the recommendation of the government's General Accounting Office, and said that they considered any potential health effects of rBGH to be "a manageable risk."(9) While women's health specialists are concerned that rBGH milk will lead to an increased incidence of breast cancer in women, there are other concerns as well. Michael Hansen, a biologist and research associate at Consumer's Union and Barbara Seaman, co-author of Women and the Crisis in Sex Hormones (New York: Bantam 1978) are concerned about the potential for rBGH cows to contract mad cow disease. They are concerned about a possible link between BSE's apparently easy transmissibility from infected protein supplements [read, composted diseased sheep and cattle] and "the kind of high-protein feed rBGH cows commonly eat to keep up with their increased metabolism and milk production."(9) In fact, one article goes so far as to say that several of the British dairy farmers who have died recently of CJD did so because of their practice of "drinking milk from their BSE-infected cows."(9) As a report on the purported link between rBGH and breast cancer indicates - other than Monsanto the manufacturer - it's hard to see who is in favor of using the genetically-engineered growth hormone in cattle at all.(9)

    Across the Atlantic, the United States seems to be taking what can only be construed as a "wait and see" attitude. Based on the Southwood Report's recommendations to the British government in 1989, their ministry of Agriculture, Fisheries and Food prohibited the sale of high-risk tissues (mainly brains and sweetbreads) for human consumption, and...banned the sale of any meat from animals known to be infected. The USDA followed the British lead, and banned all British beef products from import, products which had typically been limited to organ and scrap meat for pet food. Strangely enough, U.S. farmers continue their own practice of using sheep-derived feed here, a practice that has apparently been "discouraged...but...not banned outright." Some analysts think the likelihood of an outbreak in U.S. cattle seems small for several reasons: "Meat and bonemeal imported from Britain between 1980 and 1988 were used mainly in poultry feed (and birds haven't yet developed the disease [or perhaps their lifespan isn't long enough to evidence it]), scrapie is not very common here, and few rendered animal products are employed as protein supplements in cattle feed. Nevertheless, the surveillance of cattle in the USA has been stepped up."(6)

An Unsavory Iatrogenic History

    If prompt vegetarianism isn't the answer for you, it's hard to be comforted by knowing that the most common known forms of exposure to the deadly CJD are in fact iatrogenic. As the Lancet points out in a 1993 article, speaking about the cases studied in their report, "there are 62 cases of iatrogenic CJD by implantation or inoculation, but no 'case-to-case' transmissibility in 'non-iatrogenic cases'." For the truly morbid, September, 1995's FDA Consumer offers a few routes of iatrogenic CJD exposure: transplanted corneas, dura mater (a brain-associated membrane), injections of human growth hormone [and human pituitary growth hormone], and re-use of EEG electrodes that had been used on CJD patients.(10) It's also apparently possible to contract CJD from blood products, as witnessed by the "voluntary recall" by the American Red Cross, Baxter Healthcare and Miles, Inc. of all blood products from a "frequent blood donor" with CJD.(11) (Ironically, plasma products partially made from the same source have stayed in circulation, no pun intended).

A Pandora's Box of Horrors

    A look into the history of iatrogenically-transmitted CJD is a veritable Pandora's box of horrors. The literature cites cases of human growth hormones prescribed to fertility patients, human pituitary growth hormones for the vertically-challenged, and transplanted items such as dura mater, mentioned above, all obtained at post-mortem from cadaveric sources (although this practice was in fact illegal). The British government, along with an entity known as Commonwealth Serum Laboratories (CSL), have been sued in at least one class-action suit by the patients and families (and in many cases, their estates) of those who had been prescribed these various protocols and ultimately contracted CJD. An issue of the Lancet from several years ago reports that more than one hundred people were suing CSL (who prepared the growth hormones) for damages and the British government - which permitted, or encouraged, its use. The hormones at issue were hPG (human pituitary gonadotropin) for infertility, and hGh (human growth hormone) for short stature. Post-mortem sourcing of growth hormones seems to have dwindled after the death of eight children in England, who died as a result of being administered the hormones. In Australia, four women died as a result of receiving fertility hormones derived from cadaveric sources.(12) In England, lawsuits arose over the deaths of family members, but also the concerns of what they themselves termed "the worried well."

    Not surprisingly, the findings of the commissions which looked into the problem showed a disappointing array of problems with loathsome consequences that could have been avoided by better information, stronger ethics, and a greater sense of concern on the part of the doctors involved - and the government - for the patients. It was found that the women who had received fertility treatments fared worst. One commission found that the doctor/patient relationships of the women receiving the hPG were not good. "Most were not told that the source of the hormone was pituitary glands collected at post-mortem," reports the Lancet . "Few understood...that there were other sources [available]."(13) A look at the number of violations, summarized below, that the commission found in the practice of administering hPG and hGh is sobering indeed:

  • Practice was not confined as it should have been.
  • Alternatives "rarely discussed."
  • Exclusion criteria "formulated, but pathologists and mortuary attendants not informed of them."
  • Taking pituitary glands at post-mortem had been illegal since the 1970s. However, instead of taking them for "evaluation," pituitaries were being removed from cadavers "to supply CSL with raw material."
  • Cadaveric samples "not checked for viral particles" before being listed as "approved."
  • Ethical conflicts among doctors prescribing them who also stood to benefit from the transaction. [Were they shareholders in CSL?]
  • Health department stopped the practice in 1985, but "neglected its moral duty to inform recipients of the risks they faced until media pressure forced it to do so five years later."(13)

    So once again, with the BSE epidemic in England, we have an all-too familiar situation of the media bringing to light concerns that the government, and those with a vested interest in the process, work to deny. What will the eventual result be? Are we poised, as one scientist says, for the beginning of a "human epidemic" with CJD - or will the crisis pass away quietly? The worst aspect of it all, in many people's opinions, is that with a latency period of up to 40 years for the disease to manifest itself, that it will just take too long until the answer is known for sure.

    In the meantime, it seems to be a case of "caveat consumer," whether with beef products or items made from beef, from pet food to glandulars. Although the trade in glandulars (supplements intended to boost the body's own glandular functions by consuming freeze-dried raw cattle and pig glands) seems to have dropped off over the last ten years, due in part to consumer squeamishness about the items involved, and a growing vegetarian/vegan or ecological consciousness, some doctors such as Seattle's Ralph Golan, M.D., warn that we would be wise to take a cautious approach. Says Golan in his recent book, Optimal Wellness: Where Mainstream and Alternative Medicine Meet, "Due to a concern about viral contamination, I hesitate to recommend raw glandular tissue." He elaborates further, "[A]...compelling reason not to use adrenal glandular (or any glandular) substances: viral contamination. 80% of the domestic animal herds in England have been found to contain a "slow" virus (one that takes years for its symptoms to show), which causes a form of dementia in humans... It is not likely that this virus has contaminated herds in the United States or Argentina or New Zealand - frequent sources of glandular products. But until adequate detection techniques are widespread and government protective agencies decide to investigate this concern, I suggest you avoid using raw glandulars, which are essentially uncooked animal tissues."(14)

    To get involved in the rBGH boycott, and/or to obtain a list of companies who are rBGH-free, write: The Pure Food Campaign, 1130 - 17th Street NW, Suite 300, Washington, DC 20036.




1. Darnton, J, Fear of mad-cow disease spoils Britain's appetite. The New York Times 1996; 145:p:A1, col. 5.

2. Dawley, H, Mad cows and Englishmen: worries over a deadly ailment butcher British beef sales. Business Week 1995; 3456:44.

3. Collee, JG, BSE: Stocktaking, 1993. The Lancet 1993; 342:790.

4. Uncertain scientists. The Economist 1995; 337(7944)56-57.

5. Bovine spongiform encephelopathy in the United Kingdom: a memorandum from a WHO meeting. Bulletin of the World Health Organization 1993; 71:6:691.

6. Reeve, MP, Mad cows and Englishmen. Harvard Health Letter 1990; 16(1)1.

7. Bovine spongiform encephelopathy in the United Kingdom: a memorandum from a WHO meeting. Bulletin of the World Health Organization 1993; 71:6:691.

8. Ozel, M, Xi, YG, Baldauf, E, Diringer, H, Pocchiari, M, Small virus- like structure in brains from cases of sporadic and familial Creutzfeldt-Jakob disease. The Lancet 1994; 344:923.

9. Burkhalter, S. Recombinant bovine growth hormone: a breast cancer connection? The Network News 1994; 19(2)1.

10. Blood product recalled. FDA Consumer 1995; 29:5.

11. Precautions advised for blood supply. FDA Consumer 1995; 29:3.

12. The Lancet 1993: 342:672.

13. Ragg, M, Australian human pituitary hormone and CJD injury. The Lancet 1994; 344:531.

14. Golan, Ralph, MD, Optimal Wellness. Ballantine Books, New York, 1995.


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