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32nd World Vegetarian Congress 1996
[Vegetarian Summerfest '96: A World Vegetarian Congress]

The Public Health Implications of Mad Cow Disease
by Michael Greger (617) 321-9684

a talk at the World Vegetarian Congress, 1996
Updated and revised July 27, 1996. Please feel free to use and/or distribute in any manner

March 20 Announcement

Michelle Bowen, 29, died a slow painful death which ended in a coma three weeks after giving birth to her son via emergency cesarean section (Moyes, 1996). Stephen Churchill, a student, started feeling depressed and dizzy last year, then sank into a living nightmare of terrifying hallucinations; he was dead in 12 months at age 19 (Moyes, 1996). Peter Hall, 20, showed the first signs of depression around Christmas, 1994 (Victims, 1996). Within twelve months he couldn't walk, talk, or do anything for himself (Victims, 1996). They all died of Creutzfeldt-Jakob disease, a relentlessly progressive and invariably fatal dementia (Oxford, 1996) which usually attacks people in their sixties (MacDonald, 1996). Cases such as these involving people under age 30 were until recently exceedingly rare (Creutzfeldt-Jakob, 1996).

Around the next Christmas, 1995, an uproar ensued when a leading British neuropathologist Bernard Tomlinson announced he refused to feed his children hamburgers out of fear that they might contract this disease from infected beef (Schools, 1996). On Wednesday, March 20, 1996, Sir Tomlinson's fears were validated. The British government announced that exposure to a cattle disease called bovine spongiform encephalopathy (BSE) was the most likely explanation of these deaths and seven other recently diagnosed cases of Creutzfeldt-Jakob Disease among British young people (Brown, 1996a).

'Very unhappy' were the words British vet Colin Whitaker used to describe the dairy cow who became the world's first documented case of BSE on a fine spring morning in 1985 (Robinson, 1992; Birkett, 1996). Dubbed Mad Cow Disease by the British press (Shaw, 1993), BSE has so far stricken over 150,000 cattle (Ministers, 1996), affecting over half of British dairy farms. (Bovine, 1996). Several top scientists now fear that these first few human deaths may just be the tip of the iceberg (Reynolds, 1996). If so, Britain may be on the brink of the largest public health calamity since the Black Death (Cookson, 1996a) with worst case scenario estimates involving the deaths of millions of people who ate infected beef (Mad, 1996c).

Creutzfeldt-Jakob disease (CJD) is a human spongiform encephalopathy (Harrison, 1991) whose standard clinical picture involves weekly deterioration (Glanze, 1992) into blindness and epilepsy (Dealler, 1990) while the brain becomes riddled with holes (Gibbs, 1994). Some may recognize this disease as that which claimed the life of renowned ballet choreographer George Balanchine (Wlazelek, 1990a). About one in a million people spontaneously come down with it (Worl, 1996), but it is this seemingly new form of the disease striking young people that has thrown much of Europe into a panic (Britain, 1996).

The World Health Organization recently agreed with the British government's assessment linking the disease in people with the disease in cows (McGregor, 1996). They conclude that there seems to be a new variant of CJD, and its emergence is best explained by the BSE epidemic in cows because of a number of consistent, unusual features (McGregor, 1996). Other than being extraordinarily young--average age 27 as opposed to the usual age of around 63 (Brown, 1996a; Pain, 1996)--the human victims also had atypical EEGs (Dillner, 1996) and take twice as long to die as the elderly CJD victims (MacDonald, 1996). The most defining characteristic, though, was found when their brains were autopsied (Ten, 1996). Along with psychiatric symptoms unusual to CJD (Collinge, 1996), the brain pathology is vividly reminiscent (Link, 1996) of Kuru, a disease once found in a New Guinea tribe of cannibals who ate the brains of their dead (Public, 1992). Referring to this purportedly new variant of the disease, Germany's leading expert on CJD stated, "everything suggests that BSE is the cause..." (German, 1996).

Britain's Chief Medical Officer's view that the "probable" (Ministers, 1996) link between CJD and BSE was, "cause for serious concern", came as a complete reversal of the position the government held for a decade (Brown, 1996b). The day after the announcement, five European countries banned the importation of British beef (Doughty, 1996) and 10,000 British schools dropped beef from their menus (Cookson, 1996b). Within days, chains like McDonald's, Burger King and Wendy's in the U.K. stopped serving British beef (Wintour, 1996; Parker, 1996b).

Less than a week after Britain's CJD-BSE announcement was made, the European Union quarantined the British isle, voting an immediate and indefinite ban on the export of British beef worldwide (EU, 1996). The same day--in what's described as one of the biggest operations in decades--Ireland deployed extra police with troops on standby to seal off its border to prevent Britons from smuggling in their cattle (Ireland, 1996). Two days later, beef from British cattle considered to be especially high at risk was banned in Britain itself (Britain, 1996).


The seemingly novel (Harrison, 1991; Modie, 1993) infectious agents that cause spongiform encephalopathies like CJD and BSE evoke no immune response (Patterson, 1995) and consequently may slowly accumulate (Lacey, 1991) without any signs or symptoms for up to 30 years (Collee, 1993) No one knows how many people may have already been infected. John Pattison, Dean of the University College of London Medical School and Chairperson of the British government's Spongiform Encephalopathy Advisory Committee, thinks there could be 500,000 people already incubating CJD (Cookson, 1996a). "At this stage," he adds, "we have to say it's totally unpredictable." (Reynolds, 1996). Professor Pattison says he does not feed beef to his grandson (Less, 1996). Microbiologist Steven Dealler, secretary of the Spongiform Encephalopathy Research Campaign, places the possible death count at 2 million people (Hornsby, 1996b). Professor Pattison reportedly agreed with this possible worst case scenario assessment (Hornsby, 1996b). Richard Lacey, child health specialist and microbiology consultant for the World Health Organization (Lacey, 1994), believes, based on studies of Kuru incidence (McKie, 1996), that there could be up to a half million British deaths a year as the epidemic peaks in the next century (British, 1996).

It is now close to being generally accepted that the cause of both the disease in humans and cows isn't a virus or a bacteria or a fungus, but a "prion", an infectious protein (Carr, 1996). Called the "most intriguing, unsolved puzzle in modern biology" (Phillips, 1991), the whole concept of prions challenges the basic tenets of biology (BSE, 1988). Prions have also been called the "strangest thing in all biology" (Beil, 1996). It not known how they replicate (Public, 1993) and because of their unique makeup, they are practically invulnerable. They are not adequately destroyed by cooking, canning, or freezing (Taylor, 1992; Lacey, 1991). Chemicals or enzymes which degrade nucleic acids, proteolytic enzymes of the digestive tract, and usable doses of UV or ionizing radiation are all ineffective in destroying their infectivity (Dealler, 1991; Marsh, 1993). Even heat sterilization, domestic bleach (Dealler, 1990), and formaldehyde sterilization have little or no effect (Holt, 1988). One study even raised the disturbing question of whether even incineration could guarantee inactivation of prions (Brown, 1990). National Institutes of Health expert Joseph Gibbs remarked to Cornell's Food Science Department that one of the only ways to ensure one's beef is safe is to marinate it in a concentrated alkali such as Drain-O (Gibbs, 1994). Prions have been called the smallest (Keeton, 1993), most lethal self-perpetuating biological entities in the world (Hunter, 1993).

Crisis in Britain

BSE was 'almost certainly' (Kimberlin, 1992) caused by feeding cattle ground up sheep infected with an ovine spongiform encephalopathy known as scrapie (Modie, 1993). In modern agribusiness, protein concentrates (or meat and bone meal, both euphemisms for "trimmings that originate on the killing floor, inedible parts and organs, cleaned entrails, fetuses..." (Ensminger, 1990)) are fed to dairy cows to improve milk production and most other livestock as well (Flaherty, 1993; Mad, 1990). The recycling of the remains of infected cows into cattle feed has probably led to the British epidemic's explosive spread (Collee, 1993). An editorial in the British Medical Journal described BSE as resulting "from an accidental experiment on the dietary transmissibility of prion disease between sheep and cows" (Harrison, 1992). A subsequent "accidental experiment" of this kind, with humans, probably occurred in England in the late 1980's when meat contaminated with BSE entered the food chain (Harrison, 1992). The result of this experiment is awaited, "as we live through the incubation period" over the next decades (Harrison, 1992).

Widespread fear first struck years ago (Aldhous, 1990a). By 1989, BSE had grown into the most serious threat ever posed to British agriculture (How, 1990), but the government assured the public the disease probably wouldn't spread to other animals (Lacey, 1992). And then in April 1990, Max, a pet Siamese, died of a hitherto unknown feline spongiform encephalopathy (Lacey, 1994). BSE-infected pet food was considered overwhelmingly the most likely explanation (Cherfas, 1990). Then zoo animals like cheetahs, ostriches and antelope started dropping dead (Kirkwood, 1994). Together, these events sparked a public uproar (Aldhous, 1990b) with unprecedented media attention (Bradley, 1992). Fearing the spread of BSE into the British population, hospitals, nursing homes (Schrof, 1990), and over 2000 schools (Bleifuss, 1993), serving over 750,000 school children (O'Loughlin, 1990), stopped serving beef or restricted its consumption. By May 1990, a quarter of the population reportedly refused to eat beef (Tilcon, 1992). In six months beef prices dropped 25% (Modie, 1993), devastating the cattle industry. Then Australia, Israel (Pain, 1990), and a dozen other countries (United, 1990) banned the importation of British beef because of the BSE epidemic.

Britain's Meat and Livestock Commission countered the gathering fears with a $6.5 million advertising campaign touting red-meat consumption (Schrof, 1990). TV spots featured the Minister of Agriculture exclaiming, "It's delicious!" while eating burgers with his four-year-old daughter Cordelia (Caldwell, 1991; Pearl 1996a). The campaign succeeded. Schools put beef back on the menu (Bradley, 1992) and beef consumption returned to semi-normal levels. Despite continued warnings from scientists like Dr. Lacey, the European community had lifted its ban and most other countries had greatly relaxed their trade restrictions (O'Loughlin, 1990)until March of 1996 when news of the deaths of these young people broke (Britain, 1996).

The current worldwide ban forced Britain to initially agree to kill and incinerate (Culling, 1996) (or pulp and bury (Field, 1996)) millions of cattle (Gruzen, 1996) at a total cost of billions of dollars (Wolf, 1996), a decision supported by the National Farmer's Union and the Minister of Agriculture (Parker, 1996b). The President of Britain's Board of Trade has confirmed recently that the government is looking to use the bodies of the slaughtered cattle as fuel in electricity generating stations (Hornsby, 1996c). The selective culling may not eliminate the epidemic, though, as the number of animals Britain has agreed to kill has since been drastically reduced (Hornsby, 1996a) and evidence exists that prions can remain infectious for years in the soil (Brown, 1991) and/or can be harbored by insects.(Wisniowski, 1996).

A better solution would seem to be to find out which cows are actually infected instead of just killing them indiscriminately. Such a test for detecting BSE in live cattle was reportedly offered to the British government seven years ago by Harash Narang, a clinical virologist with the British public health service (Pearl, 1996b). Dr. Narang claims he was subsequently seriously harassed and fired as a result of this work (Boseley, 1996). Food Policy Professor Tim Lang describes the treatment of Dr. Narang as, "incredibly shoddy" and, "just disgraceful" (Boseley, 1996). Critics presume the government did not want the public to know how much infected beef was entering the food chain (Boseley, 1996) and therefore discouraged such tests to protect the $4.6 billion beef industry (Pearl, 1996b). In fact, Dr. Lacey claims that beyond much reasonable doubt the British government has at all stages concealed facts and corrupted evidence (Lacey, 1994).

The Labor Party in Britain charged the government with a "reckless disregard for public health" (Parker, 1996b), "seriously complacent decisions" (Cookson, 1996a), and a "pathetic" (Britain, 1996) response to the current crisis which the Prime Minister calls the worst to confront the government since the Falklands War. Others echoed similar charges of procrastination and delay (Pearl, 1996b). A _New Scientist_ editorial explained how the British government "tried to push scientific advice aside when it did not suit them." (Give, 1996). An editorial in _The Lancet_ criticized the government for making the error of equating the absence of evidence of risk with evidence of little or no risk (Less, 1996). Statements like "There's no way of predicting..." seemed to transform in the halls of government into, "There is no evidence..." (Ministers, 1996). These statements and British Agriculture Minister Angela Browning's January 1996 pronouncement that her government's stance was "ultra-precautionary" (Apocalypse, 1996) bear a certain resemblance to similar statements now coming from the United States government (United, 1996). At the same time Britain's Prime Minister was still asserting that there was absolutely no connection between BSE and CJD (Apocalypse, 1996) and still attempts to reassure the public that beef is safe to eat to this day (Less, 1996). Likewise the USDA continues to adamantly assert that there is no BSE in the USA (Garrett, 1996).

BSE and the USA

The United States has 100,000,000 cattle (Qualitative, 1991) and the highest per capita beef consumption in the world (Flaherty, 1993). The British strain of BSE hit North America in 1993 (Case, 1994). The cow was found on a ranch in Alberta, Canada and was one of many imported from the U.K. before both Canada and the U.S. banned the importation of British cattle (Chen, 1996). Of the 499 (United, 1996) British cattle imported into the U.S. before the 1989 ban, 188 of them have been rendered down (Bleifuss, 1994) (presumably for other livestock to eat) and 34 remain unaccounted for (Dateline, 1996). One of the imported bulls slaughtered had a "central nervous system abnormality" of which the USDA reported, "[t]here is no definitive evidence that [the bull] either had or did not have BSE" (Bleifuss, 1994). In fact the USDA calculated that there was a 50% chance that at least one of the cows was infected (APHIS, 1994). Although the importation of British beef has been banned from the U.S. for a decade due to an unrelated disease (O'Loughlin, 1990), over 13 tons of meat and bone meal, which has been implicated in the birth of the British epidemic, has come into the U.S. from England between 1982 and 1989 (Hueston, 1992).

Indigenous conditions in the U.S. conducive to a BSE outbreak include the presence of scrapie in 39 states (Marsh, 1991). The prevalence of the disease is not known since data on scrapie is not collected in all states (Bovine, 1996). The 40-year (Miller, 1993) USDA Scrapie Eradication Program has been called a "dismal failure" (Bradley, 1991) and was even implicated in the recent rise of scrapie-infected sheep (Marsh, 1991). Admitting defeat, the USDA scrapped the Scrapie Eradication Program four years ago and replaced it with an "entirely voluntary" control program (Bleifuss, 1993). Meanwhile 22,000 tons of sheep slaughterhouse by-products are produced in the United States every year which go primarily into animal feed (Qualitative, 1991). One of the main differences between the U.S. and Britain that helps minimize the risk of an outbreak is a dramatically smaller proportion of sheep to cattle overall (Qualitative, 1991). This is a moot point, however, if BSE is already here.

Downer Cows

A year before BSE was even reported in Britain, Richard Marsh, Chairman of the Department of Veterinary Science at the University of Wisconsin-Madison, was alerting dairy practitioners of the possibility that a, "previously unrecognized scrapie-like disease in cattle" existed in the United States (Marsh, 1985). Mink are sentinel animals like canaries in coal mines. They were the first, for example, to show toxicity from DES and PCBs (BSE, 1992) and since 1960 there have been four outbreaks of a mink spongiform encephalopathy (also called TME) on U.S. fur farms (Robinson, 1994). This perplexed researchers who were unable to orally infect mink with scrapie-infected sheep brains (Marsh, 1993). A clue came in 1985 when TME wiped out a population of minks in Wisconsin who hadn't eaten any sheep at all (Tainted, 1990). Their meat portion of their diet consisted almost exclusively of dairy cattle called "downers," (Marsh, 1991) an industry term describing cows which collapse for unknown reasons and are too sick to stand back up (Bovine, 1993) Dr. Marsh believes that there was a form of BSE in the United States and that it manifests itself as more of a "downer" cow disease than a "mad" cow disease (McNair, 1993; Marsh, 1993).

Downer cow syndrome is a major problem among dairy cattle (Radostits, 1994), with tens of thousands of cows going down for unexplainable reasons every year in the U.S. (Bovine, 1993). If even a tiny percentage of these cows are falling victim to BSE, this could have frightening implications on a grand scale. If downer cows can be kept alive long enough, they can be used directly for human consumption (Bovine, 1993) and their bones boiled (along with their "lips, head, knuckles, feet..." (Ensminger, 1987)) to make gelatin (U.S., 1996b), a main ingredient in products like marshmallows. If deemed unfit the carcasses are melted down in a process called rendering into products like animal feed or pet food (Hearing, 1995). The Downed Animal Protection Act, a bill currently before the Congress (S. 1847 and H.R. 2143) would prohibit the use of downed animals for human consumption by ensuring the cows are humanely euthanized instead of oftentimes literally dragged to market (Hearing, 1995).

Numerous tests have been performed and none exclude the possibility that U.S. dairy herds harbor some form of BSE. Mink, like many mammals, were found to be susceptible to BSE; when mink are fed BSE-infected brains from British cows they die from a spongiform encephalopathy (Robinson, 1994). The disease can experimentally be spread from mink to cows and from cows back to mink (Marsh, 1991). The critical experiments, though, involved innoculating brains from American sheep infected with scrapie into American cattle (Cutlip, 1994). In England, presumably scrapie-infected cows go mad, twitching (Caldwell, 1991) and kicking into a rabid frenzy (Robinson, 1992). But in the U.S., scrapie-infected cows instead staggered to their deaths (Hourrigan, 1990) like downer cows do (Cutlip, 1994). These experiments support belief in a form of BSE native to the United States (BSE, 1992). Based on the small number of mink farms decimated by this disease, though, it would seem to be so rare that Dr. Marsh has asserted that American beef is, "totally safe" as far as he can tell (Dateline, 1996).

U.S. Surveillance

By 1990 the USDA had 60 labs monitoring U.S. cattle herds for BSE (O'Loughlin, 1990). In 1991 the Animal and Plant Health Inspection Service (APHIS), the governmental agency which ensures the health of the nation's livestock, concluded that the, "possibility of BSE appearing in U.S. cattle is extremely low." (Bleifuss, 1993). The assumption made by APHIS and others (Hueston, 1992), however, was that, "scrapie infected sheep were the only source of the BSE agent." (United, 1993; Quantitative, 1991). This is certainly questionable in light of the evidence of an indigenous BSE strain. Likewise, the USDA surveillance program (described as slow, clumsy, and ineffective) (Moore, 1993) began looking for the rabies-like symptoms of the traditional British strain of BSE (Miller, 1993), in effect disregarding the available evidence. In June 1992 a USDA consultant group decided that changes in the research program to accommodate the possibility that BSE was already present in the U.S. were, "not appropriate at this time." (Bleifuss, 1993). The panel that made this decision included representatives of the National Milk Producers Federation, the National Renderers Association, the American Sheep Industry Association and the National Cattlemen's Association (Bleifuss, 1993).

In 1993, however, the USDA also began testing downer cows (Flaherty, 1993). In all, 2,791 brains from suspect cattle (WHO, 1996) from 43 states have been examined by APHIS (United, 1996) with plans to increase the inspection (U.S., 1996b). They report that no evidence for BSE has been found in the United States (United, 1996). Unfortunately they were evidently relying on standard techniques used by British officials (Altman, 1996d). Not only does the suspected American version of BSE differ in outward appearance, the affected brains of the cows infected with scrapie from American sheep also looked different from the British variety (Cutlip, 1994). Only a small percentage of the collected brains are therefore even being properly tested (Dateline, 1996). Even if the more sensitive techniques were utilized in all the cases, Dr. Marsh feels that this number would be insufficient to impart a sense of future security (Altman, 1996d); statistically, with this many samples a thousand infected cows could be missed (Bovine, 1996).

There is also suspicion that the USDA might try to intentionally cover up any suspected cases in an attempt to protect the $150 billion (Kahler, 1996) beef industry from collapse (Beef, 1996a). Beef is the largest revenue source for American agriculture nationwide (Weber, 1996). The U.S. beef export business alone is worth billions (Beef, 1996b) and has been described as the, "future of the American beef industry" (Webb, 1996). A single reported case of BSE could put this entire industry in jeopardy (Gibbs, 1994).

The inclination of governments and individuals to suppress information contrary to business interests has been documented. In Germany, for example, scientists have admitted that many cases of BSE were not reported (Neale, 1996). Ireland also reportedly concealed a recent BSE outbreak to protect its exports (Irish, 1996). When the monetary compensation given to the British farmer whose infected cows were incinerated by the government rose from 50% of market value to full compensation, the number of reported cases shot up 73% (Dealler, 1990). Presumably, the earlier economic disincentive persuaded farmers to overlook a few mad cows. In fact, British BSE cases have been severely under-reported with estimates of as many as 40% of clinical cases missing from government statistics. In the U.S. when indemnity payments for scrapie infected sheep tripled so similarly did the number of reported infected flocks (Qualitative, 1991). The Sunday Telegraph reported that "British officials believe that some European countries concealed or ignored evidence of 'mad cow disease' for fear of the consequences for their own farming industries." (Neale, 1996). It is estimated that thousands of infected animals went unreported throughout Europe (Cracknell, 1996).

An internal memorandum dated October 12, 1990 was leaked from the European Commission Department of Consumer Affairs (Mad, 1996b). Brought to light by a leading French consumer publication _Que Choisir_, the memo describes instructions given to the Standing Veterinary Committee comprised of veterinary officials from European Union member states (Mad, 1996b). Item 1 of the memo starts, "[w]e must take a cold attitude towards BSE so as not to provoke unfavourable market reactions. No longer should BSE be spoken of." Item 2: "We are going to ask the United Kingdom, through official channels, to stop publishing any more research results." The document concludes, "[i]n a general context, this BSE affair must be minimized through disinformation. Better to say that the press has a tendency to exaggerate" (In, 1996). On June 30, 1996 the _Journal du Dimanche_ published this confidential memo on the front page of its Sunday edition (In, 1996). The story was corroborated with the former official who drafted the memo (Helm, 1996), but an investigation through the European Parliament revealed the minutes of the meeting in question have mysteriously "disappeared" (Bodkin, 1996).

The problem, as many English pundits saw it, is that the British Ministry of Agriculture, Fisheries, and Food represents the interests of both consumers and the beef industry (Masood, 1996). A similar conflict of interest exists in the United States. The mandate of the USDA is to promote agricultural products but also to protect consumer health. In Britain, at least, it would seem that the government's attempt at protecting the beef industry by concentrating more on PR crisis management than on doing anything substantial ended up not only hurting the industry, but consumers, farmers, and the government as well (Delamothe, 1996).

U.S. Feed Ban

With scientists like Dr. Marsh saying, "[t]he exact same thing could happen over here as happened in Britain" (Tainted, 1990), and with beef consumption already at a thirty-year low (Schrof, 1990), the USDA is justifiably worried. As in the U.K. the U.S. has been feeding dead cows to live cows for over a decade (O'Loughlin, 1990). According to the USDA, "virtually all [U.S.] feed manufacturers use meat and bone meal in their feeds" (Bovine, 1996) and most U.S. cattle are fed such rendered animal tissues (Quantitative, 1991). In fact, here in the U.S. a minimum of 14% of the remains of rendered cattle are fed to cows (Marsh, 1993) (another 50% goes on the pig and chicken menu (Hueston, 1992)) and the 1993) 2)rendered cattlesand the usage of such supplements continues to increase (Qualitative, 1991). In 1989 alone the U.S. rendered two million tons of cattle for use primarily in animal feed and pet food (Qualitative, 1991). Because of greater cattle "recycling" than in the U.K., the USDA has conceded that, "the potential risk of amplification of the BSE agent is much greater in the United States" than in Britain (Qualitative, 1991). There has been a substantial increase in the use of animal protein in commercial dairy feed since 1987 (Tainted, 1990; Marsh, 1993) and the recent introduction of bovine growth hormone (BGH) will only increase the use of rendered animal proteins in the rations of dairy cattle due to increased energy requirements (Bleifuss, 1994).

Although there is case description in the New England Journal of Medicine in which colostrum from a Creutzfeldt-Jakob diseased woman was found to be infectious to mice (Tamai, 1992), cow's milk is considered safe by the World Health Organization. Feeding animal tissues to dairy cattle is considered risky mainly because of their early "retirement" into hamburger (Bradley, 1993). Americans eat 2.6 billion pounds of dairy cows annually (Bleifuss, 1994); roughly two-thirds of all cattle slaughtered come from dairy stock (Qualitative, 1991). Over half of U.S. dairy cows are killed before their fourth birthday (Walker, 1991) primarily because of either, "inadequate reproductive performance" (Strandberg, 1996) or because their milk production levels start to fall (Reference, 1996). One-fifth of all hamburger meat eaten in the U.S. each year is from these culled dairy cows (Bleifuss, 1994).

Dr. Gibbs, who recently chaired a World Health Organization investigation into the disease (McGregor, 1996), argues that one out of every million cattle naturally develops BSE (Flaherty, 1993). "Do I believe BSE is here [in the U.S.], of course I do," Gibbs said at a University of Wisconsin symposium (BSE, 1993). With more than two decades of prion research behind him, Stanley Prusiner, the scientist who coined the term "prion" reportedly agrees that mad cow disease must be present in the U.S. at low levels (Mad, 1996a). Dr. Marsh and four colleagues announced that there is a, "high likelihood of cattle-to-cattle cycle of a transmissible spongiform encephalopathy in the United States today" (AVMA, 1994). A single teaspoon of ingested high infectivity meat and bone meal is thought to be enough to cause BSE in a cow (Collee, 1996). Between this and evidence that prions may be able to adapt to their hosts and become more virulent with time (Mad, 1990), it would seem absolutely necessary to enact a ban and stop feeding cows to cows.

In June, 1993 the Foundation on Economic Trends, a Washington public interest group, petitioned the Food and Drug Administration (FDA) to ban all feeding of ruminants (cows, sheep) to other ruminants as the European Commonwealth had done three years earlier (EC, 1990). The legal petition was largely ignored (Apocalypse, 1996). The next year the FDA proposed to at least stop feeding sheep offal (intestines, lymph, and brain) to cows (Honstead, 1995), but the proposal was blocked by vehement protests from the rendering and livestock industries (Hager, 1996). The American Meat Institute disagreed with the motivation behind the proposal stating, "[n]o good is accomplished by...prejudicing segments of society against the meat industry" (AVMA, 1994).

A week after the Britain's recent admission that people may be dying from eating beef, the International Center for Technology Assessment, filed a similar legal petition against ruminant to ruminant feeding (Apocalypse, 1996). A leading consumer group, Public Voice for Food and Health Policy, has also called for a ban (Conditions, 1996). Three days after the latest petition was filed the meat industry announced a "voluntary" ban on feeding cows to cows (Apocalypse, 1996). In the U.S. this same industry promised to stop feeding sheep brains to cows seven years ago. The FDA has confirmed that this utterly failed (Honstead, 1996). U.S. officials admit that it is, "very difficult" to verify compliance with this current voluntary ban (Altman, 1996d). In fact weeks after the "voluntary" ban was announced by the industry the feeding of ruminant protein was still continuing at rates of million of pounds a day (Apocalypse, 1996). Dairy industry officials say that the voluntary ban has had almost no effect (McNair, 1996), supporting the director (Stauber, 1995) of the Center for Media and Democracy John Stauber's contention that the voluntary ban was just a "worthless PR sham" (Stauber, 1996).

On April 3, 1996 the World Health Organization called for a worldwide ban on feeding animal tissues to livestock (Altman, 1996c). The FDA has promised to "expedite" such regulations (Altman, 1996b), but this is expected to mean that putting a formal ban in place will take 12 to 18 months (Altman, 1996b). The American Feed Industry Association calls the ban, "a radical proposition" (Evans, 1996). The proposed regulations do not, however, stop cow remnants from being fed to other animals such as chickens whose manure is often then fed right back to cows (Ensminger, 1990). Even with the law in Britain, though, surprise random inspections last year showed that half of the British slaughterhouses visited were in at least some violation of the cow to cow ban regulations (McKie, 1996). "You can ban things until you're blue in the face," said one Federation of Veterinarians of Europe official, but without proper enforcement the ban may have little impact (Butler, 1996).

Gary Weber, Director of Beef Safety and Cattle Health for the National Cattlemen's Beef Association (NCBA), admitted 3 years ago that his industry could indeed find economically feasible alternatives to feeding rendered animal protein to other animals, but that the Cattlemen's Association did not want to set a precedent of being ruled by "activists" (BSE/Scrapie, 1993). Dr. Weber appeared on the Oprah Winfrey Show in April of 1996 (Dangerous, 1996). Clearly alarmed and disturbed by the fact that cows in the U.S. are fed the remains of other cattle, Oprah swore she would never eat another burger again (Dangerous, 1996). An internal U.S. government PR crisis management document showed that the government knew that the such feeding practices would be "vulnerable to media scrutiny" (Apocalypse, 1996). After Oprah tried to remind the audience that cows were supposed to be herbivores, Dr. Weber defended the practice by stating, "Now keep in mind, before you--you view the ruminant animal, the cow, as simply a vegetarian--remember that they drink milk." (Dangerous, 1996)

Cattle prices plummeted after the show aired (Texas, 1996). The beef industry blamed Oprah (Next, 1996). The president of the National Cattlemen's Beef Association called Oprah, "a cheerleader for...anti-beef propaganda." "We're not going to sit back and let trash TV trash a vital industry..." said the Texas Agriculture Commissioner in a prepared statement (Texas, 1996). Texas agriculture officials planned to bring a lawsuit against one of the guests on the show, Howard Lyman, a cattle rancher-turned-vegetarian under a 1995 state law that prohibits unfounded comments about perishable food items (Texas, 1996). Twelve states have such laws (Collings, 1996). These are some of the same Texas officials that responded to the tragic news of the human deaths in Britain by staging a mocking April 4 publicity stunt cook-out (Apocalypse, 1996). The Texas Attorney General has since decided against the suit, so a Texas cattleman is suing Oprah Winfrey directly (Oprah, 1996). Also on the show was Beryl Rimmer, whose 16 year old granddaughter lay in a vegetative coma on life support (Macintyre, 1996), blind and dying, one of the ten young people in Britain diagnosed with the new form of CJD (Dangerous, 1996). A doctor from the government's CJD surveillance unit reportedly told her not to make her granddaughter's plight public, that she should "think of the economy and the Common Market." (Lacey, 1994).

In the same show Dr. Weber asserted that no animal could ever enter a U.S. packing plant displaying BSE symptoms (Dangerous, 1996). Even if this were true, it has been argued that the majority of infected and infectious cattle become beef before clinical symptoms first arise (Patterson, 1995). In fact, for every "mad" cow incinerated in the U.K., there may be hundreds slaughtered and sold to butchers before any overt symptoms have developed (Radford, 1996). Dr. Narang estimates that a third of all British cattle going into the food chain are infected with BSE. In the _Journal of Public Health Medicine_, Dealler, the microbiologist, wrote, "in all probability most humans who have consumed British beef since the start of the BSE epidemic will have been exposed [to the infection]. . ." (Patterson, 1995). It is estimated that every adult in the U.K. has eaten on average 50 meals containing tissue from infected cattle (Boseley, 1996). In America it may be even harder to stop infected cattle from entering the food supply since dairy cattle are routinely culled earlier than in Britain (Qualitative, 1991).

Evaluation of Risk

Within a week of the British government's recent announcement of the link between CJD and BSE the National Cattlemen's Beef Association released a position paper which stated that, "[s]cientific evidence indicates that beef (meat) and milk do not present a risk as there is no evidence that the agent that causes BSE is present in meat and milk" (National, 1996). Even the USDA disagrees, stating that, "the safety of British beef cannot be demonstrated for 20 or more years" (Bleifuss, 1993). As retired professor of clinical neurology W.B. Matthews put it, "[c]laims that British beef is entirely safe to eat...are scarcely scientific when the question has not been tested and is, perhaps, untestable." (Matthews, 1990).

The Cattlemen's Association is presumably referring to a series of studies in which mice were innoculated with infected beef and didn't get sick (Middleton, 1993). The mouse model may not, however, be a reliable nor sufficiently sensitive indicator of the human risk involved (Dealler, 1995). These studies do show, though, that the brains and spinal cords of infected cows can cause disease (Middleton, 1993) and in the slaughterhouse, beef is recovered by mechanically sawing down the carcass, which may imbed brains (which at this stage have the consistency of pudding (Dealler, 1990)) throughout the meat (Dealler, 1991). Furthermore, meat (muscle, blood, peripheral nerve and lymph tissue) from a number of other species infected with spongiform encephalopathies has been shown to be infectious (Dealler, 1991). Finally, the prions are thought by some to continuously accumulate in one's system, so that even small doses could build up with time (Lacey, 1991).

Despite the disturbing circumstantial evidence, there is still no direct proof that consumption of an infectious dose of BSE necessarily leads to CJD in humans (Creutzfeldt-Jakob, 1996). The recent deaths in Britain may turn out to be entirely unrelated to beef consumption. To address this question, one experiment is currently underway to do further studies of the autopsied brains called strain typing which could provide strong empirical evidence of a BSE-CJD link (Almond, 1995). Results will not be forthcoming for at least 18 months, though, and may not even then provide definitive answers (Creutzfeldt-Jakob, 1996). The preliminary results from another study involving mice genetically engineered to express human proteins seem to minimize the risk to humans, but are not yet conclusive (BSE, 1995). It will be a year and a half before firm conclusions can be drawn from this study also (Creutzfeldt-Jakob, 1996) and even then there are doubts of the experiment's reliability (Hope, 1995). Scientists with the French government, however, claim to have found the first experimental evidence of a link between BSE and CJD (French, 1996). Macaque monkeys infected with BSE showed brain lesions identical to those previously thought to be unique to the victims of the new form of CJD (Lasmezas, 1996). This provides the strongest evidence to date to support the hypothesis that BSE is responsible for the emergence of the new variant of CJD in humans (Aldhous, 1996).

BSE has infected a dozen species which presumably ate infected tissue (Dealler, 1995; Bons, 1996). Eighty other cats have now since followed Max to the grave (Mad, 1996c). Experimentally, one can give BSE to monkeys (Baker, 1993; French, 1996), pigs, and four other species (Patterson, 1995). There does not seem to be any reason why BSE will not similarly infect humans (Bleifuss, 1994). So far, in fact, BSE has proven more infectious than most other transmissible spongiform encephalopathies (Dealler, 1993). BSE appears to infect other animals more easily, especially when transmitted through food (Aguzzi, 1996). No one knows what the odds are that humans are susceptible. When Dr. Dealler was recently asked by a member of the British Parliament what the chances of his contracting CJD from BSE-infected meat were, Dealler replied, "Between zero and 100 percent."

Recently a rhesus monkey raised in a British zoo who was fed meat products declared fit for human consumption developed a spongiform encephalopathy (Bons, 1996), but marmoset monkeys eating similar rations have not come down with the disease (Ridley, 1996). Unlike marmosets, though, rhesus and macaques are Old World monkeys which, "represent the evolutionary nearest available experimental model to humans" (Lasmezas, 1996). The latest data has come from comparing cow and human genomes (Krakauer, 1996). Two striking similarities were found between the prion genes of gorillas, chimpanzees, humans and --curiously-- cows which might have "predisposed" humans to cattle prion infections (Krakauer, 1996), a finding that, "can only be interpreted as worrying" (Gee, 1996).

Incidentally, cows aren't the only possible source of prion disease. Paul Brown, medical director for the U.S. Public Health Service (Gruzen, 1996), believes that pigs and poultry could be harboring BSE and passing it on to humans, adding that pigs are especially sensitive to the disease (Pearce, 1996). "It's speculation", Brown says, "but I am perfectly serious." (Pearce, 1996). Despite evidence minimizing such risk (Hawkes, 1996), the British government banned farmers from feeding processed cattle blood, bones, fat, and offal to pigs and poultry on March 20, 1996 (Hargreaves, 1996). A week and a half later they even halted the use of mammalian meat and bone meal as agricultural fertilizer (U.K., 1996) while the United States still feeds cows to other cows. Referring to the lack of any government regulations to prohibit such practices Dr. Brown warns, "We're playing with fire." (Gruzen, 1996).

CJD and the USA

If indeed a form of BSE exists in the United States, one might expect to see a rise in the number of cases of Creutzfeldt-Jakob disease. CJD, however, is not a reported illness in this country (Holman, 1995). Because the Centers for Disease Control (CDC) does not actively monitor the disease (Altman, 1996d) a rise similar to the one in Britain could be missed (Altman, 1996d). Already, a number of American CJD clusters have been found. In the largest known U.S. outbreak of cases to date (Flannery, 1996) a five-fold expected rate was found in Pennsylvania's Lehigh Valley which was linked to, among other things, cheese consumption among other things (Little, 1993). A striking increase in CJD was also reported in Florida (Berger, 1994) and there is an anecdotal report of an cluster in Oregon (Boule, 1996). An analysis of death certificates in a number of states, though, showed an overall stable and typical CJD incidence rate in the United States from 1979 to 1993 (World, 1996). To track the disease, the CDC has just initiated a four-state study of death certificates (Altman, 1996a), but due to the inaccuracy of death certificate diagnoses (Davanpour, 1993) the survey may not provide an accurate assessment.

The true prevalence of prion diseases in this or any other country remains a mystery (Harrison, 1991). Compounding the uncertainty, autopsies are rarely performed on atypical dementias (Harrison, 1991) because medical professionals fear infection (Altman, 1996a). The officially reported rate in this country is less than 1 case in a million people per year (World, 1996). An informal survey of neuropathologists, however, registered a theoretical range of 2-12% of all dementias as actually CJD (Harrison, 1991). And hundreds of thousands of Americans suffer from severe dementias every year (Brayne, 1994; United, 1995). Two other studies average about a 3% CJD rate among dementia patients (Mahendra, 1987; Wade, 1987). A preliminary 1989 University of Pennsylvania study showed that 5% of patients diagnosed with dementia were actually dying from Creutzfeldt-Jakob disease (Boller, 1989). It would seem CJD is seriously underdiagnosed at present (Harrison, 1991).

The most common misdiagnosis of CJD is Alzheimer's disease (Harrison, 1991). CJD was even described by Dr. Brown, our government's top CJD researcher (Wlazelek, 1990a), as, "Alzheimer's in fast forward (Wlazelek, 1990b)." The symptoms and pathology of both diseases overlap (Brown, 1989). There can be spongy changes in the brains of Alzheimer's patients, for example, and senile plaques in the brains of CJD victims (Brown, 1989). The causes may overlap as well; epidemiological evidence suggests that people eating meat more than four times a week for a prolonged period have a three times higher chance of suffering a dementia than long-time vegetarians (Giem, 1993), but this result may be confounded by vascular factors (Van Duijn, 1996). Dr. Brown even said that the brains of the young people who died from the new CJD variant in Britain look like the brains of people with Alzheimer's disease (Hager, 1996). Dr. Prusiner speculates Alzheimer's may even turn out to be a prion disease (Prusiner, 1984). In younger victims the disease could look like multiple sclerosis or a severe viral infection, according to Alzheimer's expert Gareth Roberts (Brain, 1996).

An estimated two to three million Americans are afflicted by Alzheimer's (Scully, 1993); it is the fourth leading cause of death among the elderly in the United States (Perry, 1995). Twenty percent or more of people clinically diagnosed with Alzheimer's disease are found at autopsy to not have had Alzheimer's at all (McKhann, 1984). At Yale, out of 46 patients clinically diagnosed with Alzheimer's, 6 were proven to be CJD at autopsy (Manuelidis, 1989). In another post-mortem study 3 out of 12 "Alzheimer" patients actually died from a spongiform encephalopathy (Teixeira, 1995). Carleton Gajdusek, who was awarded a Nobel Prize in Medicine for his work with prion diseases (Manuelidis, 1985), estimates that 1% of people showing up in Alzheimer clinics actually have CJD (Folstein, 1983). Hundreds more people may be dying from CJD than previously thought in the United States (Hoyert, 1996; United, 1995).

Latest Victims

In an examination of the risk of a major CJD epidemic in Britain, one of the government advisors wrote, "I can't imagine it will just stop at ten cases..." It seems he was right. By the end of March 1996 the number was revised to an unconfirmed twelve (Dillner, 1996). Then two women in their 30's died in Germany (Bradley, 1993). A 26-year old man recently died in France; French authorities concluded it was, "exactly identical" to the ten in Britain after consulting with health officials there (Identical, 1996). One of the latest suspected victims is a 24 year old woman in New York who may have contracted the disease years after receiving a Christmas gift of British beef cutlets (Illness, 1996). And by the end of April another English girl was diagnosed with CJD (Girl, 1996). At age 15 she is thought to be the world's youngest victim of the disease (Girl, 1996). After the diagnosis of BSE-pattern CJD was confirmed, leading neurologist Peter Behan made the controversial announcement that she, "picked it up through hamburgers" (Illness, 1996). By June five more suspected cases were identified (Scientists, 1996). Assuming a fifteen year incubation period, all of these young people dying of this disease in Britain over the last few months were presumably infected when there were but only a few hundred infected cows (MAFF, 1996). In the year 1990 alone, it is estimated that 250,000 BSE-infected cows were eaten, which of course begs the question how many people might be dying after the turn of the century (Arthur, 1996).

In the United States we are left with an industry that continues to risk public safety and a government protecting business interests over those of the consumer. A clue as to why the government has been so stubborn in enacting a ban on feeding cow and sheep remains to cows and sheep can be found in a 1991 internal USDA document entitled "BSE: Rendering Policy" retrieved through the Freedom of Information Act (Bleifuss, 1993). It weighed the costs and benefits of a number of preventative measures including a total ban on feeding ruminants to ruminants (Bleifuss, 1993). The supporters of this option felt that this minimized the risk to public health (Bleifuss, 1993). APHIS, however, goes on to explain that the "disadvantage" of this approach is, "that the cost to the livestock and rendering industries would be substantial" (Apocalypse, 1996). Plant sources such as soybeans work just as well, but can cost up to 30% more than meat and bone meal (U.S., 1996a); the lost revenue to cattle producers of such a ban is estimated at a nickel per cow per day (McNair, 1996). The document further asserts that such a policy, "could pose major problems for the U.S. livestock and rendering industries" (Bleifuss, 1993). The rendering, feed, and cattle industries rack up annual sales of $1.2 billion, $20 billion, and $60 billion, respectively (Bleifuss, 1994).

The German Farmer's Association blamed the central problem of the BSE crisis on, "the British greed for profits." The Archbishop of York also recently blamed the BSE epidemic on greed (and profit). Other than simply corporate profiteering, though, I think this crisis shows to what length governments will go to prevent financial harm to powerful lobbies in general, and in doing so risk immeasurable harm to those they claim to represent.