AnimaLife

[Guest guest]

I found this and thought it might be interesting to some. This may have been

circulated through the Voice group before, but I thought it was timely.

Beverly G.

Mad Cow Disease

" Much More Serious Than AIDS "

by Greger

A seemingly[59] new[50] disease popped up in 1985 among dairy cows[12] in

Great Britain. Dubbed Mad Cow Disease by the British press,[53] Bovine

Spongiform Encephalopathy (BSE) claimed the lives of just under 20,000 cows

by 1990[33] with up to 300 new cases appearing each week.[16] Only months

after the government concluded that the disease probably wouldn't spread to

other species[1], someone's cat died of a hitherto unknown feline spongiform

encephalopathy[26] of which infected pet food was " overwhelmingly the most

likely explanation. " [36] And then zoo animals started dropping dead.[4]

Together, this sparked a public uproar[19] with unprecedented media

attention.[50] Fearing its spread into the human population, hospitals[34],

nursing homes[34], and over 2000 schools[21], affecting over 750,000 school

children[7], stopped serving beef or restricted its consumption. An early

1990 survey showed that one in ten people in England seemed to agree with Dr.

Lacey[43], a microbiologist at Leeds University, that BSE " is much

more serious than AIDS. " [18]

By May 1990, a quarter of the population refused to eat beef.[38] In six

months beef prices dropped 10[5]-25%[3], devastating the cattle industry.

Declaring beef farming unprofitable, many British farmers either moved to

other crops[59] or went bankrupt.[50] The final blow came when Australia[43],

Israel[43], and a dozen other countries[24] banned the importation of British

beef because of the BSE epidemic. The USSR went even further, banning the

importation of British milk[44] and leather.

In 1991 another fifteen feline companions succumbed[47] and a half dozen more

zoo animals perished[12], all presumably from eating infected cow parts. By

1992 the disease spread to all dairy and beef breeds[12] and the number of

histopathologically confirmed cases almost tripled to 58,000.[27] And the

plague spread across the globe and into six other countries.[2] France even

pulled 32 over-the-counter drugs off the market because of BSE, totally

banning 19 and reformulating the 13 others.[51] Last year, the number of

cases quadrupled in Switzerland[12,60] and British beef consumption

reportedly plummeted 38%.[65] The epidemic is growing steadily[12] and

continuing unabated[64] with at least 1% of all cattle in England infected[8]

and estimates ranging up to 10%.[59] Trashing all official government

predictions of a plateau of around 20,000 cases[40], we are left with over

100,000 lab confirmed[3] cases with 1,000 new cases reported each week.[39]

Spongiform encephalopathies are invariably fatal[29] neurodegenerative[17]

diseases. There is no treatment[55] nor cure.[18] The novel[3] infectious

agents evoke no immune response[50] and consequently slowly accumulate[14]

for an incubation period of up to 30 years.[60] You can't detect them[28],

isolate them[35], nor purify them.[13] In fact, only an autopsy can tell if

you ever even had them.[45] They aren't viruses and they aren't bacteria.[66]

The consensus is that they are prions, or infectious proteins.[60] Without

detectable DNA nor RNA[41], not only does no one know how they replicate[6],

but the whole concept challenges the basic tenets of biology.[45]

Because of their unique makeup, they are practically invulnerable. They can

survive for years in the soil.[61] They are not adequately destroyed by

cooking[13], canning[14], nor freezing.[40] Chemicals or enzymes which

degrade nucleic acids[55], proteolytic enzymes of the digestive tract[49],

and usable doses of UV or ionizing radiation[48] are all ineffective in

destroying their infectivity. Even heat[40], domestic bleach[59], and

formaldehyde[14] sterilization have little or no effect. In fact, the only

way to ensure that your burger is safe is to marinate it in Drain-O (or other

concentrated alkali).[59] They are the smallest[9], most lethal

self-perpetuating biological entities in the world.

A member of Parliament recently called BSE " the most serious threat ever

posed to British agriculture. " [44] But so what? So some jobs are lost and

maybe a couple of hundred thousand cows perish. The real question is, are

people going to die? Lacey (MA, MD, PhD, FRC, Path, DCH) asserts that a

" substantial danger for man exists " [55] and further, that the human health

implications of BSE are " very grave. " [1] Others, however, do not share his

prediction of a " very, very grim " [8] future. After a $6.5 million advertising

campaign touting red-meat consumption from Britain's Meat and Livestock

Commission[34] and the Minister of Agriculture gamely munching burgers with

his four-year-old daughter for the press[16], the schools have put beef back

on the menu[50] and beef consumption has regained semi-normal levels.[38]

Despite continued warnings from scientists like Lacy, the European community

has lifted its ban and most other countries have greatly relaxed their trade

restrictions.[7]

The dismissals of human risk generally fall into four categories. There are

scientists who base their assertions that the danger is minimal on the

premise that none have yet died.[16,17,48,50,57,64,70] There are others who

try to quell public fears by claiming that there simply exists no evidence

that indicates a human health risk from BSE.[21,46,56,62,65,70] And finally,

there are those who doubt that the infectious agent can enter the food chain

in the first place[13,15,32,46,48,57] and/or those who question whether BSE

can jump the species barrier.[10,20,21,32,36,37,56,57,60,61] First of all,

even the wishful thinkers who see the risk to human beings to be trivial

admit that we really cannot know, and will not know, for a number of years.

This kind of " sit and wait " [3] attitude is expressed, for example, by the

United States Department of Agriculture (USDA) which has stated that " the

safety of British beef cannot be demonstrated for 20 or more years. " [21]

Second of all, the aforementioned arguments are flimsy, deceptive, based on

blatantly false assumptions, and are at best just unscientific. Before I

elucidate, some background is necessary.

" BSE was 'almost certainly'[10] caused by feeding cattle ground up, dead,

diseased sheep " [18] infected with an ovine spongiform encephalopathy known as

scrapie.[20] But aren't cows herbivores? Fragrant hay and picturesque

pastures are now mostly urbanite mythology; this is modern agribusiness.

" Protein concentrates " (euphemism for mashed- up bits of other animals left

over from the slaughterhouse) are fed to dairy cows[22] to improve milk

production,[65] for example. The real problem now, though, is not that we've

made cows meateaters but that we've turned them into cannibals as well; the

recycling of the remains of infected cows into cattle feed[60] has probably

led to the epidemic's explosive spread.[42] An editorial in the British

Medical Journal described BSE as resulting " from an accidental experiment on

the dietary transmissability of prion disease between sheep and cows. " [57] A

subsequent experiment of this kind, with humans, probably occurred in England

in the late 1980's when meat contaminated with BSE entered the food

chain.[57] The result of this experiment is awaited " as we live through the

incubation period " over the next decades.[57]

Sources that try to quell public fears by pointing out that no one has yet

[see Animal News] died do not seem to understand the term incubation period,

defined as the time span between actually acquiring the disease and the

appearance of the first symptoms. Studies of human prion diseases like kuru,

which attacked a New Guinea tribe which consumed the brains of their dead,

show incubation periods as long as 3 decades.[46] The earliest we could even

expect to see people dying from BSE is probably around 1995.[39] Having said

this, the incidence of Creutzfeld-Jakob disease (CJD), the most common human

prion disease,[37] has risen 100% in Britain since 1989.[8] Two especially

notable deaths were farmers who in fact did have BSE infected herds.[11] This

is surely coincidental, though, as they presumably didn't have time to

incubate it.[73]

The USDA has stated that, " To date, no scientific evidence indicates that BSE

is a human health hazard. " [8] To this, one writer replied, " Of course, to

date no scientific experiments have been done on humans to find out if this

is so. " [8] This isn't entirely true, but the experiments that have been done,

if anything, point to an increased risk. For example, CJD has been

epidemiologically linked to the consumption of offal.[58] More ominously,

though, is the finding that sheep inoculated with CJD-infected human brain

develop scrapie.[21] As retired professor of clinical neurology WB s

put it, " Claims that British beef is entirely safe to eat...are scarcely

scientific when the question has not been tested and is, perhaps,

untestable. " [28]

Others argue that humans would never be exposed to the disease. In 1989,

offal was banned from meat products destined for human consumption.[24]

Because British omnivores could then only eat the muscles, the food supply

was declared safe.[36] First of all, before the ban took hold, the nervous

lymphoid, and gut tissues of an estimated 2 million cows reached human

food.[59] Secondly, it is possible that muscles do in fact harbor

sufficiently deadly numbers of prions; spongiform encephalopathies of goats,

minks, and hamsters can be transmitted through muscle alone.[55] A recent

report does show that cow muscles are not detectably infectious, but these

data are preliminary and based only on mice.[48] And frankly it doesn't

matter because beef is not just muscle; it's laced with peripheral nerves and

lymphoid tissue[39] which have both been shown to be infectious.[39] No

tissue, though, concentrates the pathogens more than brain or spinal

cord.[46] In the slaughterhouse, beef is recovered by mechanically sawing

down the corpse, which may imbed brains (which at this stage have the

consistency of pudding)[59] throughout the meat.[55] Although BSE is more

prevalent in dairy cows and milk probably is not infectious[46], dairy cows

are quickly retired into hamburger. In addition, the prions are thought to

continuously accumulate in one's system, so that even small doses could build

up with time.[14]

By far the most common faulty reasoning when marginalizing human risk factors

is the argument that since scrapie gave rise to BSE and scrapie is not

transmissible to humans, then BSE is not transmissible to humans. This is

" untenable. " [39] As Heino Diringer of the Koch Institute in Berlin has

said, " We cannot assume that because [eating] sheep is relatively safe, ergo

beef is safe. " [36] This is because every time prio diseases jump from species

to species, the characteristics of the disease may dramatically change,

including the host range.[14] For example, scrapie cannot infect cats, but it

appears BSE can.[39] One also cannot infect rhesus monkeys with scrapie, but

as soon as scrapie jumps into minks (causing " MSE " ), then the minks can

infect the monkeys.[59] Scrapie can infect mice, though, and, when it's

transferred to cows, it can still affect mice, but when transferred from

sheep to mink, the mink can then not transmit it on to mice.[59] The bottom

line is that we cannot predict what species a prion disease will affect when

it jumps to a new one.[39]

But what are our chances? BSE has been able to infect and (therefore) kill

cats, antelopes, and even ostriches from presumably eating infected

protein.[1] Experimentally, one can give BSE to monkeys[56], pigs, mice,

sheep, goats[1], and chimpanzees.[8] There is no reason to believe that BSE

will not similarly infect humans.[8] So far, BSE has proven more infectious

than most other transmissable spongiform encephalopathies.[39] In fact 6 out

of 7 attempts to transfer the disease to different mammalian species have

been successful[39]. That does not bode well for the human race.

Susceptibility is not enough, though. The critical uncertainty is, how small

a dose is necessary to pass the disease along? Theoretically it doesn't

matter if BSE can infect humans if we never eat enough meat within a

lifetime. Last year, calculations were made to determine how many people will

have consumed a potentially infectious dose by 1997.[39] The conservative

estimate runs upwards of 34 million people.[39] Or as Lacey put it, virtually

a whole generation of people may die.[31] And we are not talking a quick and

simple death, either. If we assume the disease runs a course similar to CJD,

these people will wake up one morning twitching and deteriorate weekly[67]

into blindness and epilepsy[59] while their brain perforates into a

sponge.[43] If they're lucky, they will be dead within three months; if not,

it may take up to five years.[59]

But what about the United States? Not only is there the ethnocentric

relevance, but we have 100,000,000 cattle[8] and the highest per capita beef

consumption in the world.[65] Traditional bovine spongiform encephalopathy

hit North America in 1993.[15] The first cow discovered to be infected, one

of many imported from the UK before both Canada and the US banned the

importation of British cattle, was found on a ranch in Alberta, Canada.[8] Of

the 471 British cattle imported into the US before the 1989 ban, 188 of them

have been melted down into lard and protein (presumably for other livestock)

and at least 66 are untraceable.[8] One of the imported bulls slaughtered had

a " central nervous system abnormality " of which the USDA reported, " There is

no definitive evidence that [the bull] either had or did not have BSE. " [8]

Although the importation of British beef has been banned from the US for a

decade due to an unrelated disease[7], over 13 tons of meat and bone meal,

(which, if you remember, was implicated in the birth of the British epidemic)

has come into the US from England between 1982 and 1989.[2]

Indigenous conditions conducive to a BSE outbreak include the presence of

scrapie in 39 states.[54] The 40-year[52] USDA Scrapie Eradication Program

has been deemed a " dismal failure " [63] and even implicated in the recent rise

of scrapie-infected sheep.[54] Admitting defeat, the USDA scrapped the

Scrapie Eradication Program 2 years ago and replaced it with an " entirely

voluntary " control program.[21] The proportion of sheep to cattle in the US

is dramatically smaller than in the British Isles though, which helps

minimize the risk of an outbreak.[65] This is a moot point, however, if BSE

is already here.

Since 1947 there have been 25 outbreaks of Mink Spongiform Encephalopathy

(also called TME) on US fur farms.[22] This perplexed researchers who were

unable to orally infect mink with scrapie-infected sheep brains.[49] A clue

came in 1985 when TME wiped out a population of minks in Wisconsin who hadn't

eaten any sheep.[35] Their diet consisted almost exclusively of dairy cattle

called " downers, " [54] an industry term describing cows who fall down and are

too sick to get up. The possibility, then, that US dairy herds were harboring

some form of BSE intrigued University of Wisconsin veterinary scientist

Marsh.[65] To test this, Marsh inoculated US cattle with the infected

mink brains.[49] As predicted, they died.[49] And when he fed the brains of

these cows to healthy mink they too died of a spongiform encephalopathy[54]

providing what he thought was the missing link.[66] Marsh hypothesized that

the proposed BSE strain indigenous to the US manifests itself as more of a

downed cow disease than a mad cow disease.[49] With about 300,000 cows going

down for unexplainable reasons every year in the US[65], this has frightening

implications on a grand scale. The critical experiment came when Marsh

inoculated scrapie infected sheep brain into US cattle.[63] If you do this in

England the cows go mad, twitching[16] and kicking into a rabid frenzy.[12]

But in America, cows instead stagger to their deaths like downer cows do[65],

supporting the notion that a form of BSE is already here in the United

States.

By 1990 the USDA had 60 labs monitoring our country's cattle herds for

BSE.[7] In 1991 APHIS, the governmental agency which ensures the health of

the nation's livestock, concluded that the " possibility of BSE appearing in

US cattle is extremely low. " [21] The assumption made by APHIS and others[2],

however, was that " scrapie infected sheep were the only source of the BSE

agent. " [21] This is certainly questionable in light of the evidence for an

indigenous BSE agent. Likewise, the USDA surveillance program (described as

slow, clumsy, and ineffective)[66] began looking for the rabies-like symptoms

of the traditional British strain of BSE[52], in effect ignoring Marsh's

findings.[21] In June 1992 a USDA consultant group continued to disregard the

available evidence, deciding that changes in the research program to

accommodate the possibility that BSE was already present in the US were " not

appropriate at this time. " [21] No surprise really, when one realizes that

this panel included representatives of the National Milk Producers

Federation, the National Renderers Association, The American Sheep industry

Association and the National Cattleman's Association.[21] According to

newspaper reports last year the USDA has finally backed down and started

testing downer cows[65], but some doubt their resolve.[21]

For example, in Britain, when the monetary compensation given to the 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%.[59] Presumably, the earlier economic disincentive persuaded farmers to

overlook a few mad cows. Well, the USDA knows all too well that a positive

diagnosis in a single cow could put the entire dairy and beef export business

in jeopardy.[65] In Wisconsin alone this would mean a loss of a half a

billion dollars a year,[66] not to mention the effects it might have on beef

consumption patterns.

With scientists like Marsh saying " The exact same thing could happen over

here as happened in Britain, " [35] and with beef consumption already at a

thirty-year low,[34] the USDA is justifiably worried. There was even a

complaint filed recently with the FDA from a woman with CJD who had been

taking a dietary supplement containing bovine tissue.[4] Like England, we

have been feeding dead cows to living cows for decades.[7] In fact, here in

the US a minimum of 14% of the remains of rendered cattle is fed to other

cows[49] (another 50% goes on the pig and chicken menu).[2] Partly because of

this, the USDA has conceded that " the potential risk of amplification of the

BSE agent is much greater in the United States " than in Britain.[8] To make

things worse, there has been a dramatic increase in the use of animal protein

in commercial dairy feed since 1987.[35,49] The recent introduction of Bovine

Growth Hormone will only increase the need for rendered animal proteins in

the rations dairy cattle--of whom we eat 2.6 billion pounds

annually[8]--consume.[4]

In June 1993 the Foundation on Economic Trends, a national consumer advocacy

organization, petitioned the FDA to ban all feeding of ruminants (cows,

sheep...) to other ruminants, because they felt that transmissible spongiform

encephalopathies " pose a serious potential health risk to both the nation's

cattle herds and meat-eating consumers. " [8] Although the European

Commonwealth took this advice four years ago[23], the U.S. Government still

refuses.[8]

According to top encephalopathy expert ph Gibbs, one out of every million

cattle naturally develops BSE.[65] And because evidence exists that prions

are able to adapt to their hosts and become more virulent with time[22], it

is, in my view, absolutely necessary to enact the ban and stop recycling this

disease through US cattle. To make things worse, a preliminary 1989 study at

the University of Pennsylvania showed that over 5% of patients diagnosed with

Alzheimers are actually dying from a human spongiform encephalopathy.[21]

That means that maybe 200,000 people in the US[21] are already dying from BSE

each year.

So why is the government being so stubborn? Why don't they enact the ban? An

answer can be found in a 1991 internal USDA document entitled " BSE: Rendering

policy " which was recently retrieved through the Freedom of Information

Act.[21] It weighed the costs and benefits of a number of preventative

measures including a total ban on feeding ruminants to ruminants.[21] The

supporters of this option felt that this minimized the risk to public

health.[21] 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 " and that such a policy " could pose major problems for

the US livestock and rendering industries. " [21] After all, the rendering,

feed, and cattle industries do rack up annual sales of only $1.2 billion, $20

billion, and $60 billion, respectively.[8] And since when does public health

ever take precedence over corporate interests anyway? I just hope that, in

the end, the profits are worth it.

References

1. J. of Nutritional Medicine (1992) 3:149-151

2. Animal Health Insight (1992) Autumn:1-7

3. Moscow Indiana Daily News (1993) December 22:1A,3A

4. Consumer Policy Institute Testimony before Joint Meeting of FDA FAC and

VMAC (1993) May 6:5-6

5. J. of Agricultural Economics (1992) 43(1):96-103

6. Nature (1993) 365:93

7. New Age Journal (1990) Nov/Dec:8-9

8. In These Times (1994) Jan 24:12-13

9. Biological Science 5th edition (1993) by Keeton and Gould

10. Medical Laboratory Sciences (1992) 49(3):216-7

11. Nursing Times (1993) 89(38):19

12. Proceedings American Association of Bovine Practitioners Convention

(1992) 24:19

13. Medical Laboratory Sciences (1992) 49(4):334-9

14. Ecologist (1991) 21(3):117-122

15. Drovers Journal (1994) Jan:42

16. Discover (1991) Apr:69-74

17. Dev Biol Stand (1993) 80:15-23

18. Alternatives 18(3):9-10

19. Nature (1990) 345:280

20. Nature (1990) 343:196

21. In These Times (1993) May 31:12-15

22. Economist (1990) Feb 3:89-90

23. Veterinary Record (1990) Jun 30:632

24. Lancet (1990) 335:343

25. Veterinary Record (1990) Jun 23:626

26. Lancet (1990) May 26:1252

27. New Scientist (1992) Jun 13:9

28. British Medical Journal (1990) 300:412-3

29. British Medical Journal (1988) 296:1581-2

30. New Scientist (1993) Mar 20:5

31. Nature (1990) 345:648

32. Sub-acute Spongiform Encephalopathies, edited by R. Bradly (1991):179-186

33. Lancet (1990) 336:1300-2

34. US News and World Report (1990) Jul 2:44

35. Scientific American (1990) May:34

36. Science (1990) 249:1492-3

37. Economist (1990) Jul 28:69

38. British Food Journal (1992) 94(9):23-6

39. British Medical Journal (1993) 95(8):22-34

40. Veterinary Record (1992) Jul 4:2

41. Economist (1991) Jun 22:92-3

42. Veterinary Record (1992) Feb 15:146

43. New Scientist (1990) Jun 9:32-4

44. Veterinary Record (1990) Nov 3:440-1

45. Lancet (1988) Sep 10:607-8

46. Bulletin of the World Health Organization (1992) 70(2):183-190

47. Advances in Virus Research (1992) 41:257

48. Dev Biol Stand (1993) 80:157-170

49. Dev Biol Stand (1993) 80:111-8

50. Prion Diseases of Humans and Animals, edited by Bradley, B. et al.

(1992):285-299

51. Wall Street Journal (1992) Jun 29

52. Dev Biol Stand (1993) 80:119-121

53. New Scientist (1993) Oct 9:50-1

54. Sub-acute Spongiform Encephalopathies, edited by R. Bradly (1991):41-6

55. Nutrition and Health (1991) 7(3):117-134

56. Veterinary Record (1993) Apr 17:403-5

57. British Medical Journal (1992) 304:929-930

58. British Medical Journal (1992) 304:1509

59. Food Microbiology (1990) 7:253-279

60. Lancet (1993) 342:790-3

61. Sub-acute Spongiform Encephalopathies, edited by R. Bradly (1991):195-202

62. Nature (1993) 365:386

63. Sub-acute Spongiform Encephalopathies, edited by R. Bradly (1991):272-274

64. Nature (1993) 365:98

65. Wisconsin State Journal (1993) Sep 26:1C

66. Capital Times (1993) Sep 11:6A

67. Mosby's Medical and Nursing Dictionary 2nd Edition (1986)

[Guest guest]

Bev,

Thanks for sending this through, it answers my question. I think we need to

add rendering plants to our list. They are a major part of the problem. We

used to have one here in Ft. Wayne. We have friends that raised hogs and

took their dead ones there. It serves a purpose but seems to need more

regulating. I don't have the answer for it though. Maybe someone else does?

Robin