FOR IMMEDIATE RELEASE
January 24, 2001

CONTACT:
Simon Chaitowitz, Communications Director
tel: 202-686-2210, ext. 309; simonc@pcrm.org

Doctors Call for Stronger Action Against Mad Cow Disease

Washington, D.C.—The Physicians Committee for Responsible Medicine (PCRM) is calling on the U.S. government to take stronger steps to protect the public from mad cow disease and its human equivalent, the new variant Creutzfeldt-Jakob disease (vCJD). PCRM will issue a set of recommendations tomorrow to the U.S. Department of Agriculture and the Department of Health and Human Services. vCJD is a fatal brain-wasting disease that has killed almost 100 Europeans since it was first identified in 1996.

"Our government has been frighteningly slow to react to the very real threat of vCJD in America," says PCRM president Neal D. Barnard, M.D. "The protective measures taken so far are grossly insufficient. We should learn from Europe’s mistakes and implement tough precautionary measures—now, before it’s too late."

Here are PCRM’s five recommendations for protecting the public against vCJD:

1. Ban the use of animal-derived livestock feeds for any species, given the likelihood that animal byproducts will, in turn, be recycled to ruminants (that is, cows, sheep, and goats).
2. Prohibit animal byproducts in all medications, supplements, or cosmetics.
3. Label all foods containing animal byproducts (such as gelatin or "natural flavorings"), indicating both the presence of animal byproducts and the species of origin.
4. Provide warning labels on all foods that carry a risk of vCJD, using standards similar to those for tobacco and alcohol products.
5. Institute comprehensive monitoring programs to check for diseased animals and humans in the U.S.

PCRM’s Nutrition Department based its five recommendations on a comprehensive review of the scientific literature on mad cow and vCJD diseases and recent news reports. "Meat is simply a risky product," says Dr. Barnard. "And it’s not just Creutzfeldt-Jakob disease people need to worry about: Heart disease, colon cancer, diabetes, hypertension, and many other dangerous diseases—not to mention foodborne illnesses—would be greatly diminished by avoiding meat entirely."

For a copy of PCRM’s petition or an interview with Dr. Barnard, call Ms. Simon Chaitowitz, at 202-686-2210, ext. 309.

-30-

January 25, 2001

The Honorable Ann Veneman, Secretary
U.S. Department of Agriculture
12th St. and Independence Ave., S.W.
Washington, DC 20250

The Honorable Secretary of Health and Human Services
U.S. Department of Health and Human Services
200 Independence Ave., S.W.
Washington, DC 20201

Re: Petition for Protective Steps against Mad Cow Disease and Creutzfeldt-Jakob Disease

Dear Secretary Veneman and Secretary of Health and Human Services:

The Physicians Committee for Responsible Medicine (PCRM) requests that the U.S. Department of Agriculture (USDA) and Department of Health and Human Services (DHHS) take stronger measures to reduce the risk of new variant Creutzfeldt-Jakob disease (vCJD), an incurable and uniformly fatal disease first recognized in the United Kingdom in 1996. Just as the British government failed to take sufficient protective measures to prevent its spread, current U.S. regulations fail to provide adequate measures to protect Americans from the same threat.

Diseases related to vCJD are already present in animals in the U.S., and little is being done to monitor or curb their spread to other animals or to humans. For example, feed producers are blatantly violating even the limited federal prohibitions on manufacturing practices that were enacted in an effort to block the spread of the disease. Moreover, because of the lack of sufficient protective labeling requirements, there are no effective means for consumers to avoid potentially tainted foods or other products. Accordingly, PCRM offers several suggestions to proactively address this potential health risk in a meaningful manner.

Related Diseases Have Already Arrived

vCJD, like other transmissible encephalopathies, robs an affected individual of mental faculties and muscle coordination, eventually leading to coma and death. This category of illnesses is caused by prions, proteins that are normal in their molecular make-up, but abnormal in their shape, like springs that have been bent out of configuration. It is believed that vCJD results from contact with prions in tissues of cattle with bovine spongiform encephalopathy (BSE), or "mad cow disease," which, in turn, distort normal proteins in human brain and nerve cells. Only minuscule amounts of prion-tainted tissues are required in order to transmit the disease.¹   Prions are very difficult to destroy, even by the chemical or heat disinfectant methods used in hospitals. Heating to 134 degrees Celsius (273 degrees Fahrenheit) does not reduce their infectivity.²

Transmissible encephalopathies have long been documented in animals in the U.S., indicating the need to protect human populations. Scrapie, the encephalopathy analogous to BSE occurring in sheep and which may have been the origin of BSE, was first reported in the U.S. in 1947, and infected sheep flocks have been identified in virtually all parts of the U.S. where sheep are raised.^3,4 Similar diseases have been found in other species, including chronic wasting disease in deer and elk, and transmissible mink encephalopathy.²  While scrapie is not known to cause human disease, passage of the prions that cause scrapie through other animals may potentially alter their infectivity and disease presentation.

Indirect evidence that BSE has been present in at least some U.S. cattle comes from mink who were routinely fed cattle-derived offal on fur farms. In at least five separate outbreaks, mink fed in this way have developed a disease, called transmissible mink encephalopathy (TME), which is remarkably like BSE.^5,6 After a 1985 TME outbreak in Stetsonville, Wisconsin, experimenters injected brain tissue from diseased mink into Holstein cattle, finding that the cattle developed spongiform encephalopathy. They then fed remains of these cattle to healthy mink, who soon developed TME.⁷ Reviewing evidence that the mink disease came from cattle-based feeds, University of Wisconsin researchers concluded, "If this is true, there must exist an unrecognized bovine spongiform encephalopathy (BSE)-like infection in American cattle."⁷ In other words, U.S. cattle have been sporadically infected with BSE, which has shown its pathological effects when passed on to other species.

The Failure of U.S. Government Policies

While USDA officials point out that surveys have not yet identified BSE in U.S. cattle, the fact is they are not seriously looking. First, data from the National Veterinary Sciences Laboratories BSE Surveillance program from 1990 to 2000 show that, of approximately 900 million cattle slaughtered, only 11,954 brains (approximately 1 in 75,000) were examined for BSE. Second, brain examinations have generally been prompted by the presence of neurological symptoms. However, the symptoms of BSE do not commonly manifest in cattle until about five years of age, which is after the usual age of slaughter. For example, most U.S. dairy cows are slaughtered before four years of age, when even a prion-infected cow is likely to appear healthy. In the U.K., 70 percent of dairy cows remain alive past this point, making identification of infected animals much easier.⁸

USDA policies have also been slow to take steps against the potential spread of encephalopathies from one animal to another, or from animals to humans. To its credit, since 1989, the U.S. government has banned the import of live ruminants (cattle, sheep, goats) and most ruminant products from countries where BSE has been reported, and in December 2000, the USDA prohibited imports of animal-derived livestock feeds from Europe, regardless of species of origin, after determining that feed derived from non-ruminant species was potentially cross-contaminated with BSE. However, given that BSE may already be occurring sporadically in the U.S. or could be easily introduced, appropriate steps are needed to protect against its spread. The measures instituted so far by the U.S. government are inadequate, as evidenced by the following examples:

• U.S. feed producers are blatantly violating restrictions on feed production. Despite a 1997 Food and Drug Administration (FDA) ban on the feeding of most mammalian remains to ruminants—which unfortunately includes significant exceptions impairing the protective intent of the law—a January 2001 FDA report showed that, of 180 renderers, 16 percent lacked warning labels on feeds designed to differentiate those intended for ruminants from those for nonruminants, and 28 percent had no system to prevent the actual mixing of these feeds.
• There is no restriction on the use of blood and blood products, gelatin, milk, and milk products in feeds.
• There are no limits on the use of pig or horse remains in feeds, due to an exemption in the 1997 ban.
• There are no limits on the "recycling" of beef or other meat products in the form of garbage from restaurants or other institutions for use in animal feeds.
• Ruminant remains can be fed to poultry or fish, and, in turn, poultry feces and litter are routinely used in cattle feed.

Monitoring for human illness is even more haphazard. Transmissible encephalopathies are not yet reportable diseases for the Centers for Disease Control and Prevention. Individuals showing signs of dementia due to such a condition may be misdiagnosed as suffering from Alzheimer’s disease or stroke, and most dying with neurological illnesses are never autopsied, so their brains are never examined.

There is simply no way of knowing whether vCJD has begun in the U.S. or not. Death certificates from 1979 to 1990 show that 2,614 people were identified with CJD in the U.S. While the presumption is that they had the "classical" form of the disease, rather than the new variant form which is believed to come from animal tissues, this remains uncertain. While most were older (a sign of classical CJD), some were surprisingly young. Of this group, 23 were in their thirties and 3 were in their twenties.⁹ The reported cases are probably underestimates due to the problems of misdiagnosis and underreporting.

On a more optimistic note, restrictions on blood products are becoming more stringent, which is appropriate given that they may also be vectors of disease.¹⁰ Currently, people who have spent six months or more in Britain between 1980 and 1996 are not permitted to donate blood in the U.S. On January 18, 2001, an FDA advisory panel recommended extending this restriction to include long-term residents of France, Ireland, and Portugal.

Nonetheless, it is clear that diseases closely related to vCJD exist in the U.S., both in animals and humans, that these diseases should be considered highly infectious, that monitoring programs are too spotty to track the extent of these diseases, and that current preventive steps are far too lax.

Recommendations

For the protection of the public health against potentially devastating effects of vCJD passed from tainted products, we recommend that the USDA or the DHHS, as appropriate, enact the following measures:

1. Prohibit the use of animal-derived livestock feeds for any species, given that livestock feeds are indiscriminately produced and used, and, that if ruminant-derived feeds transmit disease to non-ruminants, the use of non-ruminant remains or fecal material as feed will recycle disease back to ruminant species.
2. Prohibit the use of animal byproducts from any species in medications, nutritional supplements, and cosmetics due to the risk of prions in ruminant tissues and cross-contamination in non-ruminant tissues.
3. Require labels on foods containing animal byproducts, such as gelatin or "natural flavorings," in order to indicate both the presence of animal byproducts and the species of origin.
4. Specify the risk of vCJD on consumer information labels on foods, following standards similar to those for tobacco and alcoholic beverages.
5. Institute comprehensive programs to monitor the presence of transmissible encephalopathies in animal and human populations in the U.S.

We appreciate your prompt consideration and implementation of these important steps.

Sincerely,

Neal D. Barnard, M.D.
President

References

1. Collee JG. A dreadful challenge. Lancet 1996;347:917-8.
2. Steelman VM. Creutzfeld-Jakob disease: recommendations for infection control. Am J Infect Control 1994;22:312-8.
3. Bleem AM, Crom RL, Francy B, Hueston WD, Kopral C, Walker K. Risk factors and surveillance for bovine spongiform encephalopathy in the United States. JAVMA 1994;204:644-51.
4. Miller LD, Davis AJ, Jenny AL. Surveillance for lesions of bovine spongiform encephalopathy in US cattle. J Vet Diagn Invest 1992;4:338-9.
5. Robinson MM, Hadlow WJ, Huff TP, et al. Experimental infection of mink with bovine spongiform encephalopathy. J Gen Virol 1994;75:2151-5.
6. Marsh RF. Bovine spongiform encephalopathy: a new disease of cattle? Arch Virol 1993;7(Suppl):255-9.
7. Marsh RF, Bessen RA. Epidemiologic and experimental studies on transmissible mink encephalopathy. Dev Biol Stand 1993;80:111-8.
8. Walker KD, Hueston WD, Hurd HS, Wilesmith JW. Comparison of bovine spongiform encephalopathy risk factors in the United States and Great Britain. JAVMA 1991;199:1554-61.
9. Holman RC, Khan AS, Kent J, Strine TW, Schonberger LB. Epidemiology of Creutzfeldt-Jakob disease in the United States, 1979-1990: analysis of national mortality data. Neuroepidemiology 1995;14:174-81.
10. Foster PR. Prions and blood products. Ann Med 2000;32:501-13.

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