I used to give blood regularly, but am now forbidden because I lived for months at a time in England from 1998-2001, where BSE (Mad Cow disease) emerged in the mid-1990′s. I have scoffed at this rule; from everything that I understood, Britain has far greater monitoring of beef than the U.S. True, BSE has been found in thousands of British cattle and very few North American cattle, but then again one is unlikely to find such a sneaky pathogen if one is not looking for it. Unfortunately, the U.S.D.A., which exists to serve agribusiness interests, rather than those the American public which pays for its existence, has at best dragged its feet on increased testing of cattle, and at worst actively has prevented those who would test on their own initiative from doing so.
The U.S.D.A. itself has drastically curtailed its BSE testing in the last few months. The agency presents no data on BSE testing on its website after August, 2006. However, the new policy is spelled out based on the detection rate from the previous sampling:
Since the enhanced surveillance program began, USDA has sampled more than 759,000 animals and, to date, only 2 animals have tested positive for BSE under the program. Both cases were in animals born before the United States banned the practice of feeding recycled ruminant protein to other ruminants. In line with USDA policies, neither of the affected animals detected under the enhanced surveillance program nor the imported cow detected in 2003 entered the human food or animal feed chains.
Based on the wealth of information gained during both the enhanced surveillance program and BSE surveillance conducted in the United States in the 5 years prior, USDA recently concluded that the prevalence of the disease in this country is extremely low, less than 1 case per million adult cattle, and that the most likely number of cases is between 4 and 7 infected animals out of 42 million adult cattle. Our analysis was submitted to the scrutiny of a peer review process, and the expert panel agreed with the appropriateness of our assumptions and the factors we considered, as well as with our estimate of BSE prevalence.
The new testing protocol is as follows:
The ongoing BSE surveillance program, which will sample approximately 40,000 animals each year, will continue to sample the cattle populations where the disease is most likely to be found. The statistically valid surveillance level of 40,000 is consistent with science-based internationally accepted standards. This level allows USDA to detect BSE at the very low level of less than 1 case per million adult cattle, assess any change in the BSE status of U.S. cattle, and identify any rise in BSE prevalence in this country.
The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as nonambulatory animals.
As they say, the methodology is based on standard science. But does that really protect our food supply? The unknowns about BSE are disturbing, and unfortunately the testing protocol is based on assumptions that may not be true because we still know so little about this disease.
Britain’s beef supply is not currently as safe as I thought, as a 2002 report (no longer available at its original location) spells out:
BSE: risk and regulation
A case study paper commissioned by the National Consumer Council
Prepared by Patrick van Zwanenberg & Erik Millstone
Science and Technology Policy Research, Sussex University
It turns out there are still many questions out there about how animals are contracting BSE and how to prevent it:
Indeed, to date, there have been 14 cases of BSE in animals born after August 1996; they constitute an anomaly which remains inexplicable. The mechanisms by which those animals were infected are unknown… It is therefore likely that some animals under 30 months will be sub-clinically infected with BSE and will be entering the human food chain. We cannot know how many animals under 30 months might be incubating the disease, however, because the existing short-term tests can only detect infected animals shortly before clinical symptoms appear, and the UK government has chosen not to conduct any sort of test for BSE on animals entering the human food chain. In 2001 there were 761 reported cases of BSE in the UK… A further 335 cases were also reported in that year from the, as yet uncompleted, active surveillance programme;… but in the summer of 2001, the European Commission’s Food and Veterinary Office noted that “[a]s active surveillance is practically not performed [in the UK], it has to be assumed that the BSE incidence for GB has to be seen with a considerable degree of uncertainty.”
This means that testing only sick and downer cattle doesn’t necessarily cover the possible infected animals. Clearly we have done some things that have helped reduce the risk considerably, for example not allowing cattle to be fed mammal by-products any more. Yet there are loopholes; from the FDA itself: “In August 1997, FDA established a regulation that prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants” (link no longer available). Apparently though it is still legal to feed chickens mammalian protein, but these seem to BSE may not pass this way, but we know so little about it we cannot say for sure.
And some rules put in place in the 1990s have already been relaxed:
The U.S. Food and Drug Administration today published several amendments to the July 2004 interim final rule, “Use of Materials Derived from Cattle in Human Food and Cosmetics,” that will allow the use of certain cattle-derived material in human foods and cosmetics…
As a result, FDA is amending the rule to allow use of the small intestine in human food and cosmetics, provided that the distal ileum has been removed. The U.S. Department of Agriculture is publishing today a similar amendment to its interim final rule on BSE.
The amendments also clarify that milk and milk products, hides and hide-derived products, and tallow derivatives are not prohibited for use in human food and cosmetics.
Is there any other reason for this than pressure from industry? Shouldn’t the U.S. government be erring on the side of caution in the case of such a potentially devastating health issue? Those infected with BSE take decades to show their symptoms. This is not a situation where a couple people will drop dead and the FDA will say “whoops, better change that rule” as a result. (Most original FDA links from here have disappeared; this is the latest on BSE policy.)
As a final note, among the real unknowns about spongiform encephalopathies is that despite what is reported in the popular press, it is clear from official and scientific documents that it is not known without doubt that prion proteins are the proximate cause. It is certainly the currently most popular idea, and most scientists are studying prion proteins based on this assumption, but there are still peer-reviewed papers in respected journals which assert alternative hypotheses, for example:
Manuelidis, L. 2007. A 25 nm virion is the likely cause of transmissible spongiform encephalopathies. Journal of Cellular Biochemistry 100:4.
The transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of “slow” viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, Substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch’s postulates for infection. Pathologic PrP is not proportional to, or necessary for infection, and recombinant and “amplified” prions have failed to produce significant infectivity. Moreover, the “wealth of data” claimed to support the existence of infectious PrP are increasingly contradicted by experimental observations, and cumbersome speculative notions, Such as spontaneous PrP mutations and invisible strain-specific forms of “infectious PrP” are proposed to explain the incompatible data. The ability of many “slow” viruses to survive harsh environmental conditions and enzymatic assaults, their stealth invasion through protective host-immune defenses, and their ability to hide in the host and persist for many years, all fit nicely with the characteristics of TSE agents. Highly infectious preparations with negligible PrP contain nucleic acids of 1-5 kb, even after exhaustive nuclease digestion. Sedimentation as well as electron microscopic data also reveal spherical infectious particles of 25-35 nm in diameter. This particle size can accommodate a viral genome of 1-4 kb, sufficient to encode a protective nucleocapsid and/or an enzyme required for its replication. Host PrP acts as a cellular facilitator for infectious particles, and ultimately accrues pathological amyloid features. A most significant advance has been the development Of tissue Culture models that support the replication of many different strains of agent and can produce high levels of infectivity. These models provide new ways to rapidly identify intrinsic viral and strain-specific molecules so important for diagnosis, prevention, and fundamental understanding.
I am not advocating a specific position on this at all; clearly, the current scientific consensus does not support this view, and I do not have the expertise in this area to judge. But I recommend that anyone who believes this is an important issue read up on it at the U.S.D.A. site and the British consumer report. In the meantime, I will be continuing my policy of avoiding factory feedlot beef (and not only because of the risk of BSE). I will also continue to update current research here because of my own interest in the topic.