|
Cauliflower Mosaic Virus |
How should a regulatory agency announce they have discovered something potentially very important about the safety of products they have been approving for over twenty years?
In the course of analysis to identify potential allergens in GMO crops, the European Food Safety Authority (EFSA) has belatedly discovered that the most common genetic regulatory sequence in commercial GMOs also encodes a significant fragment of a viral gene (Podevin and du Jardin 2012). This finding has serious ramifications for crop biotechnology and its regulation, but possibly even greater ones for consumers and farmers. This is because there are clear indications that this viral gene (called Gene VI) might not be safe for human consumption. It also may disturb the normal functioning of crops, including their natural pest resistance.
What Podevin and du Jardin discovered is that of the 86 different transgenic events (unique insertions of foreign DNA) commercialized to-date in the United States 54 contain portions of Gene VI within them. They include any with a widely used gene regulatory sequence called the CaMV 35S promoter (from the cauliflower mosaic virus; CaMV). Among the affected transgenic events are some of the most widely grown GMOs, including Roundup Ready soybeans (40-3-2) and MON810 maize. They include the controversial NK603 maize recently reported as causing tumors in rats (Seralini et al. 2012).
The researchers themselves concluded that the presence of segments of Gene VI “might result in unintended phenotypic changes”. They reached this conclusion because similar fragments of Gene VI have already been shown to be active on their own (e.g. De Tapia et al. 1993). In other words, the EFSA researchers were unable to rule out a hazard to public health or the environment.
In general, viral genes expressed in plants raise both agronomic and human health concerns (reviewed in Latham and Wilson 2008). This is because many viral genes function to disable their host in order to facilitate pathogen invasion. Often, this is achieved by incapacitating specific anti-pathogen defenses. Incorporating such genes could clearly lead to undesirable and unexpected outcomes in agriculture. Furthermore, viruses that infect plants are often not that different from viruses that infect humans. For example, sometimes the genes of human and plant viruses are interchangeable, while on other occasions inserting plant viral fragments as transgenes has caused the genetically altered plant to become susceptible to an animal virus (Dasgupta et al. 2001). Thus, in various ways, inserting viral genes accidentally into crop plants and the food supply confers a significant potential for harm.
The Choices for Regulators
The original discovery by Podevin and du Jardin (at EFSA) of Gene VI in commercial GMO crops must have presented regulators with sharply divergent procedural alternatives. They could 1) recall all CaMV Gene VI-containing crops (in Europe that would mean revoking importation and planting approvals) or, 2) undertake a retrospective risk assessment of the CaMV promoter and its Gene VI sequences and hope to give it a clean bill of health.
It is easy to see the attraction for EFSA of option two. Recall would be a massive political and financial decision and would also be a huge embarrassment to the regulators themselves. It would leave very few GMO crops on the market and might even mean the end of crop biotechnology.
Regulators, in principle at least, also have a third option to gauge the seriousness of any potential GMO hazard. GMO monitoring, which is required by EU regulations, ought to allow them to find out if deaths, illnesses, or crop failures have been reported by farmers or health officials and can be correlated with the Gene VI sequence. Unfortunately, this particular avenue of enquiry is a scientific dead end. Not one country has carried through on promises to officially and scientifically monitor any hazardous consequences of GMOs (1).
Unsurprisingly, EFSA chose option two. However, their investigation resulted only in the vague and unreassuring conclusion that Gene VI “might result in unintended phenotypic changes” (Podevin and du Jardin 2012). This means literally, that changes of an unknown number, nature, or magnitude may (or may not) occur. It falls well short of the solid scientific reassurance of public safety needed to explain why EFSA has not ordered a recall.
Can the presence of a fragment of virus DNA really be that significant? Below is an independent analysis of Gene VI and its known properties and their safety implications. This analysis clearly illustrates the regulators’ dilemma.
The Many Functions of Gene VI
Gene VI, like most plant viral genes, produces a protein that is multifunctional. It has four (so far) known roles in the viral infection cycle. The first is to participate in the assembly of virus particles. There is no current data to suggest this function has any implications for biosafety. The second known function is to suppress anti-pathogen defenses by inhibiting a general cellular system called RNA silencing (Haas et al. 2008). Thirdly, Gene VI has the highly unusual function of transactivating (described below) the long RNA (the 35S RNA) produced by CaMV (Park et al. 2001). Fourthly, unconnected to these other mechanisms, Gene VI has very recently been shown to make plants highly susceptible to a bacterial pathogen (Love et al. 2012). Gene VI does this by interfering with a common anti-pathogen defense mechanism possessed by plants. These latter three functions of Gene VI (and their risk implications) are explained further below:
1) Gene VI Is an Inhibitor of RNA Silencing
RNA silencing is a mechanism for the control of gene expression at the level of RNA abundance (Bartel 2004). It is also an important antiviral defense mechanism in both plants and animals, and therefore most viruses have evolved genes (like Gene VI) that disable it (Dunoyer and Voinnet 2006).
Gene VI (upper left) precedes the start of the 35S RNA
This attribute of Gene VI raises two obvious biosafety concerns: 1) Gene VI will lead to aberrant gene expression in GMO crop plants, with unknown consequences and, 2) Gene VI will interfere with the ability of plants to defend themselves against viral pathogens. There are numerous experiments showing that, in general, viral proteins that disable gene silencing enhance infection by a wide spectrum of viruses (Latham and Wilson 2008).
2) Gene VI Is a Unique Transactivator of Gene Expression
Multicellular organisms make proteins by a mechanism in which only one protein is produced by each passage of a ribosome along a messenger RNA (mRNA). Once that protein is completed the ribosome dissociates from the mRNA. However, in a CaMV-infected plant cell, or as a transgene, Gene VI intervenes in this process and directs the ribosome to get back on an mRNA (reinitiate) and produce the next protein in line on the mRNA, if there is one. This property of Gene VI enables Cauliflower Mosaic Virus to produce multiple proteins from a single long RNA (the 35S RNA). Importantly, this function of Gene VI (which is called transactivation) is not limited to the 35S RNA. Gene VI seems able to transactivate any cellular mRNA (Futterer and Hohn 1991; Ryabova et al. 2002). There are likely to be thousands of mRNA molecules having a short or long protein coding sequence following the primary one. These secondary coding sequences could be expressed in cells where Gene VI is expressed. The result will presumably be production of numerous random proteins within cells. The biosafety implications of this are difficult to assess. These proteins could be allergens, plant or human toxins, or they could be harmless. Moreover, the answer will differ for each commercial crop species into which Gene VI has been inserted.
3) Gene VI Interferes with Host Defenses
A very recent finding, not known by Podevin and du Jardin, is that Gene VI has a second mechanism by which it interferes with plant anti-pathogen defenses (Love et al. 2012). It is too early to be sure about the mechanistic details, but the result is to make plants carrying Gene VI more susceptible to certain pathogens, and less susceptible to others. Obviously, this could impact farmers, however the discovery of an entirely new function for gene VI while EFSA’s paper was in press, also makes clear that a full appraisal of all the likely effects of Gene VI is not currently achievable.
Is There a Direct Human Toxicity Issue?
When Gene VI is intentionally expressed in transgenic plants, it causes them to become chlorotic (yellow), to have growth deformities, and to have reduced fertility in a dose-dependent manner (Ziljstra et al 1996). Plants expressing Gene VI also show gene expression abnormalities. These results indicate that, not unexpectedly given its known functions, the protein produced by Gene VI is functioning as a toxin and is harmful to plants (Takahashi et al 1989). Since the known targets of Gene VI activity (ribosomes and gene silencing) are also found in human cells, a reasonable concern is that the protein produced by Gene VI might be a human toxin. This is a question that can only be answered by future experiments.
Is Gene VI Protein Produced in GMO Crops?
Given that expression of Gene VI is likely to cause harm, a crucial issue is whether the actual inserted transgene sequences found in commercial GMO crops will produce any functional protein from the fragment of Gene VI present within the CaMV sequence.
There are two aspects to this question. One is the length of Gene VI accidentally introduced by developers. This appears to vary but most of the 54 approved transgenes contain the same 528 base pairs of the CaMV 35S promoter sequence. This corresponds to approximately the final third of Gene VI. Deleted fragments of Gene VI are active when expressed in plant cells and functions of Gene VI are believed to reside in this final third. Therefore, there is clear potential for unintended effects if this fragment is expressed (e.g. De Tapia et al. 1993; Ryabova et al. 2002; Kobayashi and Hohn 2003).
The second aspect of this question is what quantity of Gene VI could be produced in GMO crops? Once again, this can ultimately only be resolved by direct quantitative experiments. Nevertheless, we can theorize that the amount of Gene VI produced will be specific to each independent insertion event. This is because significant Gene VI expression probably would require specific sequences (such as the presence of a gene promoter and an ATG [a protein start codon]) to precede it and so is likely to be heavily dependent on variables such as the details of the inserted transgenic DNA and where in the plant genome the transgene inserted.
Commercial transgenic crop varieties can also contain superfluous copies of the transgene, including those that are incomplete or rearranged (Wilson et al 2006). These could be important additional sources of Gene VI protein. The decision of regulators to allow such multiple and complex insertion events was always highly questionable, but the realization that the CaMV 35S promoter contains Gene VI sequences provides yet another reason to believe that complex insertion events increase the likelihood of a biosafety problem.
Even direct quantitative measurements of Gene VI protein in individual crop authorizations would not fully resolve the scientific questions, however. No-one knows, for example, what quantity, location or timing of protein production would be of significance for risk assessment, and so answers necessary to perform science-based risk assessment are unlikely to emerge soon.
Big Lessons for Biotechnology
It is perhaps the most basic assumption in all of risk assessment that the developer of a new product provides regulators with accurate information about what is being assessed. Perhaps the next most basic assumption is that regulators independently verify this information. We now know, however, that for over twenty years neither of those simple expectations have been met. Major public universities, biotech multinationals, and government regulators everywhere, seemingly did not appreciate the relatively simple possibility that the DNA constructs they were responsible for encoded a viral gene.
This lapse occurred despite the fact that Gene VI was not truly hidden; the relevant information on the existence of Gene VI has been freely available in the scientific literature since well before the first biotech approval (Franck et al 1980). We ourselves have offered specific warnings that viral sequences could contain unsuspected genes (Latham and Wilson 2008). The inability of risk assessment processes to incorporate longstanding and repeated scientific findings is every bit as worrysome as the failure to intellectually anticipate the possibility of overlapping genes when manipulating viral sequences.
This sense of a generic failure is reinforced by the fact that this is not an isolated event. There exist other examples of commercially approved viral sequences having overlapping genes that were never subjected to risk assessment. These include numerous commercial GMOs containing promoter regions of the closely related virus figwort mosaic virus (FMV) which were not considered by Podevin and du Jardin. Inspection of commercial sequence data shows that the commonly used FMV promoter overlaps its own Gene VI (Richins et al 1987). A third example is the virus-resistant potato NewLeaf Plus (RBMT-22-82). This transgene contains approximately 90% of the P0 gene of potato leaf roll virus. The known function of this gene, whose existence was discovered only after US approval, is to inhibit the anti-pathogen defenses of its host (Pfeffer et al 2002). Fortunately, this potato variety was never actively marketed.
A further key point relates to the biotech industry and their campaign to secure public approval and a permissive regulatory environment. This has led them to repeatedly claim, firstly, that GMO technology is precise and predictable; and secondly, that their own competence and self-interest would prevent them from ever bringing potentially harmful products to the market; and thirdly, to assert that only well studied and fully understood transgenes are commercialized. It is hard to imagine a finding more damaging to these claims than the revelations surrounding Gene VI.
Biotechnology, it is often forgotten, is not just a technology. It is an experiment in the proposition that human institutions can perform adequate risk assessments on novel living organisms. Rather than treat that question as primarily a daunting scientific one, we should for now consider that the primary obstacle will be overcoming the much more mundane trap of human complacency and incompetence. We are not there yet, and therefore this incident will serve to reinforce the demands for GMO labeling in places where it is absent.
What Regulators Should Do Now
This summary of the scientific risk issues shows that a segment of a poorly characterized viral gene never subjected to any risk assessment (until now) was allowed onto the market. This gene is currently present in commercial crops and growing on a large scale. It is also widespread in the food supply.
Even now that EFSA’s own researchers have belatedly considered the risk issues, no one can say whether the public has been harmed, though harm appears a clear scientific possibility. Considered from the perspective of professional and scientific risk assessment, this situation represents a complete and catastrophic system failure.
But the saga of Gene VI is not yet over. There is no certainty that further scientific analysis will resolve the remaining uncertainties, or provide reassurance. Future research may in fact increase the level of concern or uncertainty, and this is a possibility that regulators should weigh heavily in their deliberations.
To return to the original choices before EFSA, these were either to recall all CaMV 35S promoter-containing GMOs, or to perform a retrospective risk assessment. This retrospective risk assessment has now been carried out and the data clearly indicate a potential for significant harm. The only course of action consistent with protecting the public and respecting the science is for EFSA, and other jurisdictions, to order a total recall. This recall should also include GMOs containing the FMV promoter and its own overlapping Gene VI.
Footnotes:
References:
I was still in medical training when I was called to testify in defense of Oprah Winfrey in the infamous "meat defamation" trial. If you remember, Oprah swore she would never eat another burger again after hearing that cows were being fed the remains of other cattle. After she tried to remind the audience that cows were supposed to be herbivores, the meat industry representative defended the practice by stating, "Now keep in mind, before you view the ruminant animal, the cow, as simply a vegetarian -- remember that they drink milk." The absurdity of the statement aside, it's not even entirely accurate. In modern agribusiness, humans drink the milk. Calves typically get milk "replacer."
Like all mammals, cows can produce milk only after they've had a baby. Most newborn calves in the United States are separated from their mothers within 12 hours -- many immediately after birth -- so the mother's milk can be marketed for human consumption. Though some dairy farmers still wean calves on whole milk, the majority of producers use milk replacer, which too often contains spray-dried cattle blood as a cheap source of protein.
According to the American Protein Corporation, which boasts to be the world's largest spray-dryer of blood, the chief disadvantage of blood-based milk replacer is simply its "different color." Milk replacer containing blood concentrate typically has a "chocolate brown" color, which can leave a dark residue on the bottles, buckets, and utensils used to feed the liquid. "For some producers," a company official remarked, "the difference is difficult to accept at first, since the product does not look 'like milk.'" But the "[c]alves don't care," he was quick to add.
The calves may not care, but Stanley Prusiner does. Prusiner won the Nobel Prize in Medicine for his discovery of prions, the infectious proteins that cause mad cow disease. He was quoted in the New York Times as calling the practice of feeding cattle blood to young calves "a really stupid idea," because it could complete the "cannibalistic" circuit blamed for the spread of the disease.
The European Commission also recommended against the practice of "intraspecies recycling of ruminant blood and blood products" -- the practice of suckling calves on cows' blood protein. Even excluding the fact that brain matter may pass into the trough that collects the blood once an animal's throat is slit, the Commission report concluded a decade ago that "[a]s far as ruminant blood is concerned, it is considered that the best approach to protect public health at present is to assume that it could contain low levels of infectivity." Since then, evidence that blood can be infectious has only grown, yet dairy calves in the United States are still drinking up to three cups of "red blood cell protein" concentrate every day.
Although the U.S. Food and Drug Administration initially proposed to ban the feeding of blood and blood products to livestock, the agency ended up reneging on their much touted promise. Let's hope that the newly reported case of mad cow disease in a California dairy cow will renew interest in closing the loopholes in feed regulations that continue to allow the feeding of slaughterhouse waste, blood and manure to farm animals in the United States.
http://www.huffingtonpost.com/michael-greger-md/california-mad-cow-disease_b_1450984.html?
More than a decade ago, the World Health Organization called for the exclusion of the riskiest bovine tissues -- cattle brains, eyes, spinal cord and intestine -- from the human food supply and from all animal feed to protect against the spread of mad cow disease. Unfortunately, the United States still allows the feeding of some of these potentially risky tissues to people, pigs, pets, poultry, and fish. Cattle remains are still fed to chickens, for example, and the poultry litter (floor wastes that include the feces and spilled feed) is fed back to cows. In this way, prions -- the infectious proteins that cause mad cow disease -- may continue to be cycled back into cattle feed and complete the cow "cannibalism" circuit blamed for the spread of the disease.
Because poultry litter can be as much as eight times cheaper than foodstuffs like alfalfa, the U.S. cattle industry may feed as much as a million pounds of poultry litter to cattle each year. A thousand chickens can make enough waste to feed a growing calf year-round. Although excrement from other species is fed to livestock in the United States, chicken droppings are considered more nutritious for cows than pig feces or cattle dung.
A single cow can eat as much as three tons of poultry waste a year, yet the manure does not seem to affect the taste of the subsequent milk or meat. Taste panels have found little difference in the tenderness, juiciness, and flavor of beef made from steers fed up to 50% poultry litter. Beef from animals fed bird droppings may in fact even be more juicy and tender. Cows are typically not given feed containing more than 80% poultry litter, though, since it's not as palatable and may not fully meet protein and energy needs.
The industry realizes that the practice of feeding chicken feces to cattle might not stand up to public scrutiny. They understand that the custom carries "certain stigmas," "presents special consumer issues," and poses "potential public relations problems." They seem puzzled as to why the public so "readily accepts organically grown vegetables" grown with composted manure, while there is "apparent reluctance on the part of the public" to accept the feeding of chicken excrement to cattle. "We hope," says one industry executive, "common sense will prevail."
The editor of Beef magazine commented, "The public sees it as 'manure.' We can call it what we want and argue its safety, feed value, environmental attributes, etc., but outsiders still see it simply as 'chicken manure.' And, the most valid and convincing scientific argument isn't going to counteract a gag reflex." The industry's reaction, then, has been to silence the issue.
According to Beef, public relations experts within the National Cattlemen's Beef Association warned beef producers that discussing the issue publicly would only "bring out more adverse publicity." When the Kansas Livestock Association dared to shine the spotlight on the issue by passing a resolution urging the discontinuation of the practice, irate producers in neighboring states threatened a boycott of Kansas feedyards.
Maybe this new case of mad cow disease will reinvigorate consumer campaigns to close the "no-brainer" loopholes in feed regulations that continue to allow the feeding of such filthy feed to farm animals.
http://www.huffingtonpost.com/michael-greger-md/mad-cow-disease-california_b_1450994.html
The downer dairy cow recently found stricken with mad cow disease in California was infected with an "atypical" strain. Such cases are thought to arise spontaneously, a notion the USDA seized upon to explain how the disease could arise despite their regulations. If anything, that fact highlights the weaknesses in the current feed rules. If mad cow disease can arise out of nowhere, then it's even more important to close the loopholes and stop the feeding of cattle blood to calves and chicken manure to cows to prevent it from spreading. And what the USDA didn't mention about the atypical strain found in California is that there's evidence it's a more dangerous form of the disease
The California cow died of a particularly virulent form of mad cow disease known as BASE, bovine amyloidotic spongiform encephalopathy, also known as L-type atypical BSE. Typical BSE was first documented in the '80s in Britain. Afflicted cows often became twitchy and aggressive, giving rise to the "mad cow disease" moniker, as their brains degenerated into a characteristic Swiss cheese-like appearance. Hence the scientific name, BSE: bovine (cow) spongiform (sponge-like) encephalopathy (brain disease).
Then cats started dying. Max, someone's pet Siamese, was the first non-bovine victim of the disease. Infectious pet food was implicated as the cause of Max's death from a never-before-described feline spongiform encephalopathy.
Then young people started succumbing to a human spongiform encephalopathy called Creutzfeldt-Jakob disease, a relentlessly progressive and invariably fatal dementia, often involving weekly deterioration into blindness and seizures as their brains became riddled with holes. CJD appears sporadically in one in a million people, but typically strikes only the elderly. The new cases among teenagers were dubbed "variant" CJD, a disease now understood to be caused by consuming contaminated meat (or by getting a blood transfusion from someone who did).
Despite massive contamination of the food supply, no more than a few thousand people are expected to die, suggesting a robust transmission barrier between cows and humans when it comes to BSE. The same may not be true of the atypical forms of BSE found in California and in the last two mad cows in Texas and Alabama. Experimental models of human infection suggest that the type of mad cow disease discovered in the California case "is a more virulent BSE strain... in humans," with "higher transmissibility" and causing a swifter death.
Just as one in a million people sporadically get CJD, evidence suggests one in a million cattle get atypical BSE. The U.S. cattle population hovers around 100 million. Though there is evidence some of these sporadic human cases of CJD may be associated with infected cows or sheep, case control studies tie CJD more closely to the consumption of pork. A study co-authored by D. Carleton Gajdusek, recipient of the Nobel Prize in Medicine for his research on these diseases, found that "consumption of pork as well as its processed products (e.g., ham, scrapple) may be considered as risk factors in the development of Creutzfeldt-Jakob disease."
Though pigs have been proven susceptible to a porcine spongiform encephalopathy, the National Pork Producers Council claims that no naturally occurring cases of "mad pig" disease have ever been discovered. The Consumers Union, publisher of Consumer Reports, however, has petitioned the federal government to reopen an investigation into a case in which a USDA veterinarian may have found a cluster of suspect pigs in upstate New York.
New research just found that unlike the British strain, the atypical forms of BSE found in the U.S. cause animals to have difficulties in standing up, so instead of mad cow disease, it's more of a downer cow disease. Since we continue to feed slaughterhouse waste and blood to pigs, this raises the question whether any of the hundreds of thousands of downed pigs that arrive at slaughter plants every year in the U.S. may be infected.
It's ironic that this new case of mad cow disease was discovered in California where a law excluding downed animals from the food supply was recently overturned by the Supreme Court.
In 2008, an undercover investigation by The Humane Society of the United States of a dairy cow slaughterplant in California showing that downers were being dragged to slaughter for school lunch hamburgers prompted California to strengthen its laws to keep downer livestock out of the food supply. The meat industry, represented by the National Meat Association and the American Meat Institute, responded by successfully suing the state of California to keep meat from downed animals on people's plates on the grounds that only USDA had the authority to determine which animals should not be forced to the kill floor for humane or public health reasons.
Sick animals can lead to sick people. An unequivocal ban on the slaughter of any farm animal unable even to stand may reduce the public health risk of myriad threats from anthrax and E. coli to swine flu and Salmonella. Spongiform encephalopathies are a special case, though, as they are caused by infectious agents that cannot be eliminated by cooking, pasteurization, or the rendering process used to make pet food. In fact, infection can survive even incineration at temperatures hot enough to melt lead. It is therefore the meat industry's responsibility to prevent sick animals from entering the food chain in the first place, by instituting a "bright line" ban on the slaughter of all downed livestock. In the California case, the animal was killed before she could be slaughtered. Next time we might not be so lucky.
See also:
For more by Michael Greger, M.D., click here.
http://www.huffingtonpost.com/michael-greger-md/mad-cow-disease_b_1476074.html
After the discovery of a mad cow in its herds, Brazil is experiencing what the US went through in the early 2000′s when three mad cows were found in its food supply: rapid, across the board boycotts of its exports. Japan, China, South Africa, South Korea and Saudi Arabia have banned imports of beef from Brazil since its first suspected mad cow case came to light in December.
Mad cow disease is a fatal transmissible spongiform encephalopathy (TSE), which is called bovine spongiform encephalopathy (BSE) in cows, scrapie in sheep and goats and chronic wasting disease (CWD) in deer and elk. In humans, it is a terminal neurological brain disease called variant Creutzfeldt-Jakob disease (vCJD).
In December 2003, when a mad cow was discovered in the US, imported from Canada and slaughtered in Moses Lake, Washington, 98 percent of the US’ $3 billion overseas beef market evaporated. Mexico, Russia, Brazil, South Africa, Hong Kong, Japan, Singapore, Taiwan, Malaysia, South Korea, and 90 other countries banned US beef almost overnight. The only reason the European Union didn’t ban US beef was it was already banned for its high use of growth hormones.
The US spent most of 2004 trying to woo back its beef sales to Japan who replaced US beef with imports from Australia, New Zealand, and South America. But one month after the country finally agreed to start importing younger cattle only (which are thought to pose less mad cow risk) the unthinkable happened: a US shipment to Japan from Atlantic Veal and Lamb of New York contained veal with the backbone still attached. Spinal material is banned because it poses more mad cow risk and Japan immediately reimposed its boycott. Atlantic Veal and Lamb was subsequently accused of welfare abuses to animals.
A USDA audit designed to reassure Japan did the opposite. It found nine other meatpackers and slaughterhouses were not in noncompliance with removing animal parts that pose mad cow risk. Published reports said the gigantic Swift & Co. plant in Grand Island, Nebraska, was banned from shipping beef to Japan altogether. “The U.S. government does not take the issue seriously enough,” wrote Eiji Hirose of Yomiuri Shimbun/Daily Yomiuri about mad cow risks. And almost ten years later, Japan has still not fully restored US beef imports. Nor has China.
Since even one case of vCJD in humans from eating infected meat–variant Creutzfeldt-Jakob disease–threatens domestic and global beef markets, when suspected cases have arisen in the US, officials often assure the public the diseases are sporadic or hereditary CJD which originate spontaneously and are not from eating meat. Assurances often come before the fact since diagnosis can only be made from a brain biopsy, usually after death. But if CJD is something that “just happens,” the public is greatly reassured and federal officials don’t have investigate the beef supply–the ranches, packinghouses, feed suppliers and even stores and restaurants.
Since April, there is another harm reduction technique that is working to safeguard threatened beef markets. Faced with two mad cow scares this year, both US and Brazil authorities have debuted the concept of “atypical mad cow disease.” Spontaneously-erupting mad cow that has no known cause and may be a genetic mutation has seldom if ever been reported before. But it now seems the new, preferred diagnosis.
A mad cow found in April at a slaughter facility near Fresno whose identity officials protected (identities of mad cow producing ranches in Texas and Alabama were also protected) was “just a random mutation that can happen every once in a great while in an animal,” said Bruce Akey, director of the New York State Veterinary Diagnostic Laboratory at Cornell University. “Random mutations go on in nature all the time.” Brazil officials are similarly saying their mad cow suffered from “atypical mad cow disease.”
Designating cases of mad cow as a “spontaneous” and “atypical” certainly frees officials from lengthy, expensive investigations into the cows’ herd mates, offspring, ranches, slaughterhouses and most importantly feed. It certainly salvages threatened international and domestic beef markets and keep people eating US beef. It certainly quiets news stories when herds start to exhibit mad cow disease.
But is it true?
The complete history of BSE/mad cow disease in the US is found in Martha Rosenberg’s acclaimed food and drug expose Born with a Junk Food Deficiency (Prometheus 2012)
Martha Rosenberg is an investigative health reporter. She is the author of Born With A Junk Food Deficiency: How Flaks, Quacks and Hacks Pimp The Public Health (Prometheus).
http://www.counterpunch.org/2013/01/15/dismissing-mad-cow-as-a-random-mutation/
|