United States-New laws hit rendering industry.

You wrote, " ... The purpose of the ruling is to protect the livestock industry from bovine spongiform encephalopathy (BSE, or Mad Cow Disease), says...” However, BSE can be a naturally so not an infectious disease. WHY? Because there can be a direct link about high protein intake and neurodegenerative disease, see these relationships:
1) Mad cow disease (BSE); First case of BSE was in Britain in 1984. It was associated with the growing practice of recycling the corpses of dead farm animals in the production of protein cattle feed, scientists say. However, several new theoretical protein systems have been proposed during the mid 1970s to the mid 1980s. These „concepts“ are more fully discussed in the National Research Council (1985) publication „Ruminant Nitrogen Usage“ (http://www.nap.edu/books/030903597X/html/). There was the beginning of the higher dietary protein recommendation including undegradable protein (fish meal, meat an bone meal...) in dairy rations. It was recommended; during early lactation (0-70 days postpartum); rations may need to contain 19% of more crude protein. For example, the same high protein level is recommended in growing turkey- in animals with highest protein requirements from animals.
2) Chronic wasting disease (CWD); And what is about chronic wasting disease (CWD)?. There are also recommendations; about the high protein intake in deer and elk, see these U.S. literature sources;
White-tailed deer in most southern habitats have access to adequate amounts of forage most of the year. However, white-tailed deer need a minimum of 17% crude protein in their forage year-round for maximum body and antler-growth and other natural deer forages do not contain this minimal amount of protein. Thus food quality, not quantity, may be the limiting factor in producing high quality white-tails on a sustainable basis. There probably is no better off-season forage that one can plant for deer than soybeans. Soybean foliage is high in protein, the soybean seed is extremely high in protein and other nutrients. Soybean plants are utilized heavily from sprouting through seed production. Cowpeas are annual legumes like soybeans and produce high protein forage during the off-season. Fertilization should coincide with spring green-up or about mid-March. Around the first to the middle of May apply ammonium nitrate at a rate of 100 pounds per acre. Natural forage production can be doubled and crude protein content of many plants can be pushed well beyond the basic requirements of white-tailed deer (http://www.pfmt.org/wildlife/deer_nutrition.htm).
Reindeer are selective feeders and, if conditions permit, eat only the top (younger) portion of plants (higher protein content). Deer and elk prefer legumes over grasses because they are higher quality (higher protein content…) and resemble forbs because of their broad leaves (http://www.deer-library.com/artman/publish/article_57.shtml).
Elk that are rapidly growing or lactating and bulls recovering from the rut have higher protein needs. Maintenance rations should be at 10 - 12% crude protein, whereas rations for lactation or antler growth should provide 14 - 18% crude protein. Growing rations should contain 16 - 20% crude protein. If a single diet is fed to all gender and age groups, a 16 - 17% crude protein level is optimal. Total dietary protein content must be determined to follow these general guidelines…(http://www.deer-library.com/artman/publish/article_117.shtml).
3) BSE and CWD; ammonia-magnesium theory; Cellular prion protein (PrPC) is associated with regulation of intracellular free calcium (Ca) levels through an interaction with voltage-sensitive calcium channels. An important consequence of N-methyl-D-aspartate (NMDA) receptor activation is the influx of Ca into neurons. Overstimulation of the NMDA receptor as well as other excitatory amino acid receptors results in neurotoxicity and neuronal injury. Toxic effects displayed by PrPSc (scrapie prion protein) can be blocked by antagonists of NMDA receptor channels.
In connection with the protein surpluss, ruminants are predominant about the Mg- deficiency, so BSE can be involved (www.bse-expert.cz). See these relationships, according to my recent presentation at 29th World Veterinary Congress in Vancouver (http://www.bse-expert.cz/pdf/Veter_kongres.pdf); Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors. There is the abstract about this article;
Neurodegenerative diseases, including BSE, Alzheimer’s disease etc. are caused by different mechanisms but may share a final common pathway to neuronal injury due to the overstimulation of glutamate receptors, especially of the N-methyl-D-aspartate (NMDA) receptor subtype. It is generally accepted that the influx of Ca as a result of excessive activation of the NMDA receptor underlies the toxic actions of glutamate in many systems. Also, ammonia intoxication leads to excessive activation of NMDA receptors in brain. On the other hand, Mg competes with Ca at voltage- gated calcium channels both intracellularly and on the cell surface membrane. So, Mg can protect against NMDA- induced neurodegeneration and Ca deficiency can be important about "NMDA hypofunction" in schizophrenia. There are no scientific references to date in which high intake of crude protein (and potassium) high enough to lead to a state of hyperammonemia (and hypomagnesemia) during the incubation period of the BSE. Therefore there is the first idea of this review; to show the hyperammonemia plus hypomagnesemia"simultaneous" action on the ruminant tissues. Recently was found that elevated manganese in blood was associated with "prion infection" in ruminants. These findings about "manganese theory" act in concert with this "BSE ammonia- magnesium theory".
In addition there is also a surprising link between Alzheimer's disease and other neurodegenerative diseases!
See Alzheimer’s disease, first showed up in medical records at about the same time that world meat consumption (high protein intake) began to rise. There is a direct correlation between the rates of meat consumption and the rates of Alzheimer’s disease in various cultures across the world. In Africa and Asian countries (largely vegetarian India...) where meat consumption is relatively low, the rates of Alzheimer’s disease are much lower than in the developed countries, where meat consumption is high. On the other hand Mediterranean diet; lots of fruits, vegetables, legumes, cereals, some fish and alcohol, and little meat have a reduced risk for Alzheimer's disease. Animal studies (dog, rat) have shown that high protein intakes can result in development of symptoms and pathologic changes of magnesium (Mg) deficiency on Mg-intakes generally considered adequate. So effects of Mg-deficiency are exacerbated by high protein intake.
Also the link between variant CJD, BSE and scrapie has been widely accepted although never proved!
Two groups of eminent British scientists argued in 2001 over whether the "infectious agent" in BSE would kill 136,000 Britons or only a few thousand. And what is the reality- where is the truth, seven years later? The 1st vCJD cases were observed in 1995, and the peak number of deaths was 28 in the year 2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in 2005, 5 in 2006, 5 in 2007, and only one so far in 2008." So these findings (2008) act in concert with Dr VENTERS theory (The epidemic that never was) published in 2001 (http://www.bmj.com/cgi/content/full/323/7317/858).
Sincerely
Josef Hlasny, DVM, PhD., veterinary surgeon in Bludov, Czech Republic