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1. Josef Hlasny 16 años ago

   However, where is „mad cow risk“? What’s scarier than mad cow disease? Nothing, really — except illnesses that are 10 billion times more likely to hurt you. Think about it this way: Your risk of getting mad cow is much lower than your odds of winning the Powerball lottery… says Marc Siegel, M.D., a clinical associate professor of medicine at New York University Medical School http://www.cnn.com/2007/HEALTH/06/14/healthmag.diseases/index.html?eref=rss_health

   Recently I read the article „Critics say ‘don’t test, don’t find’ is rule for mad cow disease“ (http://www.sentinelandenterprise.com/ci_8677600?source=rss), there Jim Cullor, director of the University of California-Davis’ veterinary medical teaching and research center, agrees, saying, he is comfortable with the reductions in testing. YES very good! Why? According to my opinion mad cow disease (BSE) can be a nutritional disorder. So why a high risk about the BSE infectiosity? Where is a central role of British infectious proteins? (from meat and bone meal- MBM) in BSE- when there is not any evidence about this?

   Britain offloaded tens of thousands of tons of potentially BSE-infected cattle feed on the Third World after deciding it was too dangerous to give to herds in the UK. The MBM was exported after March 1988, when the Government realised that feed made from slaughtered animals was the probable cause of the BSE epidemic in UK cattle. No one knows how many cattle fed on the meal in those countries may now be incubating BSE (http://www.guardian.co.uk/uk/2000/oct/29/bse.focus).
   For example see Statement of Ben GILL (April, 1998) ; former chairman of the Livestock and Wool Committee of the National Farmers’ Union (NFU) , he says:
   «I have been involved in the emerging story of BSE since the NFU first learnt of the existence of a nine cattle in July 1987. I was vice chairman and chairman of the Livestock and Wool Committee of the NFU (1986-1991). Feed compounds used for feeding cattle, farmers may buy compound feed from feed producers. The actual ingredients used will vary from time to time and from producer to producer. These are commercial decisions taken by the feed producers. For example, protein could amongst others be generated by soya bean meal, or from processed meat and bone meal (MBM). At the time that feed producers switched from soya bean meal to meat and bone meal, there would have been no restrictions on them doing so. A farmer buying compound feed would not know what ingredients had been used to provide protein. He would not know if the protein source in the compound was soya bean meal or meat and bone meal(MBM). The arguments for a declaration of ingredients are well rehearsed in an NFU paper prepared in March 1983. The absence of ingredient listing meant that farmers buying compound feedstffs would not know whether or not the feed included meat and bone meal(MBM), and if so, whether it was bovine or ovine meat and bone meal(MBM)? The alternative to purchasing compound feeds is for a farmer to purchase the individual ingredients (referred to as „straights“) and to prepare feed compounds himself » (www.bseinquiry.gov.uk/files/ws/s047.pdf).
   My conclusion;
   In the second half of the 1970s and beyond, UK farmers were being encouraged to increase their milk production. However, where unpalatable «MBM was fed in cows- when a farmer buying compound feed would not know what ingredients had been used to provide protein?
   Meat products (MBM) are valuable only for simple- stomached animals. So, MBM is eaten readily only by pigs (100- 200 g) and poultry- hens (5- 10 g/ animal/ day). This product is not readily acceptable for ruminants (not acceptable- impossible in wildlife) because of the extraordinary smell. Therefore; if MBM is fed in domestic ruminants, it must be introduced into their diets gradually and continuously. So, a farmer buying compound feed would know what ingredients had been used to provide protein !!! In high milk producing cows, especially ; is not possible fed MBM one week (day) and does not next week (or day)!!!
   And what is about; to prepare feed compounds himself? This is impossible in a small farm, especially; because about the extraordinary smell and a high risk about the low feed intake in other cattle- so, the profitability is very low.
   At second, for example; why we found BSE positive animals ? three or more years after a ban on using MBM in dairy rations? (see examples from Europe, Canada, Japan)? So, there is the evidence that MBM is not an origin about the BSE when scientists only believe? (without any experiment or confirmation in field conditions?) that mad cow disease, or bovine spongiform encephalopathy, spreads when farmers feed cattle recycled meat and bones from infected animals. The disease is also only believed to be linked to the rare but fatal brain-wasting human variant Creutzfeldt-Jakob disease…

   I described an alternative «BSE ammonia-magnesium» theory (http://www.agriworld.nl/feedmix/headlines.asp?issue=3). This theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia (high protein intake?). These mechanisms have a strong influence on CNS, especially in ruminants and carnivora animals (www.bse-expert.cz).
   Also according to the recent research; BSE can be «not infectious disease «. Why? At first, authors in Journal of Pathology (March, 2006) found that prion proteins implicated in the development of transmissible spongiform encephalopathies, such as vCJD, may be markers for disease rather than the infectious agents. So, under laboratory circumstances prion-protein can be absorbed across the gut, it also shows that this is unlikely to occur in real life (http://www3.interscience.wiley.com/cgi-bin/abstract/112568745/ABSTRACT).
   And what is about the possibility of sporadic mutations- transmission of the disease gene? There is the explanation from Dr.Murphy; President of the International Committee on the Taxonomy of Viruses (October 2006), he says; » Recent research has shown that the scrapie PrP protein differs from the BSE PrP protein at only seven amino acid loci, whereas the BSE PrP protein differs from the human CJD PrP at more than 30 loci. These differences explain the concept of strains and help explain why prions from one species might jump more easily into another species than another. It is difficult to find the terms to discuss prions ? for example, can we talk about mutants when there is no DNA? What would Watson and Crick think of all this? There is a familial form of CJD, accounting for about 10% of cases. In the familial disease there is are mutations in the gene encoding the normal protein such that the protein tends to fold in the abnormal way and tends to pile up into aggregates in brain cells with lethal consequences … The prion protein in familial cases is the same in each family member that has it, and different in all other families. Sometimes the difference is as small as one amino acid, but these differences can be used to determine the pedigree of the prion. I ‘m sure such analyses are being applied to the 10 cases just reported in the UK»; says Dr.Murphy (http://www.accessexcellence.org/WN/NM/madcow96.html).
   Other authors in Journal Biol. Chem. (November, 2006) found that small amounts of detergent-insoluble PrP aggregates are present in uninfected human brains, so insoluble aggregates and protease-resistant conformers of prion protein in uninfected human brains (http://www.jbc.org/cgi/content/abstract/281/46/34848). More recently (February, 2007) authors in «Neuron» wrote; » Early functional impairments precede neuronal loss in prion disease; they occur before extensive PrPSc deposits accumulate supporting the concept that they are caused by a transient neurotoxic species, distinct from aggregated PrPSc» (http://www.neuron.org/content/article/abstract?uid=PIIS0896627307000086).
   Also other new findings (February 2007), offer significant insights into normal folding mechanisms as well as those that lead to abnormal amyloid fibril conversion (http://www.sciencedaily.com/releases/2007/02/070212182836.htm). Until about five or six years ago, everyone assumed that the large amyloid plaques, or neurofibrillary tangles, that were found in the brains of Alzheimer ‘s victims were the cause of the disease. However, recent scientific discoveries indicate that these large, insoluble aggregates might merely be markers of the disease?they do not cause the disease (http://www.sciencedaily.com/releases/2007/02/070215110558.htm).
   An international team of chemists and molecular biologists reported (April 2007); » A mystery on which the new Nature paper sheds light is what causes different strains of prions (infectious proteins) in which the protein sequence is identical. Our research gives a strong hypothesis that the origin of prion strains is encoded in the packing of the molecules in the fibrils which we are seeing in the crystals». They found that; Alzheimer’s disease, Parkinson’s disease, type II diabetes, the human version of mad cow disease and other degenerative diseases are more closely related at the molecular level. (http://www.sciencedaily.com/releases/2007/04/070430102021.htm).
   In addition, see also my «opinion- articles»; about the link between BSE and Alzheimer?s disease ( http://www.medicalnewstoday.com/youropinions.php?opinionid=11677) and the link between the hyperfunction (neurodegenerative diseases; Alzheimer?s disease?) and the hypofunction of glutamatergic (NMDA receptor) neurons in schizophrenia (http://www.medicalnewstoday.com/youropinions.php?opinionid=17968) and (http://www.medicalnewstoday.com/youropinions.php?opinionid=18538). .

   The prion protein infection from transmissible BSE is then thought to travel to the brain via peripheral nerves, perhaps with assistance from the lymphoreticular system. In 2004, a study of 13,000 appendix and tonsil samples revealed that thousands of people may be unknowingly harbouring vCJD ( http://news.bbc.co.uk/2/hi/health/6334215.stm). However, recently scientists find connection between nerve cells and immune system. They have made visible an astounding number of contacts between immune and nerve cells. These include some of the most important immune cell types, such as B-lymphocytes, T-lymphocytes and dendric cells – all of which form connections to the nerves ( http://www.news-medical.net/?id=21792).
   Also, according to the article «Should we still be worried?» (January 10, 2007) (http://www.guardian.co.uk/g2/story/0,,1986657,00.html), there is an agreement about the BSE no infectiosity; see following text from this article; » But despite billions spent on efforts to save Britain’s beef industry and protect its citizens, all the major questions remain unanswered. The origin of the disease? A mystery. The number of people infected with vCJD? A mystery. The risk that those harbouring the disease will infect others? Again, a mystery . The politicians didn’t know what to do and the scientists didn’t know what to do. We didn’t know where it came from, what caused it, how bad it might be. We didn ‘t know anything «. «The danger now is not from cattle, it’s from other human beings,» says another expert in vCJD .
   This can be in connection that the story of BSE in Britain is a consequence of intensive farming (metabolic disease disease and neurotoxicity) and belongs in the «Organic Research» ( http://organicresearcher.wordpress.com/2007/01/06/bse-an-alternative-theory/). My alternative «BSE ecological view» can be well documented concerning the example «Chronic Wasting Disease» (CWD) (http://organicresearcher.wordpress.com/bse-the-work-of-josef-hlasny/).
   In addition, recently (October 2007) was found that abnormal prion proteins assumed to be the infectious agents that cause mad cow disease and variant Creutzfeldt-Jakob disease might not be to blame after all. Experiments in mice also imply that current tests to detect and intercept meat from animals infected with BSE might miss some cases if diseased animals don’t have the abnormal proteins in their brains, so, Absent prions blow hole in BSE theory (http://environment.newscientist.com/article.ns?id=mg19626274.300&feedId=health_rss20). Other experiment shows (October 2007) that scientists find new causes for neurodegeneration (http://www.pnas.org/cgi/content/abstract/0702275104v1).
   In this connection about people, there is an article (October 2007) about Elizabeth Smith (http://news.bbc.co.uk/2/hi/uk_news/england/west_midlands/7040658.stm) ,she died from the human form of mad cow disease (vCJD). There I read; «Sometimes she would have meat with a meal, sometimes she wouldn’t. It wasn’t one particular kind of meat, either. It may be nothing to do with beef burgers».
   However, similarly it was found by experts (November 2000) into the case histories of 51 sufferers of vCJD has reportedly failed to produce a positive link with eating beef. The report from the National CJD Surveillance Unit in Edinburgh also found little evidence to support the theories that medical treatments or victims’ occupations could be a factor in developing the disease (http://news.bbc.co.uk/2/hi/science/nature/1006242.stm).
   Seven years later; There will be no epidemic of the human form of mad cow disease in Britain, despite fears that the worst is yet to come, recently (September 2007) an expert said. We are «highly unlikely» to see a resurgence in the fatal brain condition, according to Professor Bob Will, director of the National CJD Surveillance Unit, who was speaking at a medical conference in Edinburgh (PRION 2007) (http://theherald.co.uk/mostpopular.var.1717677.mostviewed.epidemic_of_vcj d_in_uk_highly_unlikely.php).
   In Britain, much of the alarmism about Mad Cow disease was never justified scientifically. It was pure, math-model-driven science fiction, just like Global Warming. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors, and is therefore likely to make the same ones again. In politicized science, public hysteria actually builds careers; in real science, it tends to ruin careers
   (http://www.americanthinker.com/2007/11/global_warming_as_pathological.html)
   Dr.David R.BROWN , lecturer and researcher at the University of Bath, is another dissident scientist who believes the entire BSE/CJD link must be completely reconsidered. He believes excessive exposure to manganese, a heavy metal that is, ironically, crucial to life and part of the daily diet, is the culprit behind both BSE and CJD.
   His research team recently found that elevated manganese (Mn) was associated with prion infection. Although some central nervous system regions showed elevated Mn, other regions did not. The most consistent finding was an elevation of Mn in blood. So sheep infected with scrapie and cows infected with BSE have elevated levels of Mn in their blood before clinical symptoms appear, according to new research. These findings, published in the Journal of Animal Science, also show the possibility of using Mn levels in the blood as a potential diagnostic marker for prion infection (http://jas.fass.org/cgi/content/abstract/85/6/1596).
   So, cooper deficiency and rich manganese diet is believed by some to be the key to the origin of BSE in British cattle. The subsequent feeding of meat and bone meal from cattle contaminated with organophosphate and/or manganese-modified prion protein may have caused the spread of the disease to other cattle. The uptake of manganese in place of copper may produce symptoms characteristic of manganese toxicity; slow movement, tremor and/or impaired postural reflexes, and spasm (http://enhs.umn.edu/hazards/hazardssite/prions/prionmetabolislm.html). However, these findings about «BSE; manganese theory»act in concert with my «BSE; ammonia- magnesium theory». So, I will perform some interpretations in my website with conclusion; why some central nervous system regions showed elevated Mn, other regions did not? and why the most consistent finding was an elevation of Mn in blood? However, in the first place, this will be published- presented at the 29th World Veterinary Congres (Vancouver, July 27-31, 2008).

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