Organic Researcher

After my posts about Mark Purdey, I have had a few emails and most interestingly from Josef Hlasny who has some of his own theories and writings on the cause of BSE. So with his agreement I’ve reproduced a lightly edited version of his email. Please explore and debate with Josef directly through his website.

I read with interest the article “Mark Purdey, explainning BSE and organ…. According to my opinion Mark Purdey was an excellent “BSE scientist” because he did not accept either of the main “scientific” BSE hypotheses- because (for example) “they do not demonstrate Koch’s postulates, despite millions of pounds’ worth of research conducted over 20 years”. He wrote “As a working livestock farmer and TSE researcher with first hand experience of BSE erupting in cattle that had been purchased into my organic farm, I was struck by the fact that no cases of BSE had ever emerged in cows that had been born and raised on fully converted organic farms, despite those cattle having been permitted access to the feed that contained the incriminated meat and bone meal (MBM) ingredient – as part of their 20% conventional feeding stuff allowance decreed in the organic standards at that time”

Also, I challenged the orthodox line about the origins of the BSE outbreak in cattle first recognised in 1986. An early inspiration for me was the australian work of MASON (1968) and later the work of British scientists (MOORBY et al. 2000) created a bovine spongiform encephalopathy (BSE) in dairy cows , without the requirement of any infectious agent (meat and bone meal). So, the official explanation for the origination and spread of BSE and nvCJD leaves a series of massive questions unanswered – Why have vegetarians succumbed to nvCJD? Why is this disease clustered in certain places when contaminated beef has been so widely consumed ?

Mark Purdey set about studying several countries affected by TSEs and those where it was completely absent. His results appeared to suggest that a combination of high manganese levels, low copper levels and a high level of environmental oxidising agents such as ultraviolet radiation could bring about TSEs in susceptible genotypes.

I am also “organic” – but also a veterinary surgeon and animal nutrition scientist; my alternative BSE theory is also “organic” but different- because is named as “ammonia- magnesium theory” (see www.bse-expert.cz).

Concerning the UK, recently I read with interest the article “BSE solution- we ´re not there yet!“ (in; Meat Info…, 27/11/2006) about the recent “Third mad cow forum” in Italy. There a senior scientist is calling for more rigorous testing and surveillance when it comes to BSE…. The calls, by Professor Malcolm Ferguson-Smith, of the Department of Veterinary Medicine at Cambridge University, were made following a conference held in Turin recently, which found that the infectious agent causing BSE is a mutation of the prion protein and is found in contaminated meat and bonemeal feed. This mutation has been reported in an animal in France and the United States. The prion gene mutation is identical to the one that causes one of the commonest forms of familial CJD.

Professor Ferguson-Smith urged the government to include tests for DNA sequencing of sporadic BSE cases to identify possible new mutations as, he said, transmission of the disease gene to the offspring of affected cattle is possible with the attendant risk of variant CJD in humans… Around 126 cattle have gone down with BSE after meat and bonemeal feed was banned in 1996 which means there is a real possibility of sporadic mutations, which is why there should be no relaxation in BSE testing, he said.

However, there are other relationships about “BSE is a mutation…” , also concerning “Third mad cow forum” (Turin; 4-6 October 2006). Sean Henahan asked Frederick A. Murphy, DVM, PhD (Dean of the School of Veterinary Medicine at the University of California, Davis, President of the International Committee on the Taxonomy of Viruses); the questions in an attempt to sort out the science from the media hysteria surrounding the announcement from the UK on March 21, 1996 that 10 people may have become infected with the BSE agent through exposure to beef.

Dr. Frederick A. MURPHY 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.

Other question; What about the political impact of the BSE epidemic?

The global political impact has been incredible. We’re now reading that this might be the ultimate crisis for Prime Minister Major’s Tory government, and could lead to its downfall. There are also huge economic costs. Some estimates go as high as $50 billion, with 300,000 jobs at risk. At the recent Turin (Italy) meeting of the leaders of the European Community, representatives of European countries even brought up questions concerning the pace of the unification of Europe. Even though it has now been decided that quite a bit of the cost of eliminating BSE from British cattle will be shared among other European governments, I don t think we ve heard the last of these tensions at the highest levels of governments.

Professor Ferguson-Smith says that there should be no relaxation in BSE testing. However, I think that the BSE disease can be eradicated “without BSE testing” in the United Kingdom if you will respect “BSE ammonia- magnesium theory” (see below)…

I have an interest in “animal nutrition“, and I am also sceptical of the present evidence for a “BSE infectiosity“ and for a „BSE-vCJD link”. I think that the official The BSE Inquiry report (October 2000); there was the begining about the “great mistake of the medicine sciences” (BSE is an infectious disease originated from meat and bone meal- MBM- feeding in ruminants in the UK) – it is the belief about the MBM feeding in Britain ruminants.

Why this can be a mistake? (according to “The BSE Inquiry”)

1st feature;

Because MBM is not readily acceptable to ruminants, and must be introduced into their diets gradually,… the cow would start to find it unpalatable. However Britain farmers; would not know (1980s) if the protein source in the compound was soya bean meal or „unpalatable“ meat and bone meal (link). So, where “unpalatable” MBM was fed in cows in the UK?

According to my practice as a veterinarian-specialist about ruminant nutrition – in the field conditions (1975- 1990) ; it is not possible in farmers to prepare feed compounds with the MBM himself… (because; high “unpalability” of MBM in dairy cows, especially…). So, I think that MBM was fed to britain cows- only in some “no significant cases”; and mostly only “fish meal” was fed to British cows.

2nd feature;

The British Cattle Veterinary Association is a specialist division of the British Veterinary Association. We have 1600 members of whom 1000 are practising veterinary surgeons working with cattle in farm animal veterinary practices- says Dr.Richard SIBLEY (25/05/1999).

The Scientific paper published in the Veterinary Record of October 1987 was the first large scale publicity that the profession received (about the BSE). The surveillance of BSE up to June 1988 and indeed the surveillance of any non-notifiable disease is based upon the vigilance and inquisitiveness of the farmer and attending veterinary surgeon, with the voluntary referral to a VI Centre. The system is informal and haphazard and is based upon a relationship between the practice and the VI Centre that may or may not exist.

The relationship is often dependent on personal contact, commercial expediency and local availability rather than the wider ramifications of national disease surveillance. The epidemiological studies of the first cases that concluded that an agent was transmitting the disease contained in meat and bone meal (MBM) provided the key to control. The control measures introduced were logical and rational as well as inspirational. Veterinary practitioners are scientists who meet practical disease control challenges on a daily basis. Such veterinary surgeons have much to offer in terms of BSE surveillance and control, including determining practical policies. However, there was scant opportunity for their voices to be heard with little formal consultation or involvement with policy making (link). So, why submission of BSE cases and samples was based on a voluntary commercial decision of the attending veterinary surgeon?

Why this can be a mistake? (according to Dr.Frederick MURPHY);

It is presumed, but will likely never be proven, that the scrapie agent jumped species and moved into cattle when sheep offal (the leftover parts of butchered animals) was included in protein supplements fed to cattle.

Protein supplements containing sheep and cattle offal were banned in the UK in 1988, but it was not until 1991-1992 that the ban was strictly enforced.

The next chapter started with the announcement on March 21, 1996 of 10 cases of CJD in people not otherwise considered at high risk. There have been statements in the press, but no details, that the pathologic changes in the brains of these 10 patients are different from those in usual CJD cases. In any case, it is the age-distribution of these 10 cases (average age 27 vs. 63 for sporadic CJD cases) that led the British expert committee to make its startling announcement.

Experts say (to date);

“BSE is an incurable fatal disease of cattle, caused by a prion. Nobody quite knows how a cow becomes infected. If a human eats infected beef there is a risk of developing the human equivalent of Mad Cow Disease , which is called vCJD“.

However, according to my opinion ;

BSE can be a nutritional disorder – and has its roots in a more common nutritional problem. This alternative “ammonia- magnesium” theory is based on the chronic Mg-deficiency- potentiated by hyperammonemia. There is the possibility that these mechanisms have a strong influence on CNS, especially in ruminants…

I described a Czech alternative „ammonia- magnesium“ BSE theory (March, 2001)- see the bulletin of „Research Institute of Cattle Breeding“ in Rapotín (Czech Republic)- see also this text reprinted in international journal “Feed-Mix“(2002). This journal is well known in European countries – so, after 2002 BSE incidence decrease in Europe? Recently I concluded my opinion about the BSE- see my website and my recent (27 September 2006) “opinion- article“; about the link between “BSE and Alzheimer´s disease”.