The current approach of the UK veterinary establishment towards the control of TB remains rooted to the reductionist mindset of bygone times; the uncivilised world of blanket slaughtering and badly managed "Badgerogeddons" that are naively aimed at achieving the impossible – to annihilate the TB agent from the face of the earth.

Whilst livestock farms have been subjected to these mandatory measures of mass slaughter for several decades, the long term epidemiological pattern of TB outbreaks would appear to have remained unaffected by these invasive modes of control. In stark contrast to the predictions of the most astute TB research teams, TB epidemics have continued to rear their ugly heads with ever increasing frequency. The ‘experts’ remain privately baffled.

The problem is that their whole policy is based upon a totalitarian science that is both derelict and defunct of academic integrity. It fails to cater for the most fundamental property of TB mycobacteria - that these agents are endemic within the open environment and can therefore never be controlled by a total wipe out mode of control. We need to be learning how best to live alongside the TB agent, and, more importantly, to be learning how best to boost our natural immunity to defend ourselves against these elusive mycobacteria. Yet, despite the obvious benefits that could be gained in building up our understanding of the answers to these questions surrounding our immunity against TB, no research has been commissioned in the UK to date which looks at this crucial perspective of TB pathogenesis.

In light of the fact that the incidence of this disease is currently escalating out of all proportion across the UK, it is high time that the Veterinary establishment let go of its intransigent position on TB control, and adopted a more open minded and inquisitive approach towards solving the problem.

Whilst it is encouraging that the likes of the UK Minister of Agriculture , Margaret Beckett, has repeatedly stated " what’s the point in killing badgers if it is not going to achieve anything in the fight against TB ", it is sad that so few other people in positions of power seem to be listening to such a common sense approach.

Last week I experienced the Pavlovian -like response of the British Veterinarian Association towards my plea to develop an investigation into an alternative ‘environmental/dietary’ strategy of control - as a best means of strengthening resistance to TB infection. Their dismissal was no doubt based upon their inability to stomach the radically different perspective that I had presented to them. – one which would not only require a radical about turn in their position on the pathogenesis of TB , but in their position on the pathogenesis of a plethora of other parasitic infections – the ironmonger group of pathogens whose survival is totally dependent upon the free iron supply in their host’s tissues.

If this concept is ever shown to be correct in respect of playing a causal role in bovine TB , then it would seriously threaten the credibility of the UK establishment’s mass slaughter programme, as well as undermining the vested interests and professional reputations of the powerful egos involved in the upper echelons of the UK veterinary establishment.

I had written a mere letter to the editorial of the Vet Establishment’s flagship publication which was submitted as an attempt to woo the vets away from their unilateral policy of ‘overkill’. It presented a nutshell version of the science surrounding the causal role of elevated iron in the foodchain, and how this can compromise the relevant component of our immunity, placing mammals at an increased risk of contracting TB infection. As I had recently written in RedFlagsdaily, the growth and survival of the TB mycobacteria is totally dependent upon a supply of free iron within the host’s tissues. This high iron facet pinpoints a golden opportunity for devising a means of dealing with this disease. If you can influence the levels of free iron within the host, then you can control the overall outcome of the disease; eg; The TB infection could be arrested by starving the agent of its iron supply, which could effectively cure the disease.

But, true to form, my letter was rapidly subjected to a short sharp burst of "heavy vetting", and I was not surprised to receive the classic prudish rejection for lack of scientific rigour at the end of the day – the stereotype response that is wielded onto anyone who is out front about promoting fresh ideas. But I can’t help but wonder why they do not apply the same style of rigorous scientific scrutiny when reviewing the volumes of data that have been published in support of the popular ‘infectious badger’ theory of TB origins ? The whole conventional consensus on TB science appears to have been founded upon a series of unproven assumptions that have never really been called to question.

It is ironic that the Vet Establishment had rejected the science proposed in my letter, even though it was founded upon hard experimental data of reputable international research teams. Yet, despite referencing these studies, they had conveniently ignored the supporting publications and then rejected my letter on the illusory notion that my arguments were exclusively based upon some bar-stool whims derived from my own amateurish observations down on the farm !! In this respect, one begins to question the real motives for their rejection.

The UK scientific community needs to educate itself and recognise the redoubtable role that is played by elevated iron in the pathogenesis of TB and a myriad of other parasitic infections. To the contrary, the merest mention of the iron-TB association to their scientific counterparts in the USA is met with a totally opposite reception. For example, when I casually mentioned my own observations of increased iron on my TB farm to a colleague at the US EPA, he instantly responded by saying , " Iron and TB. You bet. We are cleansing land of mycobacteria by directly spraying the open environment with iron microcrystals. These chelate the mycobacteria, diverting the dirty little fungal buggies into an early grave."

In the light of the repeated failure of the badger culls to eradicate bovine TB, why on earth aren’t the UK veterinary authorities paying serious attention to the positive results of these foreign studies by the Americans and Germans? Why are they resisting this alternative ray of hope?

Isn’t it time that they begin to capitalise upon the highly successful trials where TB affected mice were treated with the iron chelator protein, lactoferrin, which reduced the incidence of TB by 100 fold ? Or the trials where lime was spread on the soil of farms infested with mycobacteria across Michigan reducing the incidence of TB infection ten fold as a result – highly impressive results which should be instantly taken aboard by any open minded and intelligent authority who is working to design foolproof control programmes to safeguard public/animal health.

Nonetheless, the following reviewer comments comprised the mainstay of the veterinary establishment’s response to my letter ;

I responded to this by pointing out that I had only submitted a letter to the editor which was largely intended to alert veterinary readers to this fresh perspective on TB aetiology, and to further ask the vet practises whether I could be connected to additional TB farmers in the hotspot zones in order to expand my geochemical survey.

I also informed the Veterinary establishment that their comments were too fastidious and ‘over the top’ for a mere letter; particularly since they had implied that I ought to be providing the full spectrum of hard evidence for TB cause within the limited confines of my first letter on this subject to the academic literature!

Whilst the reviewers had correctly raised the issue that hotspots of TB are not always sited in areas where iron mining has existed (albeit only two areas that I can see), their comment had failed to grasp the bottom line prerequisite of the theory which distils down to "elevated iron in the bovine food chain", a problem which can arise in various contexts where iron ore beds are not sufficiently concentrated in local bedrock to justify the economic mining of the ore, but nonetheless, where iron is still highly concentrated in top soils for a raft of other geochemical reasons. I had merely capitalised my argument upon this striking correlation between the iron mining areas and TB hotspot zones, and then utilised this as a means of providing a generalised yardstick for demonstrating that the high iron factor offered a plausible explanation for the distribution of TB incidence across the UK.

There are always going to be different environmental influences that will bring about exactly the same end effect of elevated iron within the biosystem, which, in turn, will influence the outcome of any TB infection in the same way.

For example, use of the anti-lactoferrin insecticide wormer, Levamisole, is currently very prevalent on UK livestock farms where it is used in various drench or systemic pour-on wormer formulations. Although exposure to this molecule will initially create an acceleration in the synthesis/secretion of the immune protein ‘lactoferrin’, thereby creating an unnatural boost to the immune defence, the long term repercussions of such an exposure are going to be a bit like driving a car at full throttle throughout its entire road life. You will burn the car out, driving it to a premature grave in the scrap yard. In this respect the long term effect of exposures to levamisole causes a down regulation of lactoferrin secretion; due to the disrupting effects of this chemical at its target receptors on the T lymphocytes – eg; the receptors which mediate the secretion of lactoferrin.

This down regulation effect represents a well known toxicological mechanism by which a receptor can adapt to a toxic insult, by becoming sensitised and/or reducing the rate at which receptors are replenished. The net effect is a long term, perhaps permanent, deficiency in the secretion of lactoferrin, which , in the context of this study, brings about a markedly decreased level of immunity to TB infection.

Lactoferrin is an immune protein that is a component of exocrine secretions. It is manufactured in the epithelia of the gut, lungs, tear ducts (as well as in the granulocytes) where it is used as an iron chelator/antioxidant in the armoury of immune defence against invading pathogens. In this respect, Lactoferrin performs a pivotal role in the defence against invading TB, where it competes against the mycobacteria for the supply of free iron within the tissues, ultimately ‘ironing out’ the lifeblood of the TB agent.

In this respect, the simultaneous exposure of mammals to high iron food-chains and anti-lactoferrin toxic agents (eg the pesticide wormer) could be sufficient to escalate the levels of free iron in the tissues to a threshold that is ripe for a full blown TB takeover.

Whilst I understand the reviewer's point that the elevation of iron on my own TB affected farm does not supply an adequate amount of hard evidence to substantiate the theory, my letter did not actually attempt to convey any pretentions to this effect. In the light of the published experimental evidence surrounding high iron and TB infection, I had merely indicated that these observations on my own and other farms could turn out to be extremely important, and were sufficient to warrant the expansion of a full scale comparative geochemical investigation covering all of the main TB foci regions across the UK.

I feel that the higher impact mainstream journals ought to be publishing the more plausible speculative creative leaps in scientific thinking, rather than rejecting them outright. For the history of science has repeatedly shown that the majority of advancement within academia has invariably stemmed from intuitive sparks of speculative insight – usually originating from the layperson. Yet whenever these so called heretic ideas have been successfully suppressed by the mainstream in the past - due to peer prejudice, commercial or political pressures, etc – the healthy evolution of scientific knowledge usually always suffers a severe set back as a result.

Consider the negative outcome for medicine, if Jenner's original observations on the immunisation of milkmaids against small pox had been outright rejected at the start? For his initial observations were based upon a group of milk maidens who were working with cowpox infected cattle in a cowshed on a single farm in Gloucestershire. The, milkmaids had unwittingly immunised themselves against small pox as a result. If Jenner’s hypothesis had been blocked on grounds that his initial observations were only sourced from a single farm (and therefore could not be shown to hold true for every milk maid operating across the UK) then his important discovery may never have been permitted to see the light of day.

Likewise, where would we be in our understanding of the role that vitamin C performs in the prevention of scurvy, had the solo observations of the "limey sailor" been ignored .

I also take issue with the veterinarian establishment where they state that the arguments in my letter were not based upon rigorous scientific studies. Whilst my own analytical studies to date clearly provide a limited amount of hard evidence, I feel that their comments are misappropriated in respect of the true validity and relevance of the experimental data that was referenced in my letter.

In relation to the veterinary critique written above, I should point out that my letter had clearly indicated that these experiments had involved mice rather than bovines, and mycobacteria paratuberculosis rather than mycobacteria tuberculosis. Furthermore, I cannot see how the differences between the species/strains involved in these experiments should weaken the overall relevance of these trials to the context of bovine TB outbreaks in the UK. In fact, It is counterproductive to be ignoring this work.

My letter had also pointed out that all strains of mycobacteria require a source of iron to manifest their pathogenicity, irrespective of whether the paratuberculosis or tuberculosis strain is involved .

I was particularly annoyed over their failure to recognise the potential relevance of the positive study in which the number of TB pathogens in infected mice had been reduced 100 fold after treatment with the iron chelator lactoferrin. The Vet Establishment had rejected this valuable research on the basis that the work relates to TB in mice and not TB in bovines.

Aren’t the reviewers aware of the universal use of misfortunate lab mice in millions of drug licensing trials where animal reaction to pharmaceutical exposure is exploited as a best means of assessing the potential health effects of those chemicals upon human beings. Furthermore, the entire global establishment has heralded the results of the mice studies carried out by Dr Moira Bruce at Edinburgh, as a plausible means of proving the causal connection between human consumption of BSE affected cow tissues and the development of variant CJD in humans  - presumably because Moira Bruce’s conclusions were in support of the prevailing 'politically correct' theory at that time!

Once again, it seems that the work of outsider scientists has to rank at the top end of the scale; where the quality of their protocols and presentation of their data has to be as white as white can be. But it is a totally different story for those who operate from within the inner circle of incestuous expertise. They can get away with any old hotch potched piece of epidemiological data as long as it supports the establishment line.

One good example of pathological prejudice against ‘outsiders’ was enacted via the peer review system operated by "The Veterinary Record" journal. One of my own papers on TSEs was outright rejected in 2004 after being subjected to the usual stereotype accolade of "lack of scientific rigour", despite having presented some ground breaking data from the analyses of 200 soil and antler samples that I had collected across chronic wasting disease cluster zones in the USA/Canada. Ironically, a few weeks later, a hopelessly unscientific paper aimed at discrediting my data by Chihota et al ( from the prestigious Compton Labs in the UK) was published by the Vet Record despite the admission by the author that they could not afford to carry out any analyses !! ...... " to carry out blood testing and analysis on the necessary scale would have been prohibitively expensive. Instead, we sent a questionnaire survey to farmers asking them what minerals were deficient in their area and compared this with data from the National Soil Inventory".

But the Chihota paper had completely misrepresented the bottom line prerequisite of my published research into TSEs, which decrees that the loss of copper binding at the prion protein is a primary prerequisite of TSE pathogenesis. This can be achieved via several routes; copper deficiency in the environment, copper lock up in the biosystem due to contamination with copper chelating chemicals, or displacement of copper binding at PrP due to competitive binding at the protein ligands by substitute metals such as silver, etc, etc.

Chihota et al had only considered one of the many possible routes for achieving the all important end point that induces scrapie; so when they had failed to stand up their select criteria (eg environmental copper deficiency) in all of the scrapie clusters that they had studied , they arrogantly pronounced the theory as totally flawed!

Back on the TB battle front, the British veterinary establishment’s Pavlovian-like rejection of the widely recognised ‘high iron’ perspective of TB pathogenesis, betrays their determination to remain wedded to the deadlock of the current slaughter strategy – a universally adopted policy of control that is rigidly upheld across the more affluent sectors of the developed world. Furthermore, these uncivilised strategies of mass slaughter are by no means exclusive to the control of TB. They have been repeatedly implemented over the last century to suppress the outbreaks of a whole raft of supposedly ‘infectious’ diseases; for example, the pseudo infectious TSEs (mad cow group of diseases).

In one respect, it is both sad and ironic to witness such a mindset for the mass murder of animals amongst those who are trained in the skills of saving animal life. Why are they so eager to close the door on any serious alternative that offers a more plausible and lucrative strategy for dealing with this problem? Surely, it is the foremost duty of any responsible authority to try to provide a more civilised option of disease control before resorting to the final, farcical solution of blanket slaughter?

But the infectious myth surrounding TB controls has been transmitted across the entire rural community – to the extent that various vigilante groups have been taking the law into their own hands and illegally gassing the badgers into oblivion within the TB areas.

I was appalled to learn that one of these insidious cyanide sessions had taken place on my own farm, down at the most vibrant badger sett in our valley. The Local badger community had become the full scale target of one of these moonlight gas attacks, where the intruders were acting so complacently, that they had forgotten to take their empty gas bottles away. I had found the steely cylinders not far from the entrances to the sett - slumped incongruously across a clump of bluebells .

If only these insensitive idiots had been aware that the bluebell tubers provide the dietary source of concentrated iron that actually enables a TB infection to take a hold in the badgers.

In this respect, these badger bashers would have carried out a much more effective job at cleansing the animal kingdom of TB, if they had uprooted the bluebell tubers and left the poor old badgers well alone

But perhaps the most positive piece of news from behind the iron curtain of the TB hazard zone involves the results of some pilot studies that I had conducted on a batch of "inconclusive" TB reactor cows residing on my farm.

I had intensively fed these cows with a mineral-protein formulation that was designed to chelate the iron, as well as impair the uptake of iron into the cow. I was running this pilot experiment with the aim of starving the TB parasite to death, The results so far have been encouraging;

With a total of six inconclusive animals residing on my farm, five were milking cows who had been fed the formulation during each milking over a one month period. At the TB test last week, the government vets decreed that four out of the five treated animals had recovered and reverted to TB-free status, whilst the remaining one had retained her TB ‘inconclusive’ status. The sixth TB inconclusive animal - who was a beef steer and never fed the formulation - was found to have progressed to full ‘TB reactor’ status and is committed to slaughter. 

Whilst the positive results of this pilot study are hardly significant in scientific terms – because of the small numbers of animals involved - they do however indicate the possibility that all bar one of these inconclusive cattle are no longer reacting to the TB test because they had been treated with a feed that was designed to chelate and compete for the iron supply upon which the TB agent survives. In this respect, it is imperative that this investigation is advanced to the next stage, and tested upon a much larger group of animals.

Sadly, independent researchers such as myself, who invariably have to spend their own money to kick off pioneer investigations that go against the Establishment grain, are all too frequently ignored by the mainstream - irrespective of the true value of the data that they can produce at the end of the day.

Just as the UK veterinary association have subjected my letter to their classic ‘knee-jerk’ rejection, the infectious myth surrounding TB is gathering momentum and spreading to all quarters of the UK Establishment. Today, my farm and family find ourselves subjected to a steady derisory trickle of ridicule and dirty tricks, all for the crime of trying to get to the root cause of disease, so that the needless and reckless slaughter of mammalian life can be prevented. We are sadly living in retrograde times.