European livestock farmers dread the day when their cattle succumb to a tuberculosis breakdown. The implications are severe; a ruthless cull of infected cattle and local badger populations, with all remaining healthy cattle impounded behind an iron curtain of government-mandated movement restrictions and red tape. The consequences have virtually paralyzed small farming businesses into a state of financial meltdown.
But the official procedures of TB control are archaic and outmoded. They are founded upon the age-old hypothesis that humans develop TB as a sole result of exposure to TB infected-animals, and fail to accommodate the more recent front line revelations in the multifactorial science surrounding mycobacterial disease. In this respect, we need to question whether such cruel and costly strategies that are currently involved in TB control programmes are actually fulfilling their desired effect—to protect the human population against the TB agent.
Earlier this summer, I was forced to come to terms with my own cattle joining the ever increasing ranks of TB infected herds that are currently blighting the UK.
TB Breakdown: A Testing Time
At daybreak, I scaled the hill to collect the cattle from the furthest fields. The earth still held the heat of the previous day, and I was forced to coerce the cows a little, for they seemed more reluctant to rise and amble the few feet to the green lane than usual. Perhaps the cows were more perceptive than I was: their sixth sense receptive to the fate that was about to befall them in a few hours’ time.
As we hit the steeper gradients of the shillet track, the cattle accelerated a little, rutting up the dust with their hooves. The tail swish of a cow disturbed an early morning bee that droned off beyond the bank of bluebells and into the obscurity of the dazzling sun. Gradually, the entire caravan of cattle had snaked its way down the track to the valley bottom below. On the last stretch to the farm, a patch of giant foxgloves towered over us like a myriad of mauve lanterns on stalks, their luminescence still reflecting the brilliance of first light. But I failed to heed their red alert, and just drove the cows on without a second thought.
Back at the yard, the vet was ready and waiting, so we led the cows straight down to the inspection pens. The procedure was simple: to measure the size of any lumps that had erupted on the cows’ necks which served as a yardstick for gauging the extent of allergic response to the TB skin test—an intradermal injection of tubercle bacillus that had been administered by the vet three days earlier.
Hardly a few minutes passed, when I saw the vet stand back abruptly. “Oh,” he said in a concerned tone, popping on his spectacles slightly askew. “We could have a problem here, Mark.” I watched him fumbling through his pockets for the callipers, and now knew that he had to take a more precise measurement of what obviously looked like a colossal reaction lump on the cow’s neck. I became anxious, and my mouth was beginning to parch up in anticipation of what was coming next.
The air seemed to hang heavy, much like the prolonged period of suspense before an encroaching thunderstorm. Even the robins, busy in the yard a moment earlier rustling among the brittle leaves, seemed to have stopped dead in their tracks for the duration of that eternal moment. The vet raised his glasses and wiped the sweat off his forehead. “You have a reactor, I’m afraid, Mark.”
A few minutes later there was another reactor, and then a bit later several more. My mouth had gone completely dry and my stomach twisted with nausea. I became angry at the thought of these fine young pedigree animals just entering high summertime in their prime, now doomed for slaughter under the government’s animal health diktat.
Furthermore, like many other cattle farmers in the UK, I was confused by the perfect condition of the TB-reactor cows, since I had always assumed that TB was a debilitating disease. Although these cows had reacted to the skin test and were therefore deemed to carry TB, I began to wonder whether they had successfully adapted to the infection by knocking out the greater majority of the invasive mycobacteria. In this respect, the TB slaughter program could actually be annihilating the resistant animals—culling the genetically robust individuals that we really needed to preserve as breeding stock for future generations.
Badgering the True Evidence
The next stage of the so-called “crisis” procedure was to retire to the farmhouse for a tree’s worth of form filling, where I was presented with several sheets of TB questionnaire. I was amazed by the reductionist contents of the questions that followed, in which each one had been designed on the hypothetical assumption that the transmission of the TB agent from infected badgers to cattle was the sole cause of bovine TB. In this respect, “Baddie the badger” had been daubed as the guilty culprit before the necessary detective work had even begun. The exact same “back to front” investigation was applicable to the questionnaire which the government presented to farms that had experienced a case of mad cow disease, where every question was based upon the assumption of a meat and bone meal feed cause—despite the diversity of evidence which indicated that this theory was totally flawed.
The Search for Susceptibility Factors: The Seeds of TB?
But the real question that was revolving around my brain at that time focused on the fact that my farm had always boasted a TB-free status, despite being surrounded by TB-affected cattle and badgers for many years. I began to wonder what changes had been integrated into our farming practices over recent years; changes that could be responsible for switching on the susceptibility of our cattle to the TB agent. I felt that this was the relevant question that I should be asking right now.
TB is virtually endemic in the soils, waters and atmospheres of the majority of ecosystems, where mycobacteria have co-existed with mammalian life for centuries. Despite its widespread prevalence, the TB agent has produced relatively few major outbreaks across the world. It seems that an epidemic of clinical TB can only erupt once some anti-TB component of our immune defense has been disrupted. In this respect, the primary event is a disruption of immunity which enables the TB agent to breach the body’s defenses and opportunistically take hold.
A historical study of the epidemiology of TB demonstrates that epidemics of TB have occurred since the Iron Age, and that this disease has always been rife amongst specific population groups who are nutritionally impoverished in some way. For example, TB was rife amongst 19th century city slum dwellers who had no choice but to breathe the industrially polluted air 24 hours a day, as well as amongst the half-starved Scottish/Irish crofters who were evicted and forced onto boats bound for North America. Another more recent example involves AIDS victims whose immune systems are so severely compromised that they invariably develop TB as a secondary complication.
A Limey’s View of TB Cause
So what is the key factor that has suddenly unleashed TB susceptibility amongst my cattle following so many years of TB-free status? After much thought about the specific changes that I had integrated into my farming system over recent years, I began to wonder whether the TB breakdown in my herd could be connected to the drastic cost-cutting measures which I have been forced to adopt in order to survive the current agri-economic crisis.
Along with most other hard pressed livestock farmers across the UK, we had foolishly cut back on the use of the so called “non essential” lime/calcified seaweed-based fertilizers. Furthermore, the trend in reduced usage of lime-based fertilizers has been exacerbated by recent conservation measures that have debarred the harvesting of Cornish calcified seaweed altogether—thereby preventing future usage of this material on the farm.
It is the general reduction in use of lime fertilizers, combined with the recent increases in winter rainfall across the western UK that has acidified the topsoil as a result, whilst other eco-influences such as acid rain and the continued use of so-called “essential” artificial fertilizers will undoubtedly be playing their contributory roles in the acidification of agricultural ecosystems.
The pH alkaline/acidic value of the soils on our farm has dropped from an acceptable neutral pH 6 to an acidic pH 5 over the last three years—evidenced by the invasion of buttercups into our pastures where clover used to flourish.
Research has shown that there is a correlation between areas of high mycobacteria incidence and regions where the soils are acid. This association is strengthened by the results of studies where lime was spread on farms in Michigan that were suffering from high rates of mycobacterium infection (albeit the paratuberculosis strain of mycobacterium). The study concluded that the lime treatment had produced a tenfold reduction in the infection of cattle after a three-year period had passed.1
Branding the Iron on TB Cause
The relevant issue in respect to TB infection and soil acidity hinges on the fact that acidification of the topsoil leads to an excessive accumulation of available iron,2 particularly in the regions where soil iron is naturally elevated and rainfall is high. The iron is taken up by the pasture herbage (especially ryegrass, plantain,3 bluebell tubers, etc.) and percolates into the local water supplies as a result, which, in turn, is taken up by any animals that thrive upon the local iron rich ecosystem—particularly those individuals that are genetically predisposed to an increased uptake/retention of iron within their biosystems.
Interestingly, the key hotspot zones of bovine TB across the UK are the Forest of Dean, Exmoor, Cornwall, Devon and the Mendip hills. These regions all correlate with the areas where iron has been mined in abundance4 and rainfall is high.
Preliminary pasture sampling from the specific fields on my own farm in June of 2005 where the TB reactors had been pastured has consistently shown an excessive elevation of iron (average 378 mg/kg) in comparison to levels of 143 mg/kg recorded three years previously. This research is being expanded to cover TB-free and TB-positive farms across the key TB cluster areas of the UK.
What is the relationship between elevated iron and increased susceptibility to TB?
Much research is published in the scientific literature which demonstrates that iron represents an essential prerequisite in the pathogenesis of TB, enabling TB and other strains of mycobacteria to proliferate, metabolize and survive within the mammalian biosystem.5 In this respect, it is the supply of “free” iron within the host which provides the TB agent with its “fire power” capacity to unleash its deleterious pathogenicity, thereby invoking the devastating, often fatal consequences that result from TB infection.
Although TB victims adapt to their parasitic attacks by stashing away their iron supplies in tissues that are inaccessible to the mycobacteria, the grand finale of the TB disease process usually culminates in the parasite getting the upper hand; whereby the host develops the classic iron deficient anemic state that is a central clinical feature of TB.
Mycobacteria acquire their iron from the host’s own transferrin/ferritin molecules—the iron binding transport/storage proteins that are integral to the healthy metabolism of iron within the mammalian biosystem. The mycobacteria rob their host’s iron by releasing a type of iron-capturing siderophore called an exochelin, which, in turn, transfers and donates the iron back to the mycobactins which exist in the cell walls of the mycobacteria themselves.6
This hijacking of the host’s iron supply is beneficial for the survival of the TB mycobacteria in more ways than one. Not only does the TB agent utilize the host’s iron for its own proliferation and survival, but it also utilizes this metal to indemnify its own long term security within the host, by disabling the host’s immune defense against the TB bacterium. The parasite achieves this means of self protection by curtailing the viable synthesis of the iron-binding beta-2-microglobulin molecules whose role is to activate the killer T lymphocytes—the host’s main line of immune defense against mycobacteria infection.7
This could explain why individual humans whose T immune systems have become compromised through nutritional deprivation or AIDS toxicity are at a significantly greater risk of developing TB as a secondary complication.
But TB is not the only pathogen which depends upon the host’s iron for its maintenance and growth within the body. The infamous Clostridium botulinum (implicated in grass sickness of horses), leprosy, HIV, candida, listeria, salmonella, malaria, etc., are all members of this insidious family of iron-thieving pathogens to which TB belongs.8 Only last week, champion horsebreeder Gail Dunsbee had been in touch with me over the sudden death of one of her horses as a result of grass sickness—a devastating paralysis of the autonomic nerve endings in the horse’s gut due to infection with Clostridium botulinum. But much like TB, botulinum is virtually endemic in the gastrointestinal tract of horses where it rarely produces any adverse health effects at all. So what environmental factor had suddenly switched on the susceptibility of her horse’s gut to the infection?
Dissatisfied with the professional ignorance surrounding the root causes of grass sickness, Gail had taken matters into her own hands in order to safeguard the future of her surviving horses. Once again, it looks like the results of her preliminary soil analyses have provided the causal clues that might address this catastrophic problem for horse breeders.
Apart from the low potassium reading, the extremely excessive reading for iron (at 1344 ppm) was the only other element of the twelve elements tested which had deviated from its respective reference range. This result could explain why grass sickness,like TB, has invariably remained confined to acid soil districts where iron levels are generally elevated.
Ironing Out the TB Pathogen
Since elevated iron increases TB risk, it is easy to understand how the management of dietary iron can influence the outcome of TB.5,9 For example, when TB-infected mice were treated with the iron-chelating lactoferrin protein (a natural ingredient of colostrum milk), there was a one hundred-fold reduction in the number of pathogens present in the mice.7
Likewise, TB-diseased individuals used to be regularly treated with the iron-chelating compound p-aminosalicylate with some success.5 In this respect, it could prove beneficial from a preventative as well as a curative perspective to introduce copper or zinc bicarbonate supplements into the diet of TB-affected populations.2 Whilst these anionic compounds do not act as iron chelators as such, they will impair the absorption of iron across the gastrointestinal tract by competing for its uptake system of transport proteins. Furthermore, any foodstuffs containing phytic acids, such as legumes (alfalfa, clover, etc.) and grains3 will produce the same anti-iron effects.
Use of inorganic phosphorus as an inclusion in fertilizers or mineral feed supplements would also assist in reducing the amount of free iron that is rendered available in the soil, or taken up into the animal respectively.10 The phosphorus competes for the iron-binding site on the transport proteins that normally convey iron across the gut wall, thereby arresting the uptake of iron at its initial point of entry into the body.
It is also important to consider the consequences that iron chelators might have upon the horror chamber of other pathogens which need to bite the iron bullet before they can trigger disease. For instance, it has already been demonstrated that the iron-chelating compounds deferoxamine and 8-hydroxyquinoline-5-sulfonic acid have produced beneficial effects in the treatment of leprosy and Clostridium botulinum respectively.8,11
Iron in the Ecosystem
It is proposed that badgers and cattle that co-exist within the same environments will both develop TB due to their separate co-exposure to the same iron-rich food chain, and not necessarily due to a cross-infection from one animal to the other.
Bluebell and other iron-rich tubers constitute a large part of the badger’s diet and these will gradually load up the badger’s biosystem with a concentrated source of iron until threshold levels are exceeded, thereby providing any mycobacterial pathogens that are present with the sustenance to proliferate to pathogenic levels. Likewise, the high incidence rates of human TB that have been recorded amongst steelworkers and slum dwellers (who lived beside their workplaces during the industrial revolution) could have been induced by the high levels of iron in the atmospheres of their local environment.
The Politics of TB
I believe that government ministers in the UK have been correct in resisting pressures to re-enact wholesale slaughter of badgers as a means of controlling TB in the bovine/human populations. The badger culls of bygone years have achieved nothing in terms of eradicating TB. The disease has continued to recur in spite of the various slaughter measures that have been put in place. In this respect, we need to consider what is actually achieved each time that we re-enact this final farcical solution for TB control—that is, badger gassing and blanket cattle culls.
Furthermore, it is scientifically naïve to think that we will ever be able to eradicate a pathogen that is endemic in the environment at large. As long as optimum eco-conditions for the survival of TB mycobacteria are allowed to exist (eg., high iron/soil acidity), then TB epidemics will continue to rear their ugly heads, as and when alterations in weather conditions and husbandry methods permit.
Whilst it is high time that governments should say farewell to their archaic strategy for TB control, some viable alternative will be needed to replace it. In this respect, governments should begin to examine the considerably cheaper and animal welfare-friendly option of encouraging farmers (via subsidies) to adopt husbandry practices which prevent cattle from succumbing to TB infection in the first instance. For example, subsidizing the spreading of lime fertilizers across the TB endemic/high iron regions, as well as promoting the feeding and fertilizing with iron-chelating and anti-iron compounds on farms in the TB-risk areas would reduce the amount of iron that is flowing up the farm food chain, and which, in turn, would reduce the levels of TB mycobacteria infection.
Such a radical approach which curtails the susceptibility of cattle to the TB agent could produce some major advantages over the existing system which slaughters out the end results of TB infection. This would achieve a considerable reduction in the overall incidence rates of TB, thereby reaping major savings for both human and animal life, farmers’ livelihoods and the tax payers’ expense.
Because the incidence of TB is increasing amongst the human population, it is high time that we adopted a more intelligent, civilized and updated strategy for dealing with the prevention of TB. In this respect, we need to take a closer look at the underlying causes of iron overload in the human food chain and ecosystem at large. This would entail looking at the impact of acid rain and how it brings about a rise in the levels of available iron within the soil and water supplies. Issues surrounding the industrial emission of iron particulates into the atmosphere, as well as the supplementation of our foods with iron additives represent important areas that warrant investigation and the development of controls.
Likewise, the indirect impact of various toxic or mutagenic environmental agents upon the metabolic processes that regulate iron homeostasis is an area that also needs to be considered. A whole range of environmental chemicals and metals are recognized to disrupt or mutate the body’s capacity to regulate the balanced uptake, storage and/or excretion of iron, thereby representing an alternative means through which iron levels could become elevated in the biosystem, and which, in turn, switch on an increased susceptibility to TB infection.
Meanwhile, back on the farm, the knackerman had arrived to collect the TB reactors at nightfall. I led the unsuspecting cows to the loading pen, feeling guilty that I had betrayed them by failing to mount any kind of resistance against the government’s strategy of senseless slaughter. The cows waited, absorbing their final moments of life in the half light. Their backs were steaming and heads held low.
The monster lorry rattled in like an aluminum alien, and then backed up to the loading pen. The ramps came down, and after a rapid fire of whelpings and whip lashings, the cattle reluctantly surrendered themselves to their fate, hooves sliding and clattering up the metal ramp into the dark hold of the lorry.
When the truck turned the top corner, I caught my last glimpse of the cows, their noses frantically pressing through the six-inch slats—a last ditch attempt to escape their premature and pointless execution.
As I walked back to the farmhouse in the half light, I caught a glimpse of the foxglove patch on the hill—their petals glowing like red hot irons, reflecting the last light of the evening sun. It was a timely reminder that our TB problem had not been extinguished by the removal of our reactor cows from the farm, but was still very much alive and well, and rooted in the acidity of our soils. As I returned to the farmhouse, I remembered that the presence of foxgloves indicates high iron and high manganese levels in the soil.
A Brief History of Tuberculosis
Tuberculosis is a common, and if untreated, usually fatal infectious disease caused by the microorganism Mycobacterium tuberculosis in humans and Mycobacterium bovis in cattle. TB most commonly affects the lungs but also can involve almost any organ of the body. Many years ago, this disease used to be called “consumption” because without effective treatment, these patients often would waste away.
Evidence of tubercular infection in human populations has been found since earliest antiquity. Skeletal remains of prehistoric humans from 4000 BCE show tubercular decay, which has also been definitively identified in mummy spines from 3000-2400 BCE. Interestingly, the earliest undisputed detection of M. tuberculosis was found in the remains of bison dated 17,000 BCE. However, scientists have yet to determine whether tuberculosis originated in cattle and then transferred to humans, or diverged from a common ancestor.
According to the World Health Organization, one third of the world’s population, or almost 2 billion people, is infected with the tuberculosis bacterium. Most infected people do not in fact develop active TB however, either effectively fighting off the bacterium or maintaining it in a latent state in their bodies. Only one in ten latent cases will ever lead to active disease, but about half of those resulting active cases risk succumbing to TB if it is not treated.
Most new cases of TB infection occur in the developing world, where poverty, malnutrition, increasing rates of AIDS infection and chronic exposure to environmental pollution all depress immunity and increase susceptibility to TB transmission. The neglect of earlier established TB control programs, along with rising populations with HIV/AIDS infection, substance abuse, and the use of immunosuppressive drugs are also causing a resurgence of TB in the world’s developed countries. According to WHO data, 14.6 million people had active TB in 2004, with 8.9 million new cases and 1.7 million deaths, most (95 percent) occurring in developing countries.
Raw Milk and Tuberculosis: The Role of Lactoferrin
Although health officials often accuse raw milk of causing TB, many doctors have recognized the fact that raw milk contains special factors that protect against the disease. One of these factors is lactoferrin, an enzyme that kills pathogens by binding and removing iron. In a study involving mice bred to be susceptible to tissue iron overload and hence to tuberculosis, treatment with lactoferrin significantly reduced the burden of tuberculosis organisms.7 And mice injected with Candida albicans, another iron-loving organism, had increased survival time when treated with lactoferrin.12 Lactoferrin is plentiful in raw milk. It is destroyed by pasteurization.
TB Etiology and Treatments
In 1720, British physician Benjamin Marten first conjectured that “wonderfully minute living creatures” might be the cause of TB, and he even proposed that if one were “to draw in part of the breath [that an infected person] emits from the Lungs, a consumption may be caught by a sound person.” This quite sophisticated epidemiological reasoning predated by 145 years the work of Jean-Antoine Villemin, a French military doctor who revolutionized contemporary understanding of TB. In 1865, Villemin successfully demonstrated that consumption (TB) could be transmitted from humans to cattle and from cattle to rabbits, and via this evidence postulated that a specific microorganism was responsible for the disease. In 1882, Robert Koch developed a staining technique that would allow him to see and prove the existence of Mycobacterium tuberculosis.
Tuberculosis bacteria, slow-growing microorganisms which exist natively in the environment the world over, find opportunity to proliferate within people who suffer from the health-corroding conditions most associated with urban poverty: over-crowded living conditions, stagnant and industrially polluted air and water, and desperately poor nutrition. The research of Mark Purdey points up important collaborative factors such as soil pH and mineral imbalances that can prepare the terrain for tuberculosis to take hold in non-urban locales as well. The work of several eminent soil scientists, including Dr. William Albrecht, has illuminated the relationship between soil health and human health. Mineral imbalances as well as trace mineral deficiencies plus inadequate nutrition all create conditions that destroy natural immunity and provide fertile ground for disease.
The 19th century introduction of the sanatorium cure offered tuberculosis sufferers their first real hope for recovery, although raw milk therapy protocols had existed since the time of Hippocrates, who prescribed it in the case of tuberculosis. In 1854, Hermann Brehmer, a medical student who himself had recently been cured of tuberculosis by an extended stay in the Himalayan mountains, produced a doctoral dissertation with the ambitious title, “Tuberculosis is a Curable Disease.” That same year, he built several cottages (soon to grow to accommodate 300 beds) in Görbersdorf, Germany, where, at high altitude and with excellent nutrition, patients were exposed to continuous fresh air and sunshine. The results of this cure were universally regarded as highly successful, surpassing any previous treatment, and became the blueprint for sanatoria around the world.
Fresh, raw milk was often a hallmark of sanatorium treatment, and it is ironic that raw milk would eventually come to be blamed for the spread of the disease. During the 1920s, Dr. J.E. Crewe of the Mayo Foundation used an exclusive diet of raw milk to successfully cure tuberculosis. The British medical journal The Lancet reported in May 1937, “Resistance to tuberculosis increased in children fed raw milk instead of pasteurized, to the point that in five years only one case of pulmonary TB had developed, whereas in the previous five years, when children had been given pasteurized milk, 14 cases of pulmonary TB had developed.” In the United States, sanatoria designs often included a nearby dairy farm to be managed for the exclusive supply of raw milk to the sanatorium patients. In Russia, even into the Soviet era, sanatoria typically utilized kumiss (fermented mares’ milk), which had a long tradition of benefiting lung ailments, in the treatment of tuberculosis.
The other typical sanatorium protocols of enforced rest, exposure to clean, fresh air and sunshine, along with nutritious, generous meals and gentle exercise built up patients’ strength and immunity. The treatment, however, which might require many months, could only be chosen by those whose families could afford it, and the sanatoria remained out of bounds for impoverished TB sufferers.
It was only in 1943 that successful drug therapy was developed for TB treatment with the introduction of the antibiotic streptomycin. Although hailed at first as a wonder drug in the fight against tuberculosis, the disease often rebounded in just a few months of antibiotic treatment. Many more anti-TB drugs were developed in the following years, and the sanatoria fell into universal disuse. By administering two or even three drugs simultaneously, physicians appeared to overcome the problem of drug resistance, although mutant strains have always continued to appear.
Current clinical treatment protocols include the administration of four anti-TB agents, and new drugs are being developed, at ever-increasing toxicity, to meet the challenge of ever-stronger, resistant strains. The familiar pattern of using bigger and bigger drug arsenals begs the question of whether this approach is really appropriate for anyone other than the pharmaceutical industry, while the greater health deficiencies of tuberculosis sufferers today remain largely ignored.
The Pharmaceutical Journal and Pharmacist: Milk and Tuberculous Meningitis
The following debate appeared in the pages of The Pharmaceutical Journal and Pharmacist over several weeks in 1914. The discussion centers on tuberculous meningitis, the most serious form of tuberculosis, which causes severe neurologic deficits or death in more than half of cases. The pattern of tuberculous meningitis in the population is different in different areas of the world. In areas with much tuberculosis, tuberculous meningitis usually afflicts young children. Medical texts report that it develops typically three to six months after the primary tuberculosis infection, a fact of interest when assessing the argument against raw milk of J. Young Sutherland, below. Many thanks to Maury Silverman for uncovering this fascinating exchange.
Report on April 18, 1914
In a letter to the Times on April 15, Dr. Ralph Vincent combated the thesis that tuberculous meningitis in children was of bovine origin and came from drinking cows’ milk. The immediate cause of the disease, Dr. Vincent maintained, was the tubercle bacillus which was derived from the inhalation of dust containing it. In a healthy and properly nourished child, the tissues would rapidly destroy the bacilli. But in an improperly nourished child, they would be unable to do so. And this condition would arise in the case of a child fed entirely on cooked, boiled and sterilised food. Dr. Vincent stated that since 1904 he had been searching for a case of tuberculous meningitis in a child fed on raw milk, but had never found one, whereas since the beginning of this year he had seen three cases in children fed on cooked milk.
Letter published April 25, 1914
In last week’s issue of The Pharmaceutical Journal, there appears an interesting paragraph [on milk and tuberculous meningitis], which refers to a letter contributed to the Times by Dr. Ralph Vincent. The last sentence of the paragraph reads: “Dr. Vincent stated that since 1904 he had been searching for a case of tuberculous meningitis in a child fed on raw milk, but had never found one, whereas since the beginning of this year he had seen three cases in children fed on cooked milk.” This is thoroughly consistent with Dr. Vincent’s steady insistence that sterilisation “irretrievably injures the food of the infant, definitely destroying vital elements essential to nutrition.” It is interesting to turn to another authority, viz., Dr. G. F. Still, who, in dealing with the subject of tuberculous meningitis writes:—”with regard to the drinking of unboiled milk, I think there is no reasonable doubt that this is one source of tuberculous infection in general, and in particular leads to tuberculous meningitis.” I have been very much impressed by cases in which a child remained apparently in perfect health upon scalded or boiled milk, and then a change was made, sometimes because the family had moved to a district in which the milk was reported to be specially reliable; the milk was given unboiled, and within a month or two the child has died of tuberculous meningitis. I have noted this sequence sufficiently often to make me suspect very strongly that unboiled milk is a real danger in respect of tuberculous meningitis.” Truly, “when doctors differ, who shall agree?”
-J. Young Sutherland, Drumsheugh, Edinburg
Letters published May 2, 1914
Mr. Sutherland truly quotes “when doctors differ,” etc. but there can be no doubt about the lessened nutritive value of cooked milk for young children, nor the fact that boiling, by destroying the natural protective ferment, renders milk much more susceptible to infection to pathogenic bacteria. The danger of tubercular disease from milk, I think, is largely due to newspaper origin. I have examined a large number of samples of milk for B. tubercule, under the Tuberculosis Order (Animals) and only find the tubercle bacillus present in about 1 percent, and these are all suspected cases, many of the cows have reacted to the tuberculin test; this makes the number of cows giving tubercular milk very small indeed, if it is a cause at all. Expert opinion is pretty sharply divided:—(a) Whether the bovine tuberculosis can be communicated to man; (b) that all infection in man is caused by inhaling the dried human tubercle bacillus. We may reason as follows: The motor-car does not give milk, but it may cause tubercular disease.
-J. Beetham Wilson, Dorking
I have read with much interest the observations of Dr. Vincent, regarding the sterilisation of milk, and I have no hesitation in stating that I cordially agree with him on every point. From my own observations on this matter, covering a good many years, I have come to the conclusion that the methods of sterilisation of milk, as generally carried out in the every-day process of infant feeding, is little short of a blight and a curse upon the health of little children. The instructions to scald the milk in preparing the infant’s food are generally carried out by boiling it, with the result that the albumen is coagulated to a leathery substance, and the natural enzymes and digestive ferments are destroyed.
It is quite true that certain tuberculosis germs may be destroyed (if there are any present), but the result, on the one hand, in no way compensates for the other. Feed a child on this so-called sterilised milk every two or three hours and the infant will suffer all the agonies of the rack, with indigestion, flatulence, and a degree of constipation which amounts almost to paralysis of the bowels. This last is overcome by the mother, with the use of aperient medicines of every description, suppositories and injections, all of which point to the fact that some elementary law of nature is being interfered with. Boiled milk will in many cases cure the worst forms of diarrhoea, a fact which is taken advantage of by farmers, when calves are suffering with that disorder. It is, therefore, a waste of time to attempt to reason that a child can digest, or have its natural functions in good condition, when fed on heated, sterilised or boiled milk.
A veterinary surgeon has informed me that there is not a herd of cattle with cows over the age of four years, but what is infected by tuberculosis, and that milk from those cows is not contaminated by the tuberculosis bacilli, unless there is tuberculosis of the udder. He drank much milk, but never boiled or sterilised it, as in that state it was an abomination. I was pleased to note that a large firm of manufacturing chemists in London, in recommending their malt extract as a valuable addition to cows’ milk for infant feeding, are careful to give instructions that the milk should not be heated, but hot water only used [for gentle heating], which is undoubtedly the correct method. I have known cases of infants recovering, after they had been given up as hopeless, by resorting to this last method of feeding, after all others had been tried.
-D. F. Ritchie. Newport, I.W.
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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Summer 2007.