MAD COW DISEASE (BSE): NUTRITIONAL SUSCEPTIBILITY OR INFECTIOUS CAUSE
Photo Courtesy of Merrill Clark, Roseland Organic Farms, Cassopolis, Michigan
When the news broke of Mad Cow Disease in the United States, we (your editors) e-mailed NOHA Honorary Member Michael A. Crawford, PhD, CBiol,FIBiol,FRCPath, Director, Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, United Kingdom. He replied with exceedingly interesting information, which is summarized below:
Problems with accepted view
According to the official view, Mad Cow Disease or Bovine Spongiform Encephalopathy (BSE) is caused by an infectious agent, which is spread by consuming infected brain tissue from the same or other animal species. However, as far as Professor Crawford knows, no known replication of BSE has occurred by feeding the purified, deformed prion protein at the concentrations, which would have initiated the epidemic.
Specifically, how did one genetically mutated scrapie virus (deformed prion protein) in one sheep brain, mixed into the animal feed, infect virtually the whole of the intensively fed English herd within the 12 months from 1986 to '87 and be found right across the UK by the end of 1988? You have to propose that thousands of sheep were affected with the mutated scrapie virus to obtain a rational, infective level in the animal feed of the nation. If that had happened it would have been obvious in the sheep. Attempts to prove the presence of such a mutation in the sheep herd have failed miserably.
. . . the [past and current] principle applied by the animal industry was grow them fast, fatten them fast, and sell them fast. The BSE epidemic has proved that the system was gravely flawed. There is a crying need for a new approach to animal husbandry-where the health of both humans and animals is given priority. With rising obesity and mental ill health creating alarms in the USA and across Europe, the high calorie, high fat product of beef, pig, sheep, and poultry is no longer an option.
In stark contrast to the EFA status of these wild animals, extensive data has been published over many years, showing the effect of conventional intensive feeding on the loss of essential fatty acids in intensively fed animals.5,6,7
BSE in the London
Zoo: Crossed species or evidence of spontaneity
Right from the start of the BSE epidemic in cows, the same disease was found in zoo animals. Did it cross species from the cow herd to the Zoological Society of London's collection in Whipsnade?
Animals in the Zoo's collection died with BSE. Analysis by The Institute of Zoology's Biochemistry Department showed that the Zoo herbivores were clearly deficient in the omega-3 fatty acids. Of particular note is the loss of alpha-linolenic acid (18:3,n-3) in the Zoo BSE animals compared to those of matching species fed naturally in Africa. The possibility that this difference is due to chance is less than one in 100,000.8
Either BSE crossed species with extraordinary ease, or, similar to crazy chick disease, it was induced by their Zoo diet, which ignored the species evolutionary diet. These Zoo animals were being mistakenly fed on similar principles to the cows.
Access to BSE cows to compare with the Zoo animals and with non-BSE Scottish and New Zealand herds was refused by the Government in the UK. We now know from data from New Zealand and Japan what the answer would have been. Research workers at Ruakuru have shown that bringing cows off green pasture onto conventional intensive diets results in a loss of alpha-linolenic acid.
Japanese Meat Implies a Serious Essential Fatty Acid Deficiency
In Japan cattle were also intensively fed, without including dead animal parts, but, nevertheless, cattle were found to have BSE. Japanese meat compared to natural range meat showed the same EFA deficiencies as were found when comparing the zoo animals with their wild relatives. The extent of the essential fatty acid deficiency found in Japanese meat has two implications:
Brain lipids have
the same fatty acid composition in all mammals.
Thus far, 42 species have been studied with brain EFA compositions similar to those in the following bar graph:
BRAIN ESSENTIAL FATTY ACID COMPOSITION9
Thus, in the brains of all mammals, we find that the long chain (22 carbons) omega-3 fatty acid DHA (docosahexaenoic acid) (22:6) is the most abundant (See the NOHA NEWS, Fall 2003, article, "Why Is DHA Essential for Our Eyes and Brains?"). Within the bodies of animals, including ourselves, it is possible to obtain DHA from the essential omega-3 alpha-linolenic acid, which has an 18 carbon chain and three unsaturated bonds (18:3). To get DHA we have to elongate the chain to 22 carbons and further desaturate to six double bonds.
The essential omega-6 linoleic acid (18:2) is the precursor for our brains of arachidonic acid (20:4). Among other functions, these omega-6 fatty acids are crucially important for the health of the immune system and proper blood flow.
The prion protein is a cell surface glyco-protein expressed by neurones (the specialized cells that transmit nerve impulses). There is now strong evidence that the prion protein has a role in normal brain copper metabolism.10 It is involved in copper uptake11 and copper incorporation into superoxide dismutase, which is a large molecule "that can actually grab and subdue oxidative stress before [an anti-oxidant such as] vitamin C comes to the rescue."12 The prion protein in the cell membranes of the brain can act as an anti-oxidant defence in a similar manner.
Under conditions, which induce an abnormal ion balance across the cell membrane, it has been shown that the prion protein falls out of the membrane and undergoes a conformational change to an isoform, which contains exactly the same atoms but is folded differently. This deformed prion is the one that causes neurodegenerative diseases and BSE.13
Consequently, spontaneous induction of BSE would occur if there was a perturbation of the brain cell membranes, which is precisely what happens in omega-3 or frank essential fatty acid deficiency. The modern, intensive cereal diet of cows is omega-3 alpha-linolenic acid deficient but whilst they were being fed soya meal, they would at least have had some omega-3 alpha-linolenic acid. However, when the price of soya rose uncomfortably and the UK switched to using cheap, processed animal protein recovered from the slaughter houses, they removed this last protection. Just as flocks of chickens went down across the board with crazy chick disease when fed old diets [in which anti-oxidant and omega-3 fatty acid properties had been lost], so the same change would explain the sudden, widespread collapse of the intensively reared UK herd. Notably, none of the grass fed animals in Scotland, for example, succumbed.
BSE: Evidence of EFA deficiency and Brain Disorder Known Since 1967! History:
speculation claims vCJD, which is the human form of a spongiform encephalopathy,
is caused by BSE
There is no direct evidence that vCJD (a variant Creutzfeldt-Jakob disease, which is the human form of a spongiform encephalopathy) is caused by BSE.
The epidemiology of vCJD in the UK is wrong. Most of those affected are in the North. The North had the least BSE. Most BSE started in the South, where there is the least vCJD. Intensive feeding systems of cows and other animals, were at a maximum in the South and Midlands. Moreover, the incidence of heart and other chronic diseases which includes multiple sclerosis, low birthweight and associated neurological disorders is greatest in the north and least in the south where BSE was at its most virulent.
Food for humans has been manipulated in many ways, including loss of EFAs. "Undoubtedly the most serious manipulation problem in food processing centres on the essential structural fats because they are unstable. These components are protected inside the cell but deterioration commences once the architecture is damaged."16 Hence they have a short shelf life!
[First,] . . .several cows died with [BSE] on the same farm. The farmer put the rest of his herd of cows out onto the grass pasture. From that day onwards, no more cows died in his herd. . . . Note well that in the North, in Scotland, where the animals were reared on pasture, there was no BSE.
There is a changing global panorama of mental ill health.17 Mental ill health has risen in the last few decades to be in the top 10 in the list of the burdens of ill-health. By 2020 it will be in the top three. One specific example: the incidence of cerebral palsy amongst low birth weight infants rose three fold between 1967 and 1987 in the UK. Hence vCJD could be simply a symptom of the changing neural susceptibility especially in the Northern regions. It is notable that the much publicised and feared vCJD epidemic did not appear. With the appearance of BSE in the UK and Europe, Japan and the USA, people are now looking more closely at brain disorders than they were forty years ago. However, this argument does not preclude the possibility that the misfolded prion did get into the food chain at the beginning of the bovine epidemic, in large amounts, consequent on the recycling of what are called downers in the USA, into the animal feeds.
The reduction in incidence of BSE in cows with return to natural diet
In the UK, with the exception of parts of the North and Wales, intensive feeding of bovines had become very heavily practiced. When it became apparent that BSE was in crisis numbers, it was then impossible for farmers to sell their animals. The greater the crisis became, the more regulations were enforced. The farmers did not wish to kill healthy animals nor did they want to spend money on feeds for animals they could not sell, so they put them out to eat grass. For the first time in decades, cows in England were seen suckling their calves on green pastures! Thus, the cows began eating green foods rich in the omega 3, alpha-linolenic acid, anti-oxidants, etc., and the calves had proper milk.
When BSE was first discovered, several cows died with it on the same farm. The farmer put the rest of his herd of cows out onto the grass pasture. From that day onwards, no more cows died in his herd. This experience is identical to crazy chick disease in chickens found in Budowski's 1980 paper.1 The flock was dying in numbers and the day alpha-linolenic acid was introduced to the diet no more died. Although no more of this farmer's cows died after being re-introduced to grass, the cows in England began to die across the country until all the intensively fed herds had BSE.
Note well that in the North, in Scotland, where the animals were reared on pasture, there was no BSE.
BSE Conclusion I: Cow mothers fed EFA deficient diets, threaten the fetal brain
An essential fatty acid (EFA) deficient diet influences the brain, liver, and milk. Milk replacers for calves, missing EFAs and nerve growth factors, distort calf brain development (a well established fact since the 1970s).
An intense, high protein diet (protein pellets made from dead animals), which is aimed at physical growth, lacks brain nutrients and adversely affects brain growth and integrity. The rendered animal products are grossly imbalanced (protein far greater than EFAs) and specifically deficient in omega-3 EFAs, which are needed for the brain and the blood brain barrier. Indeed several others find the evidence on BSE unsatisfactory and have proposed similar causes to do with trace element deficiency or excess protein. Such ideas are not mutually exclusive as nutritional distortions involve many nutrients simultaneously. In other words, poor maternal diet, deficient milk replacers, and unbalanced growth diets deplete the developing brain, distort membrane composition, and make young animal brains susceptible.
Conclusion II: Natural Prion changes to infective BSE type. Consequence from well established and robust science:
EFA deficiency causes brain membrane leakage and structural distortion of the membrane. Thus, the EFA deficiency destabilizes neural membranes. A classical sign of EFA deficiency is leaking membranes. Membrane prion leaks from the membrane with protein conformational change, followed by spontaneous generation TO the infectious isoform, which equals BSE.
This explains the rapid appearance of BSE all over the UK intensively fed herds, after the introduction of EFA deficient animal rendered protein. The collapse of the whole herd so rapidly cannot be explained by a single scrapie rogue mutation, as was suggested. It is ludicrous to imagine that one mutated brain diluted in the animal feeds for hundreds of animals, never mind the many thousands, could have been sufficient to explain the suddenness of the BSE epidemic in the UK. The nutritional causation explains the suddenness and wide spread nature of the crisis.
However, this is not to deny that, once the infective prion had moved into the food chain en masse, it could spread in nutritionally susceptible animals. At the same time, note that once the farmers returned their herds to natural grazing with proper EFA diets, the epidemic subsided. However, with unecological intensive feeding, BSE is still endemic in the UK with many still affected.
. . . incorrect brain nutrition can singly destroy the brain. . . . The EFAs are exceedingly important for both the nutrition and health of animals and as food for humans.
Last century the principle applied
by the animal industry was grow them fast, fatten them fast, and sell them
fast. The BSE epidemic has proved that the system was gravely flawed. There
is a crying need for a new approach to animal husbandry-where the health
of both humans and animals is given priority. With rising obesity and mental
ill health creating alarms in the USA and across Europe, the high calorie,
high fat product of beef, pig, sheep, and poultry is no longer an option.
An ecologically fed and reared animal would be healthy both for the animal
and for human nutrition. If public confidence in the industry is to be restored,
then it is time for a radical re-think.
We ask ourselves why this type of evidence of the nutritional cause of BSE has been ignored and pointedly, not investigated. Huge sums of money have gone into research on prions but nothing has been invested in the nutritional distortion. Why? We wonder if one possible reason is that the Government and the animal feed experts would expose themselves to a class action claim for huge damages by admitting that BSE was caused by the experts misleading the farming community on how to feed their cows and by their ignorance of the scientific literature.
BSE is still present in the UK and has spread across much of Europe. Yet there is none in New Zealand where naturally, omega 3 rich grass pasture is used in abundance.
The important point is that there is enough closely related evidence and detailed biochemistry in peer reviewed journals to assert that the nutritional concept, should have been tested. Had it been correct, it would have saved many animals, restored confidence in the system, and allayed public fears of the impending vCJD epidemic. BSE, like crazy chick disease, would become a feature of the past. As it is, the public has lost confidence in Government scientists with an adverse effect on science as a whole.
1Budowski, P., Hawkey, C.M., and Crawford, M.A., "L'effet protecteur de l'acide alpha-linolenique sur l'encephalomalacie chez le poulet," Annals de Nutrition Alimentaire, 34: 389-400, 1980.
2NOHA tape: Michael A. Crawford, PhD, "Essential Fatty Acids for the Brain and Heart," #161, audio and video, April 1997.
3Crawford, M.A., Gale, M.M., and Woodford, M.H., "Muscle and adipose tissue lipids of the Warthog (Phacochoerus aethiopicus)," International Journal of Biochemistry, 1: 654-8, 1970.
4Crawford, M.A., Gale, M.M., and Woodford, M.H., "Linoleic acid and linolenic acid elongation products in muscle tissue of Syncerus caffer and other ruminant species," Biochemistry Journal, 115: 25-7, 1969.
5Crawford, M.A., "Fatty acid ratios in free-living and domestic animals," The Lancet (1): 1329-33, June22, 1968.
6Crawford, M.A., Gale, M.M., and Casperd, N.M., "Comparative studies on fatty acid composition of wild and domestic meats," International Journal of Biochemistry, 1: 295-305, 1970.
7Crawford, M.A. and K. Ghebremeskel, "The equation between food production, nutrition and health," Food Ethics, Ben Mepham, editor, Routeledge, London, pp. 64-100, 1996.
8Crawford, M.A., Budowski, P., Drury, P., Ghebremeskel,K., Harbige, L., Leighfield, M., Phylactos, A., and Williams, G., "The nutritional contribution to Bovine Spongiform Encephalopathy," Nutrition and Health, 7: 61-8, 1991.
9Crawford, M.A., and Sinclair, A.J, CIBA Symposium, "Lipids, malnutrition and the developing brain," pp. 67-92, Elsevier, Amsterdam, 1972.
10See the immediately following NOHA NEWS article, "NUTRITION AND ALZHEIMER'S DISEASE," by John W. Crayton, MD, specifically see the material "on regulation of copper, zinc, iron, and other metals" by the metallothionein proteins (MT-3 in the brain). Dr. Crayton also writes eloquently on how "free radical oxygen destroys brain tissue" and the consequently vital need for antioxidants to quench the free radicals. It is fascinating that the prion (when not deformed) is involved in "normal brain copper metabolism" and in the formation of antioxidants.
11Brown, D.R., "Copper and prion disease," Brain Research Bulletin, 55(2):165-73 Department of Biochemistry, Cambridge University, Cambridge, UK, May 15 2001. HYPERLINK "mailto:firstname.lastname@example.org" email@example.com
12Baker, S.M., Detoxification & Healing, page 72, Keats, 1997.
13Darwin, O. V., et al., Department of Medicinal Chemistry, University of Washington, Seattle, WA 98195-7610; Pathology (Neuropathology), and Molecular and Cellular Pharmacology, University of California, San Francisco, CA 94143, "Mapping the early steps in the pH-induced conformational conversion of the prion protein," Early publication September 2001
14 Clausen, J., and Moller, J., Acta Neurologica Scandinavica,43:375-88, 1967.
15Harbige, L.S., Yeatman, N., Amor, S., and Crawford, M.A, "Prevention of experimental auto-immune encephalomyelitis in Lewis rats by a novel fungal source of gamma-linolenic acid," British Journal of Nutrition, 74: 701-15, 1995.
16Crawford, Michael and Sheilagh, What We Eat Today, page 42, London, Neville Spearman Limited, 1972.
17See www.globalforumhealth.org and Joseph R. Hibbeln and Norman Salem Jr., "Omega-3 Fatty Acids and Psychiatric Disorders: Current Status of the Field" in: Vitamin D: Molecular Biology, Physiology, and Clinical Applications, Chapter 18, Edited by: M. F. Holick © Humana Press Inc., Totowa, NJ, 2001.
Article from NOHA NEWS, Vol. XXIX, No. 2, Spring 2004, pages 1-4.