During the recent heated debates about the bovine spongiform encephalopathy
(BSE) disease, the controversial discussions and hard decisions for drastic
solutions, there was an appeal on CNN International, on March 22,
1996, from a British lady-farmer, with a request for any opinions or suggestions
about the disease to be heard, in order to be able to make attempts to
solve the crisis in the United Kingdom. Soon afterwards, on April 30, 1996,
such a request was repeated by the British Minister of Agriculture, Fisheries,
and Food (MAFF), on Sky News (London), asking for "constructive
suggestions to be heard," for 45,000-150,000 cows are to be destroyed.
This communication is an attempt to respond to the solicited requests and
With a sense of urgency, the following humble suggestion is made for a scientific study with practical aims. Before any mass destruction of the cattle stock begins, an attempt is made to carry out a possible preventive experimental action against the disease (BSE) in the United Kingdom, Switzerland, or any other European country affected by the disease in the cattle. Supported by the evidence of a certain experimental study (1), the BSE ("mad cows") disease could potentially be controlled by a preventive administration of Prostaglandins (PGs). The Prostaglandins are a group of one of the most active hormonal substances in nature, known to be present in highest amounts in the seminal fluid of humans and animals.
The expected results of and criteria for a successful preventive prostaglandin treatment of the healthy cows, in a short period of time, possibly from two to five years, would be a substantial reduction of BSE incidence, from the 12,000 recorded cases in 1995 (2), to perhaps a half or less new cases in the next year, and a further lowering of the incidence of cases until the eradication of the disease in the subsequent years of continuing action. The preventive intervention for BSE control could be inaugurated promptly, in close cooperation with the veterinary institutions and colleagues and other British scientists.
In a nutshell, between 1988 and 1994, the mentioned experimental study in preventive treatment of breast and pelvic lesions in small laboratory animals was initiated and carried out at the Faculty of Medicine of Kuwait University, in collaboration with other researchers (one of them from the UK). The objective of the study, on a colony of 300 female and 110 male Wistar rats, was to provide experimental evidence and corroboration, if any, of the retrospectively tested semen-factor (deficiency) hypothesis in the etiology of breast cancer and the potential for prevention of the epidemic disease in married American women (3). The experimental evidence validated the postulated cause-and-effect relationship of the semen-factor-deficiency (mainly because of the use of condoms) and breast cancer association, as presented evidence in the prior field, ecological, and correlative hypothesis-testing study on breast cancer. Since it is well known that breast cancer in women is not a random or only local disease, but a systemic disease, with an ill-defined condition of hormonal dysfunction and with a non-specific carcinogenic process, the experimental study was also intended to ascertain and quantify all antecedent events, and degenerative and neoplastic manifestations in the laboratory animals.
During the initial few months of the randomized experimental trial, a number of female animals, about seven, in the two exposed groups (totaling 100), behaved strangely, started running in circles, became slim, restless, and sick, reminiscent of the bovine spongiform encephalopathy condition. The first such case of tentative "BSE" in pseudopregnant animals was observed early, in the third month of the 13-month observation. No growth hormone or any other exogenous hormone was used to induce the BSE-like condition. Other subsequent cases of female animals moving in circles, inordinately, with heads extended and twisted downwards, were isolated and further observed in the study, and died shortly. The incidence and death rate from the condition was estimated at seven percent in the two exposed groups of animals, versus none in the other four groups of animals (totaling 200). The assumption for this unexpected but not surprising development was that some kind of pituitary changes might have been involved in the fatal outcomes. In contrast, no female animal developed such a fatal, exorbitant condition, reminiscent to BSE, in the other four groups of animals, equally exposed to the same risk factor (sterile mating), but prophylactically treated with Prostaglandins.
Cognizant of the Creutzfeldt-Jakob’s disease (CJD) in human females, and of its equivalent, BSE, in animals, cows and apparently rats, it might be presumed that the scientific evidence of the two conditions is consistent with the conclusion that they are not contagious and are not linked to each other in a one-way direction through consumption of goods and other contacts with the cattle. This was also the consensus of the group of veterinarian and medical experts at the recent WHO conference about the threat of a feared BSE and CJD transmission, held in Geneva, at the beginning of April, 1996 (4). In the meantime, talks about eradication of the disease surfaced, without a clear program to achieve it but with a mass slaughter of the present livestock, and with a hope which is not sustained that the disease will not surface again. Within the framework of the tested semen-factor hypothesis in breast cancer, and because of the universality of the reproductive processes in humans and animals, what may seem to be common to these two grave conditions, sporadic CJD and BSE, is the deprivation of seminal factors, most probably the Prostaglandins, during the respective reproductive lives of females. For the purposes of this study, a sporadic (idiopathic) case of CJD is defined as a manifestation of the fatal encephalopathy in patients who have never been treated with either pituitary human growth hormone (hGH) or with any other "irrelevant" hormone therapy. The iatrogenic CJD cases (5,6) do not fall into this category. Approximately 85% of all CJD cases in the United Kingdom are considered "sporadic" (7), and are presumably predominant in females. The confirmed BSE incidence was highest in the dairy herd, 53.3%, and the total herd incidence was 18.2% in Great Britain, in 1995 (8). Weighed as an "inverse" ecological factor, the absence or elimination of the protective seminal factors in the intimate biological environment, the cause of the condition(s) could be amenable to correction and removal.
The preventive intervention against BSE should consist of prostaglandin administration and possible changes in the high-technology processes of the beef industry, i.e. termination of hormone application. The application of the prostaglandins should be carried out perhaps twice a year, at the estrus, per cow, with quantities yet to be determined. The preventive prostaglandin treatment could complement and enhance the cost-effective technology of stock breeding for meat and dairy foodstuff or for the market. It may eventually prove to be highly unlikely that the eradication of the disease be achieved and the disease not reappear in the incoming new generations of cattle, without taking into account the proposal for a technological semen-factor (prostaglandin) supplement. Some further details and consultations would be needed for drafting an urgent, nationwide operative program for BSE prevention in the United Kingdom, Switzerland, and across Europe.
We convey this information to your readers and to the health and government authorities, along with the suggestion and proposal for an immediate implementation of the postulated potential for a preventive experiment and action against the extensive BSE epidemic in the cattle of the United Kingdom, Switzerland and elsewhere in Europe, in order to try to achieve a practical solution of the dramatic beef crisis and eradication of the disease.
P.S. A recently published molecular study (9), comparing the various strains of prion proteins (PrP), related to both diseases, has established a physical link between the ‘new variant’ CJD and BSE. Yet, the laboratory studies did not show whether the PrP, with its apparent toxic pathogenicity, is a cause or an effect of the common conditions leading to the manifestations of the encephalopathies. To what extent the laboratory findings will conform to the known epidemiological evidence and other descriptive facts of both diseases, remains to be determined.
A.N., Junaid, T.A., Burns, G.R, Temmim, L. Breast and Pelvic Lesions
and Prostaglandin Preventive Treatment in Rats. An Experimental Study.
Final Report of the Project MC 030. Kuwait University, Kuwait, 1994 (Mimeographed).
2. James, B. Ban on British beef widens but experts call it unjustified. Internat’l Herald Tribune, March 23-24,1996, p. 1.
3. Gjorgov, A.N. Barrier Contraception and Breast Cancer. S.Karger, Basel-New York, 1980: pp. x+164.
4. World Health Organization. Consultation on Public Health issues related to Bovine spongiform encephalopathy and the emergence of a new variant of Creutzfeldt-Jakob disease. JAMA 275(17): 1305-06, May 1, 1996.
5. Fradkin, J.E., Schonberger, L.B., Mills, J. et al. Creutzfeldt-Jakob disease in pituitary growth hormone recipients in the United States. JAMA 265: 880-884, February 20, 1991.
6. Brown, P., Preece, M.A., Will, R.G. "Friendly fire" in medicine: hormones, homographs, and Creutzfeldt-Jakob disease. Lancet 340: 24-27, July 4, 1996.
7. Dealer, S., Lacey, R. Beef and bovine spongiform encephalopathy: the risk persists. Nutrition & Health 7:117-133, 1991.
8. Gore, S.M. More than happenstance: Creutzfeldt-Jakob disease in farmers and young adults. BMJ, 311: 1416-1418, November 25, 1996.
9. Collinge, J., Silde, K.C.L., Meads, J., Ironside, J., Hill, A.F.. Molecular analysis of prion strain variation
and the aetiology of ‘new variant’ CJD. Nature 382: 685-690, 1996. (Internet, 24 October 1996).
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