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
appeals.
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.
1. Gjorgov,
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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