Drugs, Farmers, and Disease; Saccharine Disease (Part I)
Contents in in this issue:
- “Drugs, Farmers, and Disease,” by Geoffrey Hull,
- “The Saccharine Disease (Part I)” by T.L. Cleave and G.D. Campbell.
The following is a transcription of the June 1967 issue of Dr. Royal Lee’s Applied Trophology newsletter, originally published by Standard Process Laboratories.
Drugs Farmers, and Disease
The need to awaken public opinion to the dangers of public health of the use of antibiotics in agriculture was the theme of a series of articles in the Evening Post (Reading) last June. Among medical scientists these dangers have been known for a long time, and many of them consider that not enough is done to safeguard the public. Geoffrey Hull discusses some of the issues involved.
Farmers have been encouraged for many years to feed antibiotics to farm animals and birds to promote growth, and they are able also to dose their animals with other drugs, unsystematically, without proper recourse to the veterinary surgeon. Many of these drugs are used in treating human illness, and warnings have been heard from time to time of the potential risks in allowing so many to apply indiscriminately these tools of science in whose proper use they are unversed. The safeguards that apply to the combination of medicine and pharmacy may be less strict than we should like, but those applying to the complex of veterinary science, farming, and the drug industry seem hardly to exist.
Risks foreseen as long ago as 19551 are now becoming dangers recognizable by the general public; but even in 1955, the volume of broiler chicken production in the United States (around 1,090 m. birds) could not have been sustained without the use of growth-stimulating antibiotics.2 At that time the consumption of antibiotics in farm feed was around 700,000 lbs. ($46 million worth), and it was said that the production of antibiotics for such purposes in the United States was so large that it determined the economics of production for medical use.
Since then somewhat similar practices have developed in Britain, partly through high sales pressure of the international pharmaceutical industry, so that it is now almost impossible to get compound animal feed without additives, which commonly includes antibiotics. Some of these additives do occur in nature and may be demanded by the animal, but not necessarily in the circumstances and amount in which they are being artificially used. The way in which these additives promote growth is still not fully understood, and scientists who proposed using many of them emphasized that there was no substitute for good farm management, although their proposals might seem at first to suggest this. Surveys by Ruth Harrison and others suggest that the principle has been widely disregarded.
A recent series of articles by a journalist, John Fielding,3 draws public attention to these matters. Like others, he concludes after examining regulations concerning intensive production of farm animals and birds that “there is a frighteningly superficial interest on the part of the Ministries of Agriculture and Health in the implications of an industry that has written its own rules” during the past 15 years. Fielding points to mounting evidence that new dangers should be studied urgently and to extraordinary facts such as the dissimilarity between the safeguards for red meat and poultry, neither of which seem adequate to meet changing methods of production and distribution. The truth in many of Fielding’s arguments have been known for a long time in the pharmaceutical industry and in scientific circles elsewhere, but as Fielding suggests, government seems usually to act after the mare has bolted—and only afterwards tends to consult those who previously said it would not do so. He quotes a case typical of these early prophesies. A Staffordshire farmer had treated his animals with antibiotics over a considerable period to cure a disease of the udder. His treatment was ineffective, but it resulted in building up in the animals a virulent organism, Staphylococcus aureus, which was resistant to the antibiotics. The farmer was eventually infected and died. The Staphylococci had already become immune to the antibiotics used against them by the doctors because of their overuse by the vets.
That resistance to antibiotics can be acquired is well known to everybody. It is not so well known to the public that there are cases of the transference of immunity from one strain of bacteria to another. This has alarming implications—how alarming we don’t yet know. But the fact of its existence should make us more cautious in their use until we do know more precisely how widespread this transference may become and what can be done to control it. Fielding explores the epidemiology of of Salmonellosis, a disease which is occasionally fatal, though strangely not notifiable, and which is becoming more common as “food poisoning,” associated with the increase in intensive farming and new techniques of distribution. There are apparently about 1,000 people poisoned in Britain each week by eating meat or meal products. In one area of Hampshire alone, two outbreaks in the last seven months resulted in three deaths and 80 cases of medical treatment.
Much of the support for Fielding’s arguments come from a paper by Anderson and Lewis,4 who have studied the relationships between animal and human infections of Salmonella typhimurium strains and their acquired and transmissible resistance to antibiotics. The evidence and implications of this paper are in major part those feared by many scientists for a long time. Fielding concludes that the organism causing typhoid fever is only one step away from immunity to the drug used to treat it. Of concern to farmers, Salmonella can be distributed all over the country by cattle transportation. A recent estimate Fielding quotes is that calf deaths attributed to Salmonella and associated organisms amount to over 4 percent, or about 160,000 per year.
Economists may note that 4 percent is of about the same order as the OECD target for European growth of gross national product, and that this kind of loss to British farming is likely to increase—perhaps catastrophically—unless something is done fairly quickly. But the economic loss does not stop there. Food quality and its economic impact on the national health bill enter in. About 28 percent of barley beeves are said to suffer from liver abscess, and more than 31 tons of poultry from four packing stations in the Bury St. Edmunds area alone were condemned in 1965. Inspection is believed to be inadequate, so that the public may well wish to know how much dangerous food is reaching the shops. In days gone by, one dangerous locally grown chicken might infect one family. Today, chicken produced by modern methods could infect a whole town. We may well inquire whether the profit motive has taken priority over public safety.
It cannot be left entirely to a few firms with socially enlightened policies to set the pace: the matter is too urgent and there are other considerations. In the continuing search for means of increasing world food production, governments of the developing countries are looking naturally towards the highly industrialized countries for advice. The danger here is that they may jump with too much enthusiasm on to the last bus of industrialized modernity whose brakes we are beginning to recognize are defective. The result would be not only there: in modern conditions, food, infection, and contamination travel fast and far, and influence many before anybody has realized quite what has happened.
—Mother Earth, Vol. 14, No. 5, January 1967
- First International Conference on Antibiotics in Agriculture 1956. U.S. National Academy of Science. National Research Council. Publication No. 397. Washington, DC.
- Personal visit. USDA Beltsville Minnesota, 1955.
- John Fielding, Evening Post, June 8–14, 1966. Tessa Road, Reading, Berks.
- Nature, May 8, 1965. Anderson and Lewis.
The Saccharine Disease (Part I)
Surg. Captain Cleave, MRCP (London), RN, and Dr. Campbell, MB, FRCP (Edin.) physician to the Diabetic Clinic, King Edward VIII Hospital, Durban, coauthors of Diabetes, Coronary Thrombosis and the Saccharine Disease, published by John Wright and Sons, Ltd.
The above title covers the conception of a single basic disease, with various systemic manifestations, produced entirely by the consumption of refined carbohydrates, notably sugar, and white flour—which in the body is digested to and absorbed as sugar (as regards its carbohydrate content). The English word “saccharine,” meaning related to sugar, is pronounced like the river Rhine, which sharply distinguishes it from the word for the chemical sweetener. The Saccharine Disease includes diabetes, obesity, coronary thrombosis, and certain infections with the Bacillus coli, together with dental caries, varicose veins, and peptic ulcer. This essentially simple conception is based on both evolutionary and epidemiological evidence, which we have martialed in our joint work and of which we are able to present here only a few details.
This conception the human body, after 3,000 million years of evolutionary adaptation to its environment, is regarded as correctly constructed, and its breakdown in the above conditions as due to exposing it to a new environmental factor to which it cannot yet possibly be adapted. In short, in this condition, the body is regarded as “Built rightly but being used wrongly.”
It is true that an exception to the body being built correctly exists in the case of hereditary defects, such as harelip and clubfoot, but even under the protection of modern civilization the frequency of any such defect never exceeds the figure of 5 per 1,000 births—a frequency some 20 times smaller than occurs in many of the conditions enumerated above. This crucial difference in frequency demonstrates the weakness in ascribing such conditions to hereditary defects, a weakness that is clinched by the very recent appearance of these conditions in the time-scale and by their rarity in races still living under primitive conditions, as we intend to show.
At this point we must consider the totally different question of personal build. For a man’s personal build, even though an absolutely healthy one, may render him highly vulnerable to a new environmental factor. In our work we cite the case of tall men, though perfectly healthy, being in war especially vulnerable to machine gun fire; and similar variations in personal build, which involve every organ of the body, readily explain why certain persons suffer from a disease produced by a new environmental factor, whereas other persons do not. And it is easy to see the fundamental difference between a disease produced in this way and one based on hereditary defect. The distinction is not only highly important but of great practical value, because in the personal-build case the basic external cause of the disease can be removed at once, whereas in the bodily defect case the cause can never be removed, though it may be remedied.
It is also seen how deceptive hereditary features in disease can be, since normally these concern a vulnerable personal build and not a bodily defect. Such hereditary features may therefore be virtually disregarded and attention directed to removal of the cause, in the shape of the unnatural environmental factor responsible. At the present time, in our opinion, much time and energy are being expended in the disease conditions set out above in pursuing hereditary characteristics, which are nothing less than a snare and a delusion. Let us, instead, regard the body as built rightly but being used wrongly, and aim at removing the relevant cause.
Against this most essential background we now present in outline the new environmental factor constituted by the refining of flour and sugar, and the following chart summarizes the position as regards sugar.[Chart in original document, with caption:] The rise in sugar consumption in the United Kingdome over the last century and a half.
It will be seen in the round that the 15 lbs. of sugar consumed per head per year in 1815, jumped in only 150 years to the 8-fold figure of 120 lbs. in 1965. The latter figure equals a daily consumption of 5 oz. per person—which is the amount of sugar contained in some 2¼ lbs. of sugar beet. And it is precisely this unnatural concentration in the sugar, through 2½ lbs. of sugar beet giving place to 5 oz. of crystalline sugar, that exemplified the new environmental factor we have been discussing, which in this case deceives the tongue and leads to startling increases in consumption. For who on the same diet could replace his sugar intake by 2½ lbs. of sugar beet?
Turning now to the case of flour, we we may say that in the refining of wheat, which dates on a massive scale from only about 200 years ago, approximately a third of the grain is stripped off and discarded—and this third is the one that contains much of the protein and nearly all of the fiber, the importance of which will be seen later. The concentration produced is much less than in the case of sugar, but nevertheless is again easily revealed in the eating. Since the starch in flour is digested to, and absorbed as, sugar, the disease conditions caused by the refinement of wheat will largely resemble those caused by the refinement of sugar, and we shall not here specially distinguish the two. Such conditions will be grouped under two headings.
1. Conditions produced by over-consumption
Diabetes. In this condition the pancreas is subjected to such acute strains by short, massive consumptions of sugar that it is no longer able to manufacture the necessary insulin. As a result, the sugar absorbed cannot be utilized and is excreted in the urine, and unless the patient is given other insulin he dies. In our work we show how the rise in the frequency of diabetes in Westernized countries follows the rise in sugar consumption already charted. Thus, from being 27th in the list of causes of death in the statistics of the Metropolitan Life Assurance Company in 1900, it became third by 1950. In the “rule of 20 years” established by one of us (GDC) in racial studies, we show that it takes on the average 20 years’ exposure to refined carbohydrates to produce diabetes, but even wartime sugar rationing immediately affected the actual death rate from the disease.
(See Part II in the July 1967 issue of Applied Trophology.)