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Prevention of coronary heart disease

SIR,-Surgeon Captain T L Cleave and Dr W W Yellowlees (29 May, p 1340) both remain unaware of, or choose to, ignore, the fact that the fat of the intensively reared animals that they get from their butchers differs from that eaten by hunter-gatherers at the time of Moses and by nomadic peoples like the Masai today. My colleagues and I have described these differences,1-4 World Medicine has reviewed them,5 and we have written a general book on the subject6; the same query on animal fats was raised and answered in the Lancet five years ago.7 Body tissues contain two distinct types of lipid(a) structural lipid that forms cell membranes and is rich in the polyunsaturated fats (PUFA) that provide membrane integrity8 and fluidity,9 and (b) storage fat that acts as an energy source and is rich in the triglycerides of saturated, non-essential fatty acids. The first type changes in composition only under extreme deprivation; the second is very responsive to dietary change. Free-living animals and nomadic herds build muscle, which is a rich source of structural lipid; they accumulate only small amounts of carcass storage fats.1 4 6 10 This is what Moses ate, what the hunters and gatherers ate and still eat, and doubtless what turned up at Smithfield after the drovers had marched their cattle and geese from Wales in the time of Queen Victoria. Modern intensive farming methods in which the animals are fed on high-energy foods and deprived of exercise produce pathological tissues loaded with saturated fat (see figure) and deficient in the muscle cells that carry PUFA in their membranes. The ratio of non-essential fatty acids to PUFA in free-living animals is about 2:1 and in the modern domestic animal about 50:1.1 Dr Yellowlees also omits to mention that the Masai and Samburu mix blood with their milk and thus consume a rich source of PUFA in addition to the non-essential acids of the milk fat. Furthermore, the blood fatty acids of communities who eat free-living animals reflect their high degree of polyunsaturation.'1 As far as the involvement of diet in coronary heart disease is concerned, one would not deny that dietary constituents other than fats have changed and are changing, and that the time scales were different for different constituents. Indeed, we

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have stressed that one cannot discuss one item without the other because of the metabolic interactions between sugars, carbohydrates, fats, and amino-acids.8 However, fats do have a special significance because of their role in the construction of cell membranes and because they include essential PUFA12 which cannot be made in the body. Most are familiar with the notion of protein quality being dependent on the balance of essential and non-essential amino-acids. The same applies to structural lipids, which are built with essential (polyunsaturated) and non-essential fatty acids. In effect, what the nutritional experiments have shown is that the wrong kind of protein can affect body growth and the wrong kind of fat can affect arterial growth. The blood platelet as well as the arterial wall is also influenced by lipid quality.13

I would agree with Dr Yellowlees that COMA14 did not make any recommendations regarding the essential fats, even though Sinclair had discussed their involvement some time ago.15 16 For me, the COMA report was unsatisfactory: their brief was to discuss the relationship between diet and coronary artery disease, but the report did not consider the part played by essential lipid nutrients used in the growth, maintenance, and repair of arteries. This is directly analogous to an attempt to relate diet to marasmus or kwashiorkor without reference to the essential aminoacids. How can one discuss diet and a disease process without discussing the "essential" nutrients involved ? On the other hand, the Joint Working Party's report17 appears to me to give advice that is sensible in the light of present knowledge. Dr Yellowlees may, of course, ignore it and eat his sugary saturated high teas, eggs, and butter in quantity, but that is irrelevant, for students of the subject are more concerned with future generations than our own. He should remember that the old Scot did not live on marbled beef.

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cholesterol level is present in these tribes only when they are living in their rural state. When they change their life style, with all that that entails in variation in personal responsibility and exercise levels as well as other unknown factors, their serum cholesterol rises rapidly. It is not possible, in my opinion, to correlate serum cholesterol directly with dietary intake.

JosE DAY London Ni Day, J, et al, Atherosclerosis, 1976, 23, 357.

Fluid therapy in malaria

SIR,-I read with considerable interest Col A P Hall's excellent review article on the treatment of malaria (7 February, p 323) and would like to make the following comment. I certainly agree with the statement that excessive fluid administration in malaria may lead to pulmonary oedema because of delayed response to water load in some patients.' However, since malarial patients can be either hypovolaemic, hypervolaemic, or normovolaemic, depending on the stage of the disease and the history of prior fluid administration,2 to make a generalisation that total fluid intake should not exceed 1500 ml/day may be too extreme and may be hazardous in dehydrated patients. Hypovolaemia is in fact one among the mechanisms responsible for renal failure in malaria.2 In the presence of volume deficit and blood hyperviscosity, adequate hydration in an attempt to improve haemodynamics is desirable. In this instance 1500 ml of fluid, as suggested in the article, may be too small. In my experience a higher amount of fluid of the order of 3000 ml/day can be safely given to who do not appear clinically MICHAEL CRAWFORD malarial patients overhydrated, with a small dose of frusemide Department of Biochemistry, administered intravenously at intervals. Nuffield Institute of Comparative Medicine, Zoological Society of London, Diuresis is assured, fluid overload can be London NW1 avoided, and renal function is not compromised. Salt and water administration and 'Crawford, M A, Lancet, 1968, 1, 1329. 2Crawford, M A, et al, International Journal of Bio- frusemide therapy are known to offer protecchemistry, 1970, 1, 295. 'Crawford, M A, Gale, M M, and Woodford, M H, tion against renal failure,3 which is not International Journal of Biochemistry, 1970, 1, 654. uncommon in malaria in our unit. 4Crawford, M A, in Proceedings of the Third World Conference on Animal Production, ed R L Reid, p 21 Sydney, University Press, 1975. 6World Medicine, 9 September, 1970, p 21. ' Crawford, M A, and Crawford, S M, What We Eat Today. London, Spearman, 1972. 7Crawford, M A, Lancet, 1, 1419. Houtsmuller, U M T, in Dietary Lipids and Postnatal Development, ed C Galli et al, p 145. New York, Raven Press, 1973. 9 Chapman, D, in Lipids, Malnutrition and the Developing Brain, ed K Elliot and J Knight, p 31. Amsterdam, Associated Scientific Publishers, 1972. "Ledger, H P, in Symposia of the Zoological Society of London No 21. New York and London, Academic Press, 1968. Crawford, M A, Crawford, S M, and Berg Hansen, I, Biochemical Journal, 1971, 122, liP. 2 Crawford, M A, and Sinclair, A J, in Lipids, Malnutrition and the Developing Brain, ed K Elliot and J Knight, p 267. Amsterdam, Associated Scientific Publishers, 1972. 13 The Role of Fats in Human Nutrition, ed A J Vergroesen. New York and London, Academic Press, 1975. '4 Department of Health and Social Security, Diet and Coronary Heart Disease. London, HMSO, 1974. 5 Sinclair, H M, in Symposia of the Zoological Society of London No 21, p 275. New York and London, Academic Press, 1968. " Sinclair, H M, in Lipid Pharmacology, ed R Paoletti p 237. New York, Academic Press, 1964. 17Joint Working Party, Journal of the Royal College of Physicians of London, 1976, 10, 213.

SIR,-Dr W W Yellowlees (29 May, p 1340) refers to the high intake of cholesterol in the Above: Moses' or hunter-gatherers' or early UK Masai and Samburu and their apparent nonfrom 1970s UK supermarket development of arteriosclerotic disease. My meat. Beliow: for comparison. From Crawford and Crawford.6 recent work' shows that in fact their low serum

VISITH SITPRIJA Department of Medicine, Chulalongkorn Hospital Medical School, Bangkok, Thailand 2 3

Miller, L H, et al, Annals of Tropical Medicine and Parasitology, 1967, 61, 265. Sitprija, V, et al, Nephron, in press. Montoreano, R, et al, Postgraduate Medical Journal, 1971, 47, April suppl, p 7.

Unexplained hepatitis following halothane SIR,-I read with interest the excellent article by Dr B Walton and others on unexplained hepatitis following halothane (UHFH) (15 May, p 1171). Like most clinical anaesthetists, over the years I have followed the halothane and hepatitis controversy with interest. I have always felt that the "sensitivity reaction to halothane" hypothesis as a cause of hepatitis is not based on very firm ground because of the many hundreds of thousands of halothane anaesthetics administered compared with the low incidence of UHFH and the fact that in general anaesthetic practice it is virtually impossible to give a halothane-free anaesthetic because of the impossibility of finding a

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19 JUNE 1976

halothane-free anaesthetic machine. As sensitivity reactions can follow very small subsequent doses of a sensitising antigen, then it would be likely that even if all second and subsequent anaesthetics were administered without added halothane there would be a greater number of instances of UHFH than seem to occur. I have always wondered whether some other factor might be involved in the production of UHFH. Some years ago two isolated and wellseparated instances of hepatitis following repeated halothane anaesthesia occurred in a hospital which I used to attend. I was not the anaesthetist concerned so am unable to go into detail, but in a subsequent general discussion with the operating theatre technician who was present when both the relevant anaesthetics were given I learnt that in the first instance there had been an episode of hypoxia with frank cyanosis during induction of anaesthesia because of difficulty with endotracheal intubation, and that there might have been some minor hypoxia in the second instance. I have often wondered whether ignored or undetected minor episodes of hypoxia during the course of halothane anaesthesia might be the trigger factor in the production of UHFH. It is interesting that Dr Walton and his colleagues record a higher incidence of UHFH in obese patients; as all anaesthetists are aware, in a spontaneously breathing obese patient (especially, for instance, when in the lithotomy position) minor degrees of underventilation can occur which could possibly cause hypoxia in the liver. I should like to suggest that in any instance of UHFH following repeated halothane anaesthesia, or of fever, prolonged nausea, or anorexia following a primary halothane anaesthetic, it might be rewarding to look closely for any major or minor degrees of hypoxia which might have occurred during the course of the anaesthetic. W K SLACK Whipps Cross Hospital, London Ell

Five separate malignancies in one patient SIR,-Dr M J Ostrowski (27 December 1975, p 736) recently reported a case of five separate malignancies in one patient, there having been only one other similar recorded case.' I should like briefly to add one further case. A 37-year-old man presented in 1965 with anaemia and vague abdominal pain. After investigation laparotomy revealed an annular carcinoma of the fourth part of the duodenum and a separate jejunal carcinoma 50 cm distally. "Curative" resection was performed. In 1970 he was investigated for painless haematuria and a transitional cell carcinoma of the right renal pelvis was found, for which nephroureterectomy was performed. Twice in 1972 papillary bladder recurrences were fulgurated. In 1973 investigation for lower abdominal pain associated with constipation resulted in a left hemicolectomy for carcinoma of the splenic flexure of the colon. During routine follow-up in November 1975 painless jaundice was noted. At exploratory laparotomy following investigation an inoperable carcinoma of the head of the pancreas was demonstrated. The para-aortic nodes, liver, and entire length of small and large bowel were normal. The patient died on the sixth postoperative day and the operative diagnosis was histologically confirmed at necropsy. There was no recurrence of the four other tumours.

large number of numerical features which vary with time. For patient management it is important to know the exact dose of drugs prescribed, numerical biochemical results, and the blood pressure readings. These continuous variables cannot be easily stored using feature cards, nor can specific information on risk factors, diagnoses, and other features of clinical importance be made available to the clinician at every visit without a computerheld system. The computer system is also the mechanism for a broadly based research effort into the treatment of hypertension. The analysis of large amounts of numerical research informaI should like to thank Mr R P M Miles, St tion requires a computer in order to eliminate Richard's Hospital, Chichester, for permission to extensive clerical and "calculating" effort. Only a computer system allows both our describe this case. managemrient and research objectives to be fully PETER JONES achieved. Surgical Unit, C J BULPITT St James's Hospital,

and Gates2 and later reiterated by Moertel.1 This patient therefore developed separate carcinomas of the duodenum, jejunum, urothelium, colon, and pancreas. There was no family history of malignancy and environmental history was unexceptional. At no time did the patient have radiotherapy. Primary carcinomas of the duodenum and small bowel are rare in themselves, together accounting for approximately 300 of all gastrointestinal malignant lesions.3 I can find no previous record of duodenal and jejunal carcinomas occuring in the same patient. It is worth noting that with single jejunal tumours the five-year survival is only 15o0.4

London SW12

Moertel, C G, Recent Results in Cancer Research, vol 7. New York, Springer, 1966. Warren, S, and Gates, 0, American3ournal of Cancer, 1932, 16, 1358. 3 Peterson, H C, and Morrisey, W J, Journal of the Iowa Medical Society, 1970, 60, 696. 4 Colcock, B P, and Adamson, N E, Suirgical Clinics of North America, 1959, 39, 737. 2

Hazards of monocomponent insulins SIR,-Dr Stephen Holt (1 May, p 1075) reports the case of an insulin-dependent diabetic who, on switching from standard insulin to monocomponent insulin, initially required a 400o reduction in dose, then after a four-month interval required another reduction in dose of 23o0.

It is well recognised that in many instances when a change to monocomponent insulin from a standard preparation is made the daily insulin requirement falls, but Dr Holt has presented no evidence to prove that the reduction in insulin dose needed by his patient after she had been using monocomponent insulin for four months was in any way related to the use of that form of insulin preparation. I could instance the case of a 48-year-old housewife, an insulin-dependent diabetic for 16 years, whose daily dose of insulin zinc suspension fell rapidly from 80 units to 36 units for no apparent reason. The occasional dramatic change in required dose of insulin is not necessarily due to a change in the type of insulin given, and frequent clinical attendances are no more obligatory for the diabetic on monocomponent insulin than for any other insulin-dependent diabetic.

COLIN M KESSON Department of General Medicine, Royal Infirmary,

Glasgow

Computer-held medical records

SIR,-Drs R McG Harden and K A Harden (17 April, p 961) make the important point that computers may be used quite inappropriately for solving a problem which could be solved more cheaply in other ways. Punched cards, whether they be organised to hold individual records or individual features, are an excellent method of storing a limited amount of data in a fixed structure. The computer-held record system which we Each tumour fulfiled the criteria of separate primary malignancies described by Warren are using (20 March, p 677), however, stores a

Department of Medical Statistics and Epidemiology, London School of Hygiene and Tropical Medicine London WC1

L J BEILIN Department of the Regius Professor of Medicine, Radcliffe Infirmary, Oxford

E C COLES SANDRA TURNER Division of Computing and Statistics, MRC Clinical Research Centre, Harrow, Middx

C T DOLLERY Department of Clinical Pharmacology, Royal Postgraduate Medical School, London W12

BRIAN JOHNSON A D MUNRO-FAURE Department of Renal Medicine, King's College Hospital, London SE5

Incidence of dermographism SIR,-In his classic investigations of the human skin Lewis' reported that in response to a single firm stroke on the skin 25%/' of the 84 individuals tested exhibited "some swelling" and 5%" exhibited a "definite weal." As part of a larger investigation2 I had the opportunity to test 104 students and hospital workers (31 male, 73 female, aged 18-58 (mean 29-7) years) for dermographism. The skin on the volar surface of each forearm was given one firm stroke with a wooden tongue depressor. Dermographism was considered to have been observed if a weal developed along the line of the stroke within three minutes. Only one woman aged 23 showed the dermographic response; one other woman aged 19, showed the flare reaction-that is, inflammation beyond the boundary of the line of the stroke but without weal formation. The woman with the flare reaction had a lengthy history of skin allergies, but the girl with the dermographic response reported no history of skin ailments. Since there was only one case of dermographism (0-96%, of the sample) the present data differ from those of Lewis. This difference may be due to any one of the following: (a) Lewis may have administered a firmer stroke to the skin; (b) he may have had a larger proportion of individuals with skin problems in his sample (44 (42%) of the present sample reported having had a skin ailment professionally diagnosed or treated); or (c) his criteria for "swelling" may have been less stringent than mine. These data, along with those of

Letter: Unexplained hepatitis following halothane.

1532 Prevention of coronary heart disease SIR,-Surgeon Captain T L Cleave and Dr W W Yellowlees (29 May, p 1340) both remain unaware of, or choose t...
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