694 which it constitutes 8% of total calories,? yet are vital for the integrity of the developing arterial wall and later for its maintenance and repair. There are also differences in minerals, vitamins, and trace elements. The Western baby is usually bottle-fed with an unnatural substitute of radically different composition to which sugar or salt is often added to maternal taste and the mixture given in excess. Weaning is then carried out, all too early, onto a modern atherogenic diet, high in saturated fat, cholesterol and refined carbohydrate and deficient in polyunsaturated fat. Full-fat dairy produce is given in excess and also fatty meat and meat products, together with fats and oils which have been hydrogenated by the food industry to change their composition from being high in polyunsaturates to high in saturates. Processing of vegetable oils and their use in many convenience foods contributes to excess, deficiencies, and imbalance of essential nutrients. The links between food, plasma-lipids, atherosclerosis, and coronary disease are strong. Your contributor is not correct in his supposition that "the chances are that even the high serumcholesterol of the atheromatous individual is unrelated to that in the plaque". Lipid in the plaque is mainly derived from that in the plasma and dietary cholesterol can be traced to that in the food.8 The probability of a causal relationship between bottle feeding and these early pathological changes seems high. Cow’s milk should be avoided for as long as possible whilst infant defences are developing and the tissues are becoming less susceptible to dietary insult. If the mother is unable or unwilling to feed her infant, then particular care should be paid to the alternative, humanised as far as possible and not neglecting the balance of fatty acids. This is rarely done in realistic terms. It seems likely that the answer to the coronary problem starts in childhood, with breast feeding followed by appropriate weaning, and infant nutrition based on correction of the radical changes man has made in the food he eats in recent years. Meanwhile, surely consideration should be given to a project which should be feasible and might well provide invaluable information ? If an accurate record of infant and early childhood feeding were made by the cooperation of maternity ward staff, midwives, health visitors, and family doctors in consultation with paediatricians and if the information were centrally stored, pathologists would sometimes have the opportunity to compare the state of the coronary arteries with early nutrition. Edinburgh University, 21 Buccleuch Place, Edinburgh EH8 9L9

R. W. D. TURNER

CLONIDINE OVERDOSE

SIR,-A 48-year-old hypertensive male was admitted to the U.S.A.F. Medical Center, Keesler 3 h after ingesting an estimated twenty-four 0.2 mg clonidine hydrochloride (’Catapres’) tablets and an undetermined amount of alcohol. The patient’s blood-pressure had been controlled with two thiazide-triamterene (’Dyazide’) capsules daily, frusemide (’Lasix’) 40 mg every other day, and clonidine 0-8 mg three times daily for approximately 6 months. On admission he was alert but complained of dizziness on standing. Supine bloodpressure was 110/78 mm Hg with pulse 78/min. On standing the blood-pressure fell to 50/30 mm Hg with pulse increasing to

98/min.

patient was given maintenance intravenous fluids, and he slept much of the first 24 h but was easily awakened. There was a variable orthostatic drop in the blood-pressure, systolic greater than diastolic, and a relative bradycardia during the first 24 h. The blood-pressure returned to pre-admission levels 1972, 1, 49.

standing blood-pressure and pulse after clonidine overdose.

the 13th hour after ingestion. On the second hospital day he was given half his usual dose of clonidine. He did not exhibit a hypertensive rebound, and he was discharged on the third hospital day with no untoward effects. Plasma samples were assayed for clonidine hydrochloride by Dr D. Davies, Hammersmith Hospital, London, using gaschromatography/mass-spectrometry. Plasma concentrations were 6.0, 5.25, and 4.9 ng/ml at 4, 6, and 8 h after ingestion. Reported average peak plasma levels 90 min after a single 03 mg dose has been 1.02+0.52ng/mI.1 The dose of clonidine hydrochloride ingested by this patient is the largest single dose

by

reported. U.S.A.F. Medical Center, Keesler Air Force Base, Mississipi, U.S.A.

Keesler,

*Present address: Renal Division, Department of School of Medicine, Winston-Salem, North Carolina

MICHAEL A. MOORE* PAUL PHILLIPI Medicine, Bowman 27103, U.S.A.

Gray

STARTING DIGOXIN

SIR,-When the new specification for digoxin tablets (not less than 75% dissolution in one hour) was introduced in October, 1975, the need for reassessment of dose was stressed. The figure summarises recent experience in the general medical department of a district hospital2 and the renal unit of a teaching hospital,3 using ’Lanoxin’ tablets (Wellcome Medical Division) manufactured in the U.K. It is intended as a guide to the initial choice of dose. Subsequent alteration may be required to achieve the maximum therapeutic effect or avoid symptoms of toxicity. The standard dose is the mean dose required by the general medical patients to achieve therapeutic serum concentrations. Previous studies 4have shown that little of the variation in requirements in patient groups with normal or slightly impaired renal function can be explained by patient variables. ReducC. T., Davies, D. S., Draffan, G. H., Dargie, H. J., Dean, C R. Reid, J. L., Clare, R. A., Murray, S. Clin.Pharmac. Ther. 1976, 19, 11 2. Dobbs, S. M., Rodgers, E. M., Parkes, J., Kenyon, W. L., unpublished obser-

1.

The

8 Connor, W. E., Connor, S. L. Prev. Med.

Serial

Dollery,

vations. 3. Dobbs, S. M., Mawer, G. E., Rodgers, E. M., Woodcock, B. G., Lucas, S B.Br. J.clin.Pharmac. 1976, 3, 231. 4. Peck, C. G., Sheiner, L. B., Martin, C. M., Combs, D. T., Melmon, K L N.Engl. J.Med. 1973, 289, 441. 5. Wagner, J. G., Yates, J. D., Willis, P. W., Sakmar, E., Stoll, R G Clin. Pharmac. Ther. 1974, 15, 291.