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DIET AND EXERCISE IN CORONARY HEART-DISEASE
1340 BREAST-FEEDING IN THE THIRD WORLD SIR,-The War on Baby Foods (April 20, p. 719) should really be seen as a campaign to maintain the tradition of breast-feeding. Certainly complex social and economic pressures account for the changing patterns in feeding and and processed milk feeds cannot be simply labelled health, " unhealthy " when in affluent societies the fall in infant mortality over many years has generally accompanied the
swing
to
bottle-feeding.
Professor Jelliffewas one of the first to alert the public to the dangers of undernutrition from artificial feeding. More recently he and others have focused concern on the problem of early obesity from the same cause in Western communities.2,33 However, Muller’s paperto which your editorial refers, has indicated the magnitude of the dangerous trend away from breast-feeding in the Third World, and commercial promotion has not always been blameless. In many countries the practice of breast-feeding is the greatest cultural asset for the nutrition of infants, and all those responsible for child health should be conscious of the situation. Responsible dialogue with the food industries and legislation both have a place (but British experience after the restriction on cigarette advertising has been
disappointing). I believe your analogy between artificial feeding and the is unfortunate. Both may be convenient but dangerous, but feeding is a more fundamental priority. The risk of road accidents may not be small, but the risk for a village child who receives no breast milk is enormous. In their careful longitudinal survey in rural Punjab, Wyon and Gordon concluded that " In the study population did not receive breast milk virtually all infants died who in the first months of life." 5 motor-car
London School of Hygiene and
Tropical Medicine, Keppel Street, London WC1E 7HT.
WILLIAM A. M. CUTTING.
DIET AND EXERCISE IN CORONARY HEART-DISEASE
SIR,-Iam at a loss to understand why some well-known colleagues are propagating by Press and radio advice to
public which is likely to disturb the life habits of many people, but with such slender evidence of likely benefit. A warning letter from Professor Mann6 in your own columns, together with your leading article,’ might have the
led
to more
caution.
(1) The International Society of Cardiology 8 has said in an advisory booklet that " an increased intake of cholesterol and fat is an absolute prerequisite for the experimental production of severe atherosclerosis ". This The lipid-fed animal model is quite unsubstantiated. does indeed get fatty deposits and even lumps in the arteries, but these lesions rarely ulcerate or thrombose. Similar fatty streaks in man may never progress to atheroma.9 Stehbens 10 has produced, by experimental arteriovenous fistulae in sheep with blood-cholesterols of only 73-83 mg., lipid-containing atheromatous plaques 1. Jelliffe, D. B. Food Technol. 1971, 25, 55. 2. Nutr. Rev. 1973, 31, 116. 3. Jelliffe, D. B. Br. med. J. 1973, ii, 546. 4. The Baby Killer. Published by War on Road, London N7 9BE.
Want, 467 Caledonian
5. Wyon, J. B., Gordon, J. E. The Khanna Study; p. 187. Harvard, 1971. 6. Mann, G. V. Lancet, Jan. 12, 1974, p. 63. 7. ibid. April 6, 1974, p. 605. 8. International Society of Cardiology. Myocardial Infarction: How to Prevent: How to Rehabilitate. 1973. 9. Mitchell, J. R. A., Schwartz, C. J. Arterial Disease. Oxford, 1965. 10. Stehbens, W. E. Proc. R. Soc. B 1974, 185, 357.
complicated by thrombosis. The mechanical stresses of these vibrating arteriovenous shunts may be similar to the jet lesions beyond aortic stenosis, coarctations, &c. Nearly forty years ago, it was fashionable to treat severe heartfailure by suppression or ablation of the thyroid. In spite of substantial elevations of blood-cholesterol over many years, these patients did not develop coronary heartdisease. 11Gillam, 1summing up the trials of clofibrate, says they have failed to demonstrate that lowering of cholesterol causes any alteration of prognosis. The report on arteriosclerosis from the National Heart and Lung Institute 13 recommends against any large-scale trials of diet in the prevention of coronary disease. (2) Now that coronary-artery bypass surgery is practised and is preceded by obligatory radio-opaque visualisation of the coronary arteries, a report from the Mayo Clinic 14 on 300 coronary angiograms states that the severity of coronaryartery disease thus precisely delineated is not correlated with the cumulation of alleged risk factors. It now seems to be established that the treatment of moderate and severe hypertension does not reduce noticeably the occurIt is said that over 80% rence of myocardial infarction. of the healthy American adult population have at least one risk factor, so that the chances of getting coronary disease are not pinpointed very clearly, except as a human hazard. (3) Exercise.-The first report by Morris et a1.,15 claiming advantages from active physical work, was based only on a marginal difference of incidence but different mode of onset of the disease in bus drivers and bus conductors. Many careful statistical follow-up reports mentioned by the National Heart Institute 13deny any beneficial effect from exercise. A striking but often forgotten paper by Wallace Yater et al.11 on 866 coronary attacks with 450 necropsies, affecting men between 18 and 39 in the U.S. Armed Forces, showed that 27% of the attacks came on during vigorous physical exercise. Considering the fraction of our time spent in such strenuous activities, this is a striking demonstration that exercise can be an important precipitating factor. Unaccustomed and violent physical exercise, such as cranking a car on a cold morning, was a familiar onset of succeeding infarction in the days of my clinical experience. No doubt those with good coronary arteries will be the better for their exercise, but some, unfortunately unidentifiable, will be exposed to the risk. We have arrived at this dilemma by the unfortunate separation of epidemiology from close clinical analysis of the data. Bronte-Stewart 17 noted a low incidence of death from coronary thrombosis in France, and assumed that olive oil used in cooking had some protective influence. Lenegre 18 pointed out in the same year that this allegedly low death-rate was quite erroneous and that an unusually " high incidence of myocarditis " in France really represented ischasmic heart-disease. In spite of this correction, the error was repeated-e.g., by the Irish Heart Foundation in 1969 19-that France had a very low incidence of coronary disease. It does our profession little credit to continue basing 11.
Blumgart, H. L., Freedberg, A. S., Kurland, 1953, 14, 665. Gillam, P. M. S. Am. Heart J. 1974, 87, 1.
G. S.
Am. J. Med.
12. 13. Arteriosclerosis 1971. Report by National Heart and Lung Institute Task Force. 14. Fuster, V., Connolly, D. C., Frye, R. L., Danilson, M. A., Elveback, L. R., Kurland, L. T. Am. J. Cardiol. 1974, 33, 138. 15. Morris, J. N., Heady, J. A., Raffle, P. A. B., Roberts, C. G., Parks, T. W. Lancet, 1953, ii, 1053, 1111. 16. Yater, W. M., Traum, A. H., Brown, W. C. T., Fitzgerald, R. P., Geisler and Wilcox, B. B. Am. Heart J. 1948, 36, 334. 17. Bronte-Stewart, B. Br. med. Bull. 1958, 14, 243. 18. Lenègre, J. Revue Pract. Paris, 1958, 8, 1723. 19. Irish Heart Foundation. Prevention of Coronary Heart Disease, 1969.
1341
rules for advice and management
on
such uncertain and
highly improbable hypotheses. 2 North Square, London NW11 7AA.
JOHN MCMICHAEL.
CORONARY CARE FOR MYOCARDIAL INFARCTION IN DIABETICS
SIR,-We were very interested in the article by Dr Soler and his colleagues (March 23, p. 475) and wonder whether they have noticed that the single classification for all forms of oral therapy conceals wide variations in the results for patients on different forms of oral therapy. Rewritten to show this, table i would appear as follows:
the small number of patients included in their be taken not to read too much sigsurvey, nificance into these figures. It is therefore to be hoped that results from further studies will become available, which may confirm the favourable comparison of metformin treatment with diet.
Owing
to
care must
Rona Laboratories Ltd., Cadwell Lane, Hitchin, Herts SG4 0SF.
C. W. KENWORTHY, Managing Director.
DIABETIC KETOACIDOSIS AND INTRACEREBRAL THROMBOSIS
SIR,-Dr Timperley and colleagues (May 18,
p.
952)
of cerebral intravascular coagulation in diabetic ketoacidosis and suggest that platelet aggregation is likely to be the primary event. It is surprising that, in support of this view, they make no reference to the increased platelet aggregation promoted by longchain fatty-acids and &bgr;-lipoprotein.I-a The serum levels of both these lipid fractions and of others may be increased in poorly controlled or untreated diabetes mellitus,4-6 and a case 6 of disseminated intravascular coagulation in fatal diabetic coma was characterised by hyperlipidsemia. Furthermore, hyperlipidaemia may encourage the formation of thrombi by increasing blood viscosity. Diabetic precoma is generally associated with an increase in blood viscosity, which is only partly explained by a raised hxmatocrit.7 The following case, seen in this hospital, illustrates the effect which severe diabetic hyperlipidmmia with hyperviscosity can have on the brain. A 6-year-old boy, known to be a diabetic for nine months,
outline
some
possible
causes
was admitted with a history of vomiting and abdominal pain for about one day and deepening coma of a few hours’ duration. He was dehydrated and ketotic. Lipmmia retinalis was noted. Blood-glucose was 670 mg., cholesterol 1700 mg., and tri-
Haslem, R. J. Nature, Lond. 1964, 202, 765. Hoak, J. C., Warner, E. D., Connor, W. E. Circulat. Res. 1967, 20, 11. 3. Farbiszewski, R., Skrzydlewski, Z., Worowski, K. Thrombos. Diathes. hœmorrh. 1969, 21, 89. 4. Bagdade, J. D., Porte, D., Bierman, E. L. New Engl. J. Med. 1968, 279, 181. 5. Chance, G. W., Albutt, E. C., Edkins, S. M. Lancet, 1969, i, 1126. 6. Kwaan, H. C., Colwell, J. A., Suwanwela, N. Diabetes, 1972, 21, 108. 7. Skovborg, F., Nielsen, A. V. Bibl. anat., Basel, 1968, 10, 145. 1. 2.
Lipid-rich thrombi in vessels of cerebral white matter, with surrounding haemorrhage ( X 2).
some
glyceride 19,800 mg. per 100 ml. Blood pH was 7-02, Pco2 27 mm. Hg, and standard bicarbonate 7-8 meq. per litre. Plasma osmolarity was 415 mosmol per kg.; owing to the lipsmia, electrolyte values were artificially low with sodium 86 meq., potassium 2-7 meq., and chloride 63 meq. per litre. Haematocrit was 37% and blood relative viscosity measured on a capillary viscometer 20°C was 15. Treatment was started with plasma and 0-5M sodiumchloride infusions, insulin, and sodium bicarbonate. Some improvement was achieved in biochemical state, but six hours after admission signs of a right hemiplegia developed. ’Rheomacrodex’ was given with little effect. At nine hours he had tonic convulsions, and papillcedema was found. Despite further treatment with dexamethasone, 20% mannitol, and then an exchange transfusion, he became decerebrate and died about thirty-six hours after onset of coma. At necropsy, the brain showed some swelling of the left temporoparietal region and a subarachnoid film’ of blood and milky lipid over the frontal poles. There was no thrombosis of the circle of Willis or its major branches, but many intracerebral
at
vessels, especially in the white matter (see accompanying figure), were occluded by a coagulum of blood and lipid; these vessels were commonly surrounded by a ring of interstitial haemorrhage In addition, two large subarachnoid 1-10 mm. in diameter. hoematomas were present, in the right superior temporal sulcus and the left Sylvian fissure; both of these disrupted parts of the related cortex, suggesting that they had arisen from subcortical haemorrhages. Histologically, vessels in the white matter were filled with laminated red thrombus and lipid, and there was extensive acute ischsemic change in neurons of cerebral cortex. Basal ganglia, cerebellum, brainstem, and spinal cord were relatively spared. In this case,
hyperlipidaemia and hyperviscosity were and were clearly the primary cause of the extensive intracerebral thrombosis. Less severe degrees of hyperlipidxmia and hyperviscosity in diabetic coma may also unusually
severe
contribute to focal thrombus formation, as described by Dr Timperley and his colleagues, and should be taken into account in any further investigations of this disease process.
swing
to
bottle-feeding.
Professor Jelliffewas one of the first to alert the public to the dangers of undernutrition from artificial feeding. More recently he and others have focused concern on the problem of early obesity from the same cause in Western communities.2,33 However, Muller’s paperto which your editorial refers, has indicated the magnitude of the dangerous trend away from breast-feeding in the Third World, and commercial promotion has not always been blameless. In many countries the practice of breast-feeding is the greatest cultural asset for the nutrition of infants, and all those responsible for child health should be conscious of the situation. Responsible dialogue with the food industries and legislation both have a place (but British experience after the restriction on cigarette advertising has been
disappointing). I believe your analogy between artificial feeding and the is unfortunate. Both may be convenient but dangerous, but feeding is a more fundamental priority. The risk of road accidents may not be small, but the risk for a village child who receives no breast milk is enormous. In their careful longitudinal survey in rural Punjab, Wyon and Gordon concluded that " In the study population did not receive breast milk virtually all infants died who in the first months of life." 5 motor-car
London School of Hygiene and
Tropical Medicine, Keppel Street, London WC1E 7HT.
WILLIAM A. M. CUTTING.
DIET AND EXERCISE IN CORONARY HEART-DISEASE
SIR,-Iam at a loss to understand why some well-known colleagues are propagating by Press and radio advice to
public which is likely to disturb the life habits of many people, but with such slender evidence of likely benefit. A warning letter from Professor Mann6 in your own columns, together with your leading article,’ might have the
led
to more
caution.
(1) The International Society of Cardiology 8 has said in an advisory booklet that " an increased intake of cholesterol and fat is an absolute prerequisite for the experimental production of severe atherosclerosis ". This The lipid-fed animal model is quite unsubstantiated. does indeed get fatty deposits and even lumps in the arteries, but these lesions rarely ulcerate or thrombose. Similar fatty streaks in man may never progress to atheroma.9 Stehbens 10 has produced, by experimental arteriovenous fistulae in sheep with blood-cholesterols of only 73-83 mg., lipid-containing atheromatous plaques 1. Jelliffe, D. B. Food Technol. 1971, 25, 55. 2. Nutr. Rev. 1973, 31, 116. 3. Jelliffe, D. B. Br. med. J. 1973, ii, 546. 4. The Baby Killer. Published by War on Road, London N7 9BE.
Want, 467 Caledonian
5. Wyon, J. B., Gordon, J. E. The Khanna Study; p. 187. Harvard, 1971. 6. Mann, G. V. Lancet, Jan. 12, 1974, p. 63. 7. ibid. April 6, 1974, p. 605. 8. International Society of Cardiology. Myocardial Infarction: How to Prevent: How to Rehabilitate. 1973. 9. Mitchell, J. R. A., Schwartz, C. J. Arterial Disease. Oxford, 1965. 10. Stehbens, W. E. Proc. R. Soc. B 1974, 185, 357.
complicated by thrombosis. The mechanical stresses of these vibrating arteriovenous shunts may be similar to the jet lesions beyond aortic stenosis, coarctations, &c. Nearly forty years ago, it was fashionable to treat severe heartfailure by suppression or ablation of the thyroid. In spite of substantial elevations of blood-cholesterol over many years, these patients did not develop coronary heartdisease. 11Gillam, 1summing up the trials of clofibrate, says they have failed to demonstrate that lowering of cholesterol causes any alteration of prognosis. The report on arteriosclerosis from the National Heart and Lung Institute 13 recommends against any large-scale trials of diet in the prevention of coronary disease. (2) Now that coronary-artery bypass surgery is practised and is preceded by obligatory radio-opaque visualisation of the coronary arteries, a report from the Mayo Clinic 14 on 300 coronary angiograms states that the severity of coronaryartery disease thus precisely delineated is not correlated with the cumulation of alleged risk factors. It now seems to be established that the treatment of moderate and severe hypertension does not reduce noticeably the occurIt is said that over 80% rence of myocardial infarction. of the healthy American adult population have at least one risk factor, so that the chances of getting coronary disease are not pinpointed very clearly, except as a human hazard. (3) Exercise.-The first report by Morris et a1.,15 claiming advantages from active physical work, was based only on a marginal difference of incidence but different mode of onset of the disease in bus drivers and bus conductors. Many careful statistical follow-up reports mentioned by the National Heart Institute 13deny any beneficial effect from exercise. A striking but often forgotten paper by Wallace Yater et al.11 on 866 coronary attacks with 450 necropsies, affecting men between 18 and 39 in the U.S. Armed Forces, showed that 27% of the attacks came on during vigorous physical exercise. Considering the fraction of our time spent in such strenuous activities, this is a striking demonstration that exercise can be an important precipitating factor. Unaccustomed and violent physical exercise, such as cranking a car on a cold morning, was a familiar onset of succeeding infarction in the days of my clinical experience. No doubt those with good coronary arteries will be the better for their exercise, but some, unfortunately unidentifiable, will be exposed to the risk. We have arrived at this dilemma by the unfortunate separation of epidemiology from close clinical analysis of the data. Bronte-Stewart 17 noted a low incidence of death from coronary thrombosis in France, and assumed that olive oil used in cooking had some protective influence. Lenegre 18 pointed out in the same year that this allegedly low death-rate was quite erroneous and that an unusually " high incidence of myocarditis " in France really represented ischasmic heart-disease. In spite of this correction, the error was repeated-e.g., by the Irish Heart Foundation in 1969 19-that France had a very low incidence of coronary disease. It does our profession little credit to continue basing 11.
Blumgart, H. L., Freedberg, A. S., Kurland, 1953, 14, 665. Gillam, P. M. S. Am. Heart J. 1974, 87, 1.
G. S.
Am. J. Med.
12. 13. Arteriosclerosis 1971. Report by National Heart and Lung Institute Task Force. 14. Fuster, V., Connolly, D. C., Frye, R. L., Danilson, M. A., Elveback, L. R., Kurland, L. T. Am. J. Cardiol. 1974, 33, 138. 15. Morris, J. N., Heady, J. A., Raffle, P. A. B., Roberts, C. G., Parks, T. W. Lancet, 1953, ii, 1053, 1111. 16. Yater, W. M., Traum, A. H., Brown, W. C. T., Fitzgerald, R. P., Geisler and Wilcox, B. B. Am. Heart J. 1948, 36, 334. 17. Bronte-Stewart, B. Br. med. Bull. 1958, 14, 243. 18. Lenègre, J. Revue Pract. Paris, 1958, 8, 1723. 19. Irish Heart Foundation. Prevention of Coronary Heart Disease, 1969.
1341
rules for advice and management
on
such uncertain and
highly improbable hypotheses. 2 North Square, London NW11 7AA.
JOHN MCMICHAEL.
CORONARY CARE FOR MYOCARDIAL INFARCTION IN DIABETICS
SIR,-We were very interested in the article by Dr Soler and his colleagues (March 23, p. 475) and wonder whether they have noticed that the single classification for all forms of oral therapy conceals wide variations in the results for patients on different forms of oral therapy. Rewritten to show this, table i would appear as follows:
the small number of patients included in their be taken not to read too much sigsurvey, nificance into these figures. It is therefore to be hoped that results from further studies will become available, which may confirm the favourable comparison of metformin treatment with diet.
Owing
to
care must
Rona Laboratories Ltd., Cadwell Lane, Hitchin, Herts SG4 0SF.
C. W. KENWORTHY, Managing Director.
DIABETIC KETOACIDOSIS AND INTRACEREBRAL THROMBOSIS
SIR,-Dr Timperley and colleagues (May 18,
p.
952)
of cerebral intravascular coagulation in diabetic ketoacidosis and suggest that platelet aggregation is likely to be the primary event. It is surprising that, in support of this view, they make no reference to the increased platelet aggregation promoted by longchain fatty-acids and &bgr;-lipoprotein.I-a The serum levels of both these lipid fractions and of others may be increased in poorly controlled or untreated diabetes mellitus,4-6 and a case 6 of disseminated intravascular coagulation in fatal diabetic coma was characterised by hyperlipidsemia. Furthermore, hyperlipidaemia may encourage the formation of thrombi by increasing blood viscosity. Diabetic precoma is generally associated with an increase in blood viscosity, which is only partly explained by a raised hxmatocrit.7 The following case, seen in this hospital, illustrates the effect which severe diabetic hyperlipidmmia with hyperviscosity can have on the brain. A 6-year-old boy, known to be a diabetic for nine months,
outline
some
possible
causes
was admitted with a history of vomiting and abdominal pain for about one day and deepening coma of a few hours’ duration. He was dehydrated and ketotic. Lipmmia retinalis was noted. Blood-glucose was 670 mg., cholesterol 1700 mg., and tri-
Haslem, R. J. Nature, Lond. 1964, 202, 765. Hoak, J. C., Warner, E. D., Connor, W. E. Circulat. Res. 1967, 20, 11. 3. Farbiszewski, R., Skrzydlewski, Z., Worowski, K. Thrombos. Diathes. hœmorrh. 1969, 21, 89. 4. Bagdade, J. D., Porte, D., Bierman, E. L. New Engl. J. Med. 1968, 279, 181. 5. Chance, G. W., Albutt, E. C., Edkins, S. M. Lancet, 1969, i, 1126. 6. Kwaan, H. C., Colwell, J. A., Suwanwela, N. Diabetes, 1972, 21, 108. 7. Skovborg, F., Nielsen, A. V. Bibl. anat., Basel, 1968, 10, 145. 1. 2.
Lipid-rich thrombi in vessels of cerebral white matter, with surrounding haemorrhage ( X 2).
some
glyceride 19,800 mg. per 100 ml. Blood pH was 7-02, Pco2 27 mm. Hg, and standard bicarbonate 7-8 meq. per litre. Plasma osmolarity was 415 mosmol per kg.; owing to the lipsmia, electrolyte values were artificially low with sodium 86 meq., potassium 2-7 meq., and chloride 63 meq. per litre. Haematocrit was 37% and blood relative viscosity measured on a capillary viscometer 20°C was 15. Treatment was started with plasma and 0-5M sodiumchloride infusions, insulin, and sodium bicarbonate. Some improvement was achieved in biochemical state, but six hours after admission signs of a right hemiplegia developed. ’Rheomacrodex’ was given with little effect. At nine hours he had tonic convulsions, and papillcedema was found. Despite further treatment with dexamethasone, 20% mannitol, and then an exchange transfusion, he became decerebrate and died about thirty-six hours after onset of coma. At necropsy, the brain showed some swelling of the left temporoparietal region and a subarachnoid film’ of blood and milky lipid over the frontal poles. There was no thrombosis of the circle of Willis or its major branches, but many intracerebral
at
vessels, especially in the white matter (see accompanying figure), were occluded by a coagulum of blood and lipid; these vessels were commonly surrounded by a ring of interstitial haemorrhage In addition, two large subarachnoid 1-10 mm. in diameter. hoematomas were present, in the right superior temporal sulcus and the left Sylvian fissure; both of these disrupted parts of the related cortex, suggesting that they had arisen from subcortical haemorrhages. Histologically, vessels in the white matter were filled with laminated red thrombus and lipid, and there was extensive acute ischsemic change in neurons of cerebral cortex. Basal ganglia, cerebellum, brainstem, and spinal cord were relatively spared. In this case,
hyperlipidaemia and hyperviscosity were and were clearly the primary cause of the extensive intracerebral thrombosis. Less severe degrees of hyperlipidxmia and hyperviscosity in diabetic coma may also unusually
severe
contribute to focal thrombus formation, as described by Dr Timperley and his colleagues, and should be taken into account in any further investigations of this disease process.