822 POSSIBLE ROLE FOR CHLORPROMAZINE IN PROTECTION AGAINST MYOCARDIAL INFARCTION
SIR,-There is increasing evidence, recently summarised,lI that the sudden
unpredictable event responsible for initiating high proportion of myocardial infarcts is the fissuring of an atheromatous plaque in the supplying artery. The associated haemorrhage into the arterial wall induces aggregation of platelets as a thrombus, just as arterial haemorrhages elsewhere induce platelet aggregation as "hxmostatic plugs." Crucial questions are, therefore, how arterial haemorrhages cause platelet aggregation and how aggregation may be prevented or reversed in coronary arteries. An explanation recently proposed’·2 is that the process depends mainly on the activation of platelets by A.D.P. coming from the red blood-cells which are subjected to excessive haemodynamic stress at the a
site of haemorrhage. Some time ago I had the idea that drugs capable of counteracting hxmolysis3 might diminish this activating effect of red cells on platelets and so inhibit their aggregation as thrombi. Experimental evidence for this idea came with the demonstration4 that chlorpromazine added to anticoagulated human blood in concentrations which in vitro diminish hypotonic haemolysis, but have no direct effect on platelet aggregation,5 prolong the bleeding-time from small holes in artificial vessels where extravasation is terminated, as in vivo, by aggregated platelets. Experiments by A. Wehmeier and myself (unpublished) support the conclusion that this effect is accounted for by the antihxmolytic action of chlorpromazine. This has led to the suggestion’’’* that other drugs possessing this effect of chlorpromazine may diminish the incidence of arterial, particularly of coronary, thrombosis when it is induced by conditions of abnormal stress on the red cells, such as through haemorrhage into atheromatous lesions. Evidence for or against this proposition could perhaps be obtained by comparing the incidence of acute coronary occlusions in populations on long-term treatment with chlorpromazine (or other drugs acting in this respect like chlorpromazine) with the incidence in control populations not on such drugs. The only conceivably relevant evidence of which I have been made aware up to now (through the courtesy of Dr J. A. Baldwin, director of the Oxford University Unit of Clinical Epidemiology) is an investigation of mortality in Norwegian psychiatric hospitals during the period 1950 to 1962.6 This concluded that mortality from circulatory disease, predominantly "coronary disease" and "infarction", was higher in the mental-hospital population than in the general population, although the excess was not as much as that from most other causes. Within the patient population, the excess mortality from coronary disease and infarction was less for schizophrenics than for all other psychoses. Furthermore, the excess mortality from circulatory disease diminished strikingly after 1957, particularly when compared with the period 1926-41, because the mortality did not rise to the same extent in the hospital as in the general population. These conclusions, if confirmed, are of course open to different interpretations. Epidemiological considerations apart, chlorpromazine has many effects in the body, and also a large number of metabolites. Furthermore, the concentration of chlorpromazine in patients’ plasma is one to two orders of magnitude lower than that required to prolong the ex-vivo bleeding-time described above. Therefore, if patients’ blood were used for determining this bleeding-time, a prolongation 1
Born, G. V. R. Plenary lecture
to
the VIIIth World
Congress
of Cardiology,
Tokyo. Amsterdam (in the press). in Blood Cells and Vessel Walls: functional interactions (Ciba Fndn Symp. no. 71). Amsterdam (in the press). 3. Seeman, P Pharmac. Rev. 1972, 24, 583. 4. Born, G. V R. Bergquist, D., Arfors, K.-E. Nature. 1976, 259, 233. 5 Mills, D. C. B., Roberts, G. C. K. ibid. 1967, 213, 35 6. Odegard, O. Acta genet , Basel, 1967, 17, 137. 7. Mackay, A V. P , Healey, A. F., Baker, J. Br. J. clin. pharmac. 1974, 1, 425.
2.
if the drug or a similarly active metaconcentrated in red cell membranes. On the other hand, it has been observed8 that single clinical doses (5-20 mg)11 of chlorpromazine injected intramuscularly into apparently healthy volunteers caused the Ivy bleeding-time to be signifi-
might
be
bolite
were
expected only
cantly prolonged. Our experimental observations with chlorpromazine make It attractive to suggest that the general introduction of this drug for the control of schizophrenic inpatients from about 1955 onwards accounts for their relative protection against cardiac mortality at a time when it was increasing rapidly in Norway and elsewhere, including Britain. It would be interesting to learn of other information which may support or, just as important, invalidate this line of thought. It may be worthwhile to investigate appropriate populations from this point of view. Department of Pharmacology, King’s College, University of London, London WC2R 2LS
G. V. R. BORN
COMPUTERISED TOMOGRAPHY AND SUBDURAL HÆMATOMAS
S!R,—Mr Galbraith and Mr Teasdale (March 3, p. 504). out that acute and chronic subdural hasmadiffer in clinical features, surgical approach, and prognosis. They also state that in my letter of Jan. 13 (p. 110) I failed to make this distinction. However, that letter was concerned with acute as well as chronic subdural hsematomas. If only acute subdural hsematomas are considered, the possibility of false-negatives in c.T. scanning still remains. An acute subdural haematoma may present as an isodense lesion if the extravasated blood has low haemoglobin concentration’ or if it arises from rebleeding into a more chronic lesion.2 Recurrent bleeding and anxmia are common among chronic alcoholic patients, .3 a group particularly prone to subdural hxmorrhage That isodense lesions occur in acute cases is corroborated by the Glasgow workers’ own report of such lesions in four of their fifty patients with acute traumatic intracranial bleeding.’ The lesions were unilateral, and thus easily diagnosed by the concomitant ventricular distortion, but had they been bilateral they could have been missed altogether. Bilateral collections are not uncommon in cases of acute subdural haemorrhage. Furthermore, Galbraith et al. selected as controls cases of trauma with a negative c.T. scan and a diagnosis of "diffuse cerebral damage". That all the cases of subdural bleeding had been excluded from their control group can only be accepted by first accepting that false-negatives never occur on c.T. scan-
correctly point tomas
ning. The diagnostic reliability of c.T. scanning in cases of acute subdural hsematoma is high. The reports so far published, however, do not support Galbraith and Teasdale’s view that there are no false-negatives. Neurology Service, Medical Center,
Portland, Oregon 97201, U.S.A.
LUIS GARCIA-BUÑUEL
SHOULD THE LAX SET THE PACE?
SiR,—Iwas most interested in Professor Schou’s letter (March 31, p. 730) dealing with the problems of conference
proceedings and multiauthor books. I think that these are two separate problems-whilst it is clearly practical to ask contributors to congresses to deliver their papers by a set date or run the risk of their papers being excluded, this is hardly prac-
Born, G. V. R.
8.
Zahavi, J , Schwartz, G. Lancet, 1978, ii, 164.
1. New, P. F J., Aronow, S. Radiology, 1976, 121, 635. 2. French, B. N., Dublin, A. B. Surg Neurol. 1977, 7, 171. 3. Merrit, H. H. A Textbook of Neurology; p. 329. Philadelphia, 1973. 4. Galbraith, S., Teasdale, G., Blaiklock, C. Br. Med. J. 1976, ii, 1371
823
ticable for
a
multiauthor book
dealing
with
a
particular
sub-
ject comprehensively.
Although there is no certain way to make sure that multiauthor books are published without severe problems, I have found that there are two golden rules which help a great deal. The first is for the volume editor to brief, in detail, all his contributors, and to give details of his briefs to all other authors so that all contributors have a complete picture of the entire book. The second rule is an elementary one-namely, to chase authors regularly and persistently, but, most importantly, to do so well in advance of deadlines, thereby identifying problems before they become acute. & Hall Ltd, 11 New Fetter Lane, London EC4P 4EE
Chapman
BARRY SHURLOCK
BREAST-FED BABIES WHO FAIL TO THRIVE
SIR,-Dr Davies (March 10,
p. 541) suggests more frequent for failure to thrive at the breast. Both Salariya Harvey2 have lately proposed that babies should routinely be fed much more often than is usually advised, but we have known for a long time that the milk supply can be increased by more frequent feeding though the mechanism is unclear.3 The usual maternity hospital regimen of 3-5 hourly feeding, with a limited time at each breast, must, from consideration of basic physiological principles, lead to an insufficient milk supply in many women. Insufficiency of milk4 is a numerically enormous problem and is by far the most common reason for mothers to stop breast-feeding before they want to. That few breast-fed babies are admitted to hospital starving only underlines the alacrity with which community health workers and mothers put babies on to complementary feeds of cows’ milk formulae. Why not start all mothers off in hospital on a feeding pattern conducive to success? Mothers are only too keen to feed their babies on an unrestricted basis if they are told this is likely to lead to successful breast-feeding for as long as they want. Nurses say that their work load is less on wards with unrestricted feeding. The idea that 15-20 min is ample time for a feed has no scientific backing, except for bottle-fed babies. My personal experience suggests that milk production depends upon the total length of time for which the nipple skin is stimulated by sucking, which can be altered by the length of feeds as well as their number. One piece of researchs backs this up, but more work needs to be done. This is not to say that there is not a small minority of babies who can thrive on six feeds a day of 10 min a side. If a baby is underfed, why not give him the chance of stimulating his mother’s milk supply by letting him sleep in her bed, so that her warmth, smell, sound, and touch can encourage him to wake for feeds? The British custom of putting babies in their own cots in their own rooms may reduce the number of feeds a baby asks for during the night but it could also reduce the mother’s milk supply. Frequent feeding together with longer feeds takes 2 or 3 days to increase the milk supply, and mothers should be warned of this delay so that they do not immediately feel a failure when one day’s increased suckling-time produces no change in the amount of milk.
breast-feeds
as
treatment et al.1 and
20
Vandyke Close, Redhill, Surrey RH1 2DS 1 2 3
University of Cambridge, School of Clinical Medicine, Addenbrooke’s Hospital, Hills Road, Cambridge CB2
2QQ
MARGARET
J. WHICHELOW
CADMIUM IN SHIPHAM
SIR,-In your March 10 issue Dr Harvey and his collaboramake the following comment on their measurements, with non-invasive system of in-vivo neutron-activation analysis, of liver and kidney cadmium among people in the village of Shipham, the site of former zinc-ore mining: tors a
"Although the liver-cadmium concentrations found in these heavily exposed people is about five times that of controls-which some commentators on the television programme on Feb. 22 found ’very alarming’-they may be compared with the very much higher values of up to
260 p.p.m. which
we
have found in studies
on over
six hundred in-
dustrially exposed workers in Britain and Belgium. Since most of these men are fit and healthy and without any signs of cadmium toxicity we believe that our pilot study at Shipham may be interpreted as being broadly reassuring rather than alarming." Thames Television asked our department to carry out ceranalyses of cadmium in blood and &bgr;2-microglobulin in urine, and I was invited to comment on Harvey’s data. Provided the data are correct-and there are no reasons to believe they are not-they are worrying. Harvey et al. found values in the liver of up to 28 p.p.m. and several values of about 20 p.p.m. This would correspond to levels in kidney cortex of at least 200-300 p.p.m. wet weight. The World Health Organisation in its evaluation of cadmium has stated that "the critical level of cadmium in the renal cortex for the appearance of tubular proteinuria was between 100 and 300 mg/kg wet weight and that the most likely estimate was about 200 mg/kg tain
wet
weight."5I
The word "critical" means that a level has been reached where the first signs of an adverse effect may occur among sen-
PENNY STANWAY
Salariya, E. M., and others. Lancet, 1978, ii, 1141. Harvey, D. Mod. Med. Oct. 1978, p. 87 Hall, D.M.B., Kay, G. Br. med. J 1977,i, 776.
4 Infant Feeding 1975: attitudes and practice in Stationery Office, 1978. 5 Hall,B Lancet, 1975, i, 779. 6 Egli, G. E., and others. Pediatrics, 1961, 27, 314.
SIR,-Dr Davies’ article will inevitably raise concern about the risk of undernourishment in breast-fed babies and about the problem most frequently encountered by lactating women in the U.K.-namely, insufficient milk. Whilst, as Davies points out, this can often be prevented by encouraging the mothers to feed frequently in the early days to establish lactation, this policy does not always correct a milk supply that fails after a few weeks. An alternative and effective remedy is to encourage the mothers to eat more and eat frequently. In a study of 258 newly delivered mothers in Cambridge who all began by breast-feeding, one group of 106 mothers was encouraged to eat much more than normal to maintain their milk supply whereas the other (control) group of 152 mothers was given no dietary advice. By three months post partum only about half as many mothers in the "advised" (eating heartily) group had weaned their babies due to insufficient milk compared with the number in the control group.I,2 The only two babies who were gaining very little weight-on average 84 g and 74 g per week during the first three months of life, and apparently content -were both breast fed and in the control group. Whereas it is often possible to increase a failing milk supply by encouraging the mother to eat much more,3 prevention is better than cure, and by ensuring that mothers are aware of their extra dietary energy requirements-500 kcal/day is the current recommendation4-fewer of them will run short of milk and become demoralised by having a baby who fails to thrive.
England
and Wales. H.M.
1. Whichelow, M. J., King, B. E., Taylor, S Int J. Obes. 1979, 3, 93. 2 Whichelow, M. J., King, B E., Taylor, S. Proc. Nutr. Soc (in the press). 3. Whichelow, M. J. Archs Dis Childh. 1975, 50, 669. 4. D.H.S.S. Recommended Intakes of Nutrients for the United Kingdom. H.M
Stationery Office, 1969. Organisation.
Environmental Health Criteria for summary. EHE/EHC/77 1.
5. World Health
Cadmium,
SIR,-There is increasing evidence, recently summarised,lI that the sudden
unpredictable event responsible for initiating high proportion of myocardial infarcts is the fissuring of an atheromatous plaque in the supplying artery. The associated haemorrhage into the arterial wall induces aggregation of platelets as a thrombus, just as arterial haemorrhages elsewhere induce platelet aggregation as "hxmostatic plugs." Crucial questions are, therefore, how arterial haemorrhages cause platelet aggregation and how aggregation may be prevented or reversed in coronary arteries. An explanation recently proposed’·2 is that the process depends mainly on the activation of platelets by A.D.P. coming from the red blood-cells which are subjected to excessive haemodynamic stress at the a
site of haemorrhage. Some time ago I had the idea that drugs capable of counteracting hxmolysis3 might diminish this activating effect of red cells on platelets and so inhibit their aggregation as thrombi. Experimental evidence for this idea came with the demonstration4 that chlorpromazine added to anticoagulated human blood in concentrations which in vitro diminish hypotonic haemolysis, but have no direct effect on platelet aggregation,5 prolong the bleeding-time from small holes in artificial vessels where extravasation is terminated, as in vivo, by aggregated platelets. Experiments by A. Wehmeier and myself (unpublished) support the conclusion that this effect is accounted for by the antihxmolytic action of chlorpromazine. This has led to the suggestion’’’* that other drugs possessing this effect of chlorpromazine may diminish the incidence of arterial, particularly of coronary, thrombosis when it is induced by conditions of abnormal stress on the red cells, such as through haemorrhage into atheromatous lesions. Evidence for or against this proposition could perhaps be obtained by comparing the incidence of acute coronary occlusions in populations on long-term treatment with chlorpromazine (or other drugs acting in this respect like chlorpromazine) with the incidence in control populations not on such drugs. The only conceivably relevant evidence of which I have been made aware up to now (through the courtesy of Dr J. A. Baldwin, director of the Oxford University Unit of Clinical Epidemiology) is an investigation of mortality in Norwegian psychiatric hospitals during the period 1950 to 1962.6 This concluded that mortality from circulatory disease, predominantly "coronary disease" and "infarction", was higher in the mental-hospital population than in the general population, although the excess was not as much as that from most other causes. Within the patient population, the excess mortality from coronary disease and infarction was less for schizophrenics than for all other psychoses. Furthermore, the excess mortality from circulatory disease diminished strikingly after 1957, particularly when compared with the period 1926-41, because the mortality did not rise to the same extent in the hospital as in the general population. These conclusions, if confirmed, are of course open to different interpretations. Epidemiological considerations apart, chlorpromazine has many effects in the body, and also a large number of metabolites. Furthermore, the concentration of chlorpromazine in patients’ plasma is one to two orders of magnitude lower than that required to prolong the ex-vivo bleeding-time described above. Therefore, if patients’ blood were used for determining this bleeding-time, a prolongation 1
Born, G. V. R. Plenary lecture
to
the VIIIth World
Congress
of Cardiology,
Tokyo. Amsterdam (in the press). in Blood Cells and Vessel Walls: functional interactions (Ciba Fndn Symp. no. 71). Amsterdam (in the press). 3. Seeman, P Pharmac. Rev. 1972, 24, 583. 4. Born, G. V R. Bergquist, D., Arfors, K.-E. Nature. 1976, 259, 233. 5 Mills, D. C. B., Roberts, G. C. K. ibid. 1967, 213, 35 6. Odegard, O. Acta genet , Basel, 1967, 17, 137. 7. Mackay, A V. P , Healey, A. F., Baker, J. Br. J. clin. pharmac. 1974, 1, 425.
2.
if the drug or a similarly active metaconcentrated in red cell membranes. On the other hand, it has been observed8 that single clinical doses (5-20 mg)11 of chlorpromazine injected intramuscularly into apparently healthy volunteers caused the Ivy bleeding-time to be signifi-
might
be
bolite
were
expected only
cantly prolonged. Our experimental observations with chlorpromazine make It attractive to suggest that the general introduction of this drug for the control of schizophrenic inpatients from about 1955 onwards accounts for their relative protection against cardiac mortality at a time when it was increasing rapidly in Norway and elsewhere, including Britain. It would be interesting to learn of other information which may support or, just as important, invalidate this line of thought. It may be worthwhile to investigate appropriate populations from this point of view. Department of Pharmacology, King’s College, University of London, London WC2R 2LS
G. V. R. BORN
COMPUTERISED TOMOGRAPHY AND SUBDURAL HÆMATOMAS
S!R,—Mr Galbraith and Mr Teasdale (March 3, p. 504). out that acute and chronic subdural hasmadiffer in clinical features, surgical approach, and prognosis. They also state that in my letter of Jan. 13 (p. 110) I failed to make this distinction. However, that letter was concerned with acute as well as chronic subdural hsematomas. If only acute subdural hsematomas are considered, the possibility of false-negatives in c.T. scanning still remains. An acute subdural haematoma may present as an isodense lesion if the extravasated blood has low haemoglobin concentration’ or if it arises from rebleeding into a more chronic lesion.2 Recurrent bleeding and anxmia are common among chronic alcoholic patients, .3 a group particularly prone to subdural hxmorrhage That isodense lesions occur in acute cases is corroborated by the Glasgow workers’ own report of such lesions in four of their fifty patients with acute traumatic intracranial bleeding.’ The lesions were unilateral, and thus easily diagnosed by the concomitant ventricular distortion, but had they been bilateral they could have been missed altogether. Bilateral collections are not uncommon in cases of acute subdural haemorrhage. Furthermore, Galbraith et al. selected as controls cases of trauma with a negative c.T. scan and a diagnosis of "diffuse cerebral damage". That all the cases of subdural bleeding had been excluded from their control group can only be accepted by first accepting that false-negatives never occur on c.T. scan-
correctly point tomas
ning. The diagnostic reliability of c.T. scanning in cases of acute subdural hsematoma is high. The reports so far published, however, do not support Galbraith and Teasdale’s view that there are no false-negatives. Neurology Service, Medical Center,
Portland, Oregon 97201, U.S.A.
LUIS GARCIA-BUÑUEL
SHOULD THE LAX SET THE PACE?
SiR,—Iwas most interested in Professor Schou’s letter (March 31, p. 730) dealing with the problems of conference
proceedings and multiauthor books. I think that these are two separate problems-whilst it is clearly practical to ask contributors to congresses to deliver their papers by a set date or run the risk of their papers being excluded, this is hardly prac-
Born, G. V. R.
8.
Zahavi, J , Schwartz, G. Lancet, 1978, ii, 164.
1. New, P. F J., Aronow, S. Radiology, 1976, 121, 635. 2. French, B. N., Dublin, A. B. Surg Neurol. 1977, 7, 171. 3. Merrit, H. H. A Textbook of Neurology; p. 329. Philadelphia, 1973. 4. Galbraith, S., Teasdale, G., Blaiklock, C. Br. Med. J. 1976, ii, 1371
823
ticable for
a
multiauthor book
dealing
with
a
particular
sub-
ject comprehensively.
Although there is no certain way to make sure that multiauthor books are published without severe problems, I have found that there are two golden rules which help a great deal. The first is for the volume editor to brief, in detail, all his contributors, and to give details of his briefs to all other authors so that all contributors have a complete picture of the entire book. The second rule is an elementary one-namely, to chase authors regularly and persistently, but, most importantly, to do so well in advance of deadlines, thereby identifying problems before they become acute. & Hall Ltd, 11 New Fetter Lane, London EC4P 4EE
Chapman
BARRY SHURLOCK
BREAST-FED BABIES WHO FAIL TO THRIVE
SIR,-Dr Davies (March 10,
p. 541) suggests more frequent for failure to thrive at the breast. Both Salariya Harvey2 have lately proposed that babies should routinely be fed much more often than is usually advised, but we have known for a long time that the milk supply can be increased by more frequent feeding though the mechanism is unclear.3 The usual maternity hospital regimen of 3-5 hourly feeding, with a limited time at each breast, must, from consideration of basic physiological principles, lead to an insufficient milk supply in many women. Insufficiency of milk4 is a numerically enormous problem and is by far the most common reason for mothers to stop breast-feeding before they want to. That few breast-fed babies are admitted to hospital starving only underlines the alacrity with which community health workers and mothers put babies on to complementary feeds of cows’ milk formulae. Why not start all mothers off in hospital on a feeding pattern conducive to success? Mothers are only too keen to feed their babies on an unrestricted basis if they are told this is likely to lead to successful breast-feeding for as long as they want. Nurses say that their work load is less on wards with unrestricted feeding. The idea that 15-20 min is ample time for a feed has no scientific backing, except for bottle-fed babies. My personal experience suggests that milk production depends upon the total length of time for which the nipple skin is stimulated by sucking, which can be altered by the length of feeds as well as their number. One piece of researchs backs this up, but more work needs to be done. This is not to say that there is not a small minority of babies who can thrive on six feeds a day of 10 min a side. If a baby is underfed, why not give him the chance of stimulating his mother’s milk supply by letting him sleep in her bed, so that her warmth, smell, sound, and touch can encourage him to wake for feeds? The British custom of putting babies in their own cots in their own rooms may reduce the number of feeds a baby asks for during the night but it could also reduce the mother’s milk supply. Frequent feeding together with longer feeds takes 2 or 3 days to increase the milk supply, and mothers should be warned of this delay so that they do not immediately feel a failure when one day’s increased suckling-time produces no change in the amount of milk.
breast-feeds
as
treatment et al.1 and
20
Vandyke Close, Redhill, Surrey RH1 2DS 1 2 3
University of Cambridge, School of Clinical Medicine, Addenbrooke’s Hospital, Hills Road, Cambridge CB2
2QQ
MARGARET
J. WHICHELOW
CADMIUM IN SHIPHAM
SIR,-In your March 10 issue Dr Harvey and his collaboramake the following comment on their measurements, with non-invasive system of in-vivo neutron-activation analysis, of liver and kidney cadmium among people in the village of Shipham, the site of former zinc-ore mining: tors a
"Although the liver-cadmium concentrations found in these heavily exposed people is about five times that of controls-which some commentators on the television programme on Feb. 22 found ’very alarming’-they may be compared with the very much higher values of up to
260 p.p.m. which
we
have found in studies
on over
six hundred in-
dustrially exposed workers in Britain and Belgium. Since most of these men are fit and healthy and without any signs of cadmium toxicity we believe that our pilot study at Shipham may be interpreted as being broadly reassuring rather than alarming." Thames Television asked our department to carry out ceranalyses of cadmium in blood and &bgr;2-microglobulin in urine, and I was invited to comment on Harvey’s data. Provided the data are correct-and there are no reasons to believe they are not-they are worrying. Harvey et al. found values in the liver of up to 28 p.p.m. and several values of about 20 p.p.m. This would correspond to levels in kidney cortex of at least 200-300 p.p.m. wet weight. The World Health Organisation in its evaluation of cadmium has stated that "the critical level of cadmium in the renal cortex for the appearance of tubular proteinuria was between 100 and 300 mg/kg wet weight and that the most likely estimate was about 200 mg/kg tain
wet
weight."5I
The word "critical" means that a level has been reached where the first signs of an adverse effect may occur among sen-
PENNY STANWAY
Salariya, E. M., and others. Lancet, 1978, ii, 1141. Harvey, D. Mod. Med. Oct. 1978, p. 87 Hall, D.M.B., Kay, G. Br. med. J 1977,i, 776.
4 Infant Feeding 1975: attitudes and practice in Stationery Office, 1978. 5 Hall,B Lancet, 1975, i, 779. 6 Egli, G. E., and others. Pediatrics, 1961, 27, 314.
SIR,-Dr Davies’ article will inevitably raise concern about the risk of undernourishment in breast-fed babies and about the problem most frequently encountered by lactating women in the U.K.-namely, insufficient milk. Whilst, as Davies points out, this can often be prevented by encouraging the mothers to feed frequently in the early days to establish lactation, this policy does not always correct a milk supply that fails after a few weeks. An alternative and effective remedy is to encourage the mothers to eat more and eat frequently. In a study of 258 newly delivered mothers in Cambridge who all began by breast-feeding, one group of 106 mothers was encouraged to eat much more than normal to maintain their milk supply whereas the other (control) group of 152 mothers was given no dietary advice. By three months post partum only about half as many mothers in the "advised" (eating heartily) group had weaned their babies due to insufficient milk compared with the number in the control group.I,2 The only two babies who were gaining very little weight-on average 84 g and 74 g per week during the first three months of life, and apparently content -were both breast fed and in the control group. Whereas it is often possible to increase a failing milk supply by encouraging the mother to eat much more,3 prevention is better than cure, and by ensuring that mothers are aware of their extra dietary energy requirements-500 kcal/day is the current recommendation4-fewer of them will run short of milk and become demoralised by having a baby who fails to thrive.
England
and Wales. H.M.
1. Whichelow, M. J., King, B. E., Taylor, S Int J. Obes. 1979, 3, 93. 2 Whichelow, M. J., King, B E., Taylor, S. Proc. Nutr. Soc (in the press). 3. Whichelow, M. J. Archs Dis Childh. 1975, 50, 669. 4. D.H.S.S. Recommended Intakes of Nutrients for the United Kingdom. H.M
Stationery Office, 1969. Organisation.
Environmental Health Criteria for summary. EHE/EHC/77 1.
5. World Health
Cadmium,
