- Email: [email protected]
PROLACTIN-LOWERING EFFECT OF GROWTH-HORMONE-RELEASING FACTOR IN CHILDREN WITH GROWTH-HORMONE DEFICIENCY
1088 EGGS AND ISCHAEMIC HEART DISEASE
SIR,-We should not, perhaps, expect Dr McNair, writing from the Eggs Authority, to do anything to discourage people from eating eggs (Sept 17, p 687). Nevertheless, he ought to try to present reliable data. The many working parties which have reviewed the evidence agree that dietary fat and hypercholesterolaemia are causal risk factors in atherosclerosis and that dietary cholesterol does play a significant role. At a recent meeting in Berlin held by the International Atherosclerosis Society in conjunction with the World Health Organisation the clear consensus was that the relation between diet and coronary heart disease (CHD) is beyond serious doubt and warrants vigorous action. As for confining the debate to "informed scientists", this is just what some regard as unethical and we agree the public has a right to know the consensus on this important topic so that they can judge for themselves how they can modify their diet. McNair presents data from the US in a way which suggests that the consumption of eggs and of saturated fat has not fallen in relation to the substantial decline in mortality from CHD over the past fifteen years or so. The most relevant data are those published by the US Department of Commerce. A table shown at the Bethesda2 Conference on the Primary Prevention of Coronary Heart Disease demonstrated that annual egg consumption per head declined steadily from 389 in 1950 to 273 in 1978 (- 29 - 8%) together with a decline in consumption of butter by 54’ 5% and of lard by 84’ 6%. The body synthesises sufficient cholesterol for all its needs, so all dietary cholesterol is surplus to requirements. In the UK average consumption has greatly increased in recent years. If consumption is not excessive, compensation takes place by increased excretion and sometimes depression of synthesis. Failure of homoeostasis, is in cholesterol and reflected overload however, hypercholesterolaemia. Glueck and Connor3have reviewed in detail the data on diet in CHD relationships over twentyyears, in a paper with more than 100 references. Prof J. Stamler has recently indicated that research has provided new data reinforcing previous conclusions. For every 100 mg change in dietary cholesterol there is a corresponding response of 6 mg/dl in serum cholesterol, and such changes can exert a significant influence on CHD risk. The assertion that people in general, including apparently healthy people, need not be concerned about dietary cholesterol and foods high in cholesterol, such as eggs, is not valid. Those attempting to inform the public are described as "misguided crusaders" and confusion is added by bringing in genetic factors. Certainly genetic factors determine response in the individual to a preventive measure, but in populations it is the changes in lifestyle, including dietary ones, which are related to changes in mortality, up or down. There is no cut-off point for hypercholesterolaemia, as McNair suggests; and the figure he presumably had in mind, but did not cite, is purely arbitrary. There are sound reasons why guidelines have been made for whole populations and they do include advice to "eat fewer eggs and more sunflower seeds". Other factors, dietary and non-dietary, are important, and not only in relation to hypercholesterolaemia. Diet is an emotional subject and a sensitive area, best desensitised by open discussion. One cannot escape the fact, however, that almost all working parties have recommended restriction of dietary cholesterol to 300 mg/day or less. Consumption in the UK is 520 mg, and official policy in the UK is out of step with this recommendation. 30% of serum cholesterol comes from dairy products and 25% from meat and meat products, but the highest contribution (35%) comes from eggs, and a medium-sized egg contains 240 mg cholesterol. Consequently one of the simplest ways of effecting a reduction is to bring down average egg consumption from 5 to 3 per week. Across the country this would amount to a reduction from 14 000 million to 9 000 million 1. Lewis B. 2. Stamler J.
Hypothesis into theory. J Roy Soc Med 1978; 71: 809-18. Primary prevention of coronary heart disease: the last 20 years. Am J Cardiol
1981; 47: 722-35. 3. Glueck CJ, Connor WE.
Diet-coronary heart disease relationships reconnoitered. Am J
Clin Nutr 1978; 31: 727-37
year. This is the nub of the matter for the Eggs Authority and well see it has commercial implications, but why should health come second? eggs
a
we can
DENIS BURLEY
Horsham, West Sussex
University of Edinburgh, 56 Buccleuch Street,
RICHARD TURNER
Edinburgh EH8 9LP
PROLACTIN-LOWERING EFFECT OF GROWTH-HORMONE-RELEASING FACTOR IN CHILDREN WITH GROWTH-HORMONE DEFICIENCY
SIR,-Your July 16 issue carried
two
papers
on
the effect of
pancreatic growth-hormone-releasing factor’ (hpGRF-40) on growth-hormone (GH) release in patient with GH deficiency. We can confirm the GH-releasing effect of synthetic hpGRF in children with isolated GH deficiency and have found that the peptide has an inherent prolactin-lowering action in such children. Five children with isolated GH deficiency (four boys, one girl) aged 10-17 years and one boy aged 16 years operated on 1 year previously for a craniopharyngioma were tested with an intravenous dose of 1 g/kg synthetic hpGRF-40 (Bachem, Bubendorf, Switzerland). All the GH-deficient children, whose height was below the third percentile, had had GH replacement therapy or GH human
3°
CHANGES IN PLASMA PROLACTIN IN FIVE PATIENTS WITH GH DEFICIENCY AND IN ONE PATIENT WITH CRANIOPHARYNGIOMA GIVEN
1
tg/kg hpGRF-40 AS AN INTRAVENOUS BOLUS AT TIME ZERO
ND = values lower than the sensmvity of the assay. Normal values in prepubertal children, 8 4± 1’ 5 5 ng/ml (mean±SEM).
*Craniopharyngtoma
and other target gland hormone replacement (craniopharyngioma) withdrawn for at least a week. GH deficiency was assessed using at least two stimulation tests with insulin and levodopa and was labelled "isolated" when pituitary investigations, including evaluation of gonadotropin secretion (LHRH test) and corticotropin secretion (insulin hypoglycaemia), were normal. On the day of the experiment, after an overnight fast, an intravenous forearm cannula was inserted and two basal blood samples were taken 15 min apart. 1 g/kg hpGRF-40, prepared as described by Thorner et al,4 dissolved in 1 ml of normal saline was given intravenously over 30 s. Normal saline alone was given as a control infusion to the same patients in separate experiments few days before or after hpGRF-40. Blood was then sampled every 15 min for 1 h and then every 30 min up to 150 or 180 min. Plasma was collected and stored at - 20° C until assayed for GH and prolactin by radioimmunoassay, with reagents provided by CEA-IRE Sorin (Saluggia) and Biodata (Milan), respectively. All five patients with isolated GH deficiencies showed a definite rise in plasma GH with peaks at 15 min ranging between 6’3and 14-77 ng/ml, whilst no GH rise was elicited in the subject with a craniopharyngioma. In four of the five patients there was at the 1.
Rivier J, Spiess J, Thorner M, Vale W. Characterization of a growth hormone releasing factor from a human pancreatic islet tumor. Nature 1982; 300: 276-78. 2. Borges JLC, Blizzard RM, Gelato M, et al. Effects ofhuman pancreatic tumour growth hormone releasing factor on growth hormone and somatomedin C levels in patients with idiopathic growth-hormone deficiency Lancet 1983; ii: 119-23. 3. Grossman A, Savage MO, Wass JAH, et al. Growth-hormone-releasing factor in growth hormone deficiency: Demonstration of a hypothalamic defect in growth hormone release. Lancet 1983; ii: 137-38 4. Thorner MO, Rivier J, Spiess J, et al. Human pancreatic growth hormone releasing factor selectively stimulates growth-hormone secretion in man. Lancet 1983; i: 24-28
1089 same time a striking lowering of prolactin levels with nadirs at 60-90 min post-infusion (see table). In patients C and E there was a rebound rise at 120 min. In patient D, who had a raised serum prolactin before the experiment, prolactin concentrations were not suppressed after hpGRF; nor were they in the boy with craniopharyngioma. No rise in plasma GH or suppression of prolactin was seen after saline. No serious adverse effects or changes in pulse rate or blood pressure were noted. These data strengthen the view that there,may, in some GHdeficient patients, be an absolute or relative defect in hypothalamic GRF function. They show that hpGRF-40 will usually induce a clear-cut lowering of plasma prolactin. This prolactin effect was not seen in the patient with a craniopharyngioma, who can be thought of as having impairment of the pituitary gland. The prolactinlowering effect of hpGRF seems not to be confined to children with isolated GH deficiency but appears to be present in normal prepubertal children also (unpublished).
University of Cagliari
CARLO PINTOR ROBERTO CORDA ROSA PUGGIONI
Department of Pharmacology, Chemotherapy, and Toxicology, Faculty of Medicine and Surgery, University of Milan, 20129 Milan, Italy
VITTORIO LOCATELLI SILVANO G. CELLA EUGENIO E. MULLER
Department of Paediatrics,
DISEASE SCORING SYSTEM IN INTENSIVE CARE
SIR,-Dr Le Gall and colleagues (Sept 24, p 741) suggested a simplification of APACHE, our prototype severity-of-disease scoring system for severely ill patients.’ We heartily agree with the need for simplification and are already taking steps in this direction.2 We cannot, however, support the simplified acute physiological score (SAPS) proposed by our French colleagues. For a severity-of-disease classification to be proved valid it must consistently and accurately stratify by risk of death acutely ill patients, on the basis of initial physiological data. It must do this for all the diseases that
special care units treat and it must be as independent as possible of therapeutic decisions. Le Gall’s reanalysis of data from our joint US/French study3did not test the performance of SAPS within diseases because data were insufficient. Its validity, therefore, remains uncertain. Because it includes information
on
independent of therapy.44
ventilator support, the SAPS is
not
We are now very close to completing a disease-specific validation of a shortened acute physiology score,using information from a national survey of 6000 intensive care admissions in the United States together with data from New Zealand and Denmark. It will require fifteen or fewer physiological measurements, should be as easy to use as the SAPS, and will not require therapeutic data. Most importantly, we feel certain that our score will stratify by risk more accurately than the SAPS, both for aggregate intensive care 5 populations and for individual diagnoses. The availability of a severity-of-disease classification system applicable to many diagnoses could have important implications for the evaluation of hospital practices worldwide. Such evaluations would be more precise, however, if we could agree on a single system. We suggest that physicians and researchers withhold final judgment until ours and our French colleagues’ work are complete. ICU Research Unit,
George Washington University Medical Center,
Washington, DC 20037, USA
WILLIAM A. KNAUS DOUGLAS P. WAGNER ELIZABETH A. DRAPER JACK E. ZIMMERMAN
RACE, NUTRITION, AND INFANT MORTALITY
IN
SOUTH AFRICA
SIR,-In your account (Aug 20, p 465) of Mr R. J. Fincham’s contribution to an international conference on ethnic health issues, held in Leeds last July, you reported that the South African Department of Health and Welfare had undertaken nutritional surveys in the Eastern Cape because ofa 1979 newspaper report that "One out of every 4 black babies born in Grahamstown last year died before the age of 12 months". The true situation in Grahamstown was not stated. This figure was drawn from only 396 registered Black births in Grahamstown. This city has a Black population of 40 000, and the birth rate of Black people in South Africa is 40 per 1000. The true number of Black births for this city would therefore be about 1600, giving an infant mortality rate of about 62 per 1000 which is only one-quarter of the rate given in your account. Since Grahamstown Hospital serves a population much larger than that of Grahamstown itself, the number of deaths would also have included some infants from outside the city area in instances where city addresses were recorded on admission. This would further tend to inflate the calculated infant mortality rate. This Department undertook the surveys because local authority clinic reports on malnutrition and potential undernutrition (based on routine examinations at clinics and using the Boston standards) did not correspond to newspaper reports. The Department has for many years been subsidising local authority clinics to prevent kwashiorkor. Your account refers to the high incidence of undernutrition in "resettlement" areas. There is only one resettlement area in the Eastern Cape, and this is the only instance where this Department renders a direct health service. Other services are all local authority ones subsidised by the Department. The incidence of undernutrition in this resettlement area is negligible, based on the Boston third percentile. Referring to this community a newspaper reported in 1980 that undernutrition was very common and based its findings on the Department’s own patient clinic cards: it turned out that the reporter based his results on the third decile instead of on the third centile. As to our questioning "the applicability of the United States standards", this was merely a discussion in the original report based on conflicting opinions among world authorities, some of which have appeared in The Lancet. }-3 Fincham was coauthor of the original report on the rural area survey in which this controversy was discussed. It was also categorically stated that these surveys were not intended to compare the situation with other Third World countries but solely to discover the true situation as compared with clinic reports-ie, they were: provide information about the nutritional status of specific population were at risk of malnutrition; (b) to provide an insight into factors which influenced nutritional status; (c) to give some indication of the proportion of these populations making regular use of local authority clinics; (d) to provide a foundation on which the Department could base future health strategies; and to provide feedback, surveillance, coordination with various bodies (State, semi-State, local authorities, welfare organisations, and the private sector), promotion of community involvement, and development is an accepted priority. 4 May I end by citing a WHO report from 1981:4 "The concept of community involvement has emerged as the most important key to success in nutrition programmes and health programmes. This is... the (a)
to
groups who
primary health care as a strategy for health for all. Community involvement is related to many important aspects of strategy development. First and foremost is the need to strengthen the capability of the people themselves in identifying their own problems". basis for the concept of
1 Knaus WA,
Zimmerman JE, Wagner DP, Draper EA, Lawrence DE. APACHE, acute physiology and chronic health evaluation: a physiologically based classification
system. Crit Care Med 1981; 9: 591-97. 2 Knaus WA, Wagner DP, Draper EA. APACHE. Crit Care Med 1983; 11: 316. 3 Knaus WA, Le Gall J-R, Wagner DP, et al. A comparison of intensive care in the USA and France. Lancet 1982; ii: 642-46. 4 Scheffler RM, Knaus WA, Wagner DP, Zimmerman JE. Severity of illness and the relationship between intensive care and survival. Am J Publ Health 1982; 72: 449-54.
5 Knaus WA, Wagner DP, Draper EA. The relationship betwseen severity of illness and outcome. Clin Res 1983; 31: 299 (abstr)
1. Goldstein
H, Tanner JM. Ecological considerations in the creation and the use of child standards. Lancet 1980; i. 582-85. 2. McLaren DS, Read WWC. Classification of nutritional status in early childhood. Lancet 1972, ii: 146-48. 3. Habicht JP, Martorell R, Yardrough C, Maluna RM, Klein RE. Height and weight standards for pre-school children: How relevant are ethnic differences in growth potential? Lancet 1974; i: 611-14. 4. World Health Organisation. The role of the health sector in food and nutrition. Tech Rep Ser WHO 1981; no 667: 11, 32, 33.
growth
SIR,-We should not, perhaps, expect Dr McNair, writing from the Eggs Authority, to do anything to discourage people from eating eggs (Sept 17, p 687). Nevertheless, he ought to try to present reliable data. The many working parties which have reviewed the evidence agree that dietary fat and hypercholesterolaemia are causal risk factors in atherosclerosis and that dietary cholesterol does play a significant role. At a recent meeting in Berlin held by the International Atherosclerosis Society in conjunction with the World Health Organisation the clear consensus was that the relation between diet and coronary heart disease (CHD) is beyond serious doubt and warrants vigorous action. As for confining the debate to "informed scientists", this is just what some regard as unethical and we agree the public has a right to know the consensus on this important topic so that they can judge for themselves how they can modify their diet. McNair presents data from the US in a way which suggests that the consumption of eggs and of saturated fat has not fallen in relation to the substantial decline in mortality from CHD over the past fifteen years or so. The most relevant data are those published by the US Department of Commerce. A table shown at the Bethesda2 Conference on the Primary Prevention of Coronary Heart Disease demonstrated that annual egg consumption per head declined steadily from 389 in 1950 to 273 in 1978 (- 29 - 8%) together with a decline in consumption of butter by 54’ 5% and of lard by 84’ 6%. The body synthesises sufficient cholesterol for all its needs, so all dietary cholesterol is surplus to requirements. In the UK average consumption has greatly increased in recent years. If consumption is not excessive, compensation takes place by increased excretion and sometimes depression of synthesis. Failure of homoeostasis, is in cholesterol and reflected overload however, hypercholesterolaemia. Glueck and Connor3have reviewed in detail the data on diet in CHD relationships over twentyyears, in a paper with more than 100 references. Prof J. Stamler has recently indicated that research has provided new data reinforcing previous conclusions. For every 100 mg change in dietary cholesterol there is a corresponding response of 6 mg/dl in serum cholesterol, and such changes can exert a significant influence on CHD risk. The assertion that people in general, including apparently healthy people, need not be concerned about dietary cholesterol and foods high in cholesterol, such as eggs, is not valid. Those attempting to inform the public are described as "misguided crusaders" and confusion is added by bringing in genetic factors. Certainly genetic factors determine response in the individual to a preventive measure, but in populations it is the changes in lifestyle, including dietary ones, which are related to changes in mortality, up or down. There is no cut-off point for hypercholesterolaemia, as McNair suggests; and the figure he presumably had in mind, but did not cite, is purely arbitrary. There are sound reasons why guidelines have been made for whole populations and they do include advice to "eat fewer eggs and more sunflower seeds". Other factors, dietary and non-dietary, are important, and not only in relation to hypercholesterolaemia. Diet is an emotional subject and a sensitive area, best desensitised by open discussion. One cannot escape the fact, however, that almost all working parties have recommended restriction of dietary cholesterol to 300 mg/day or less. Consumption in the UK is 520 mg, and official policy in the UK is out of step with this recommendation. 30% of serum cholesterol comes from dairy products and 25% from meat and meat products, but the highest contribution (35%) comes from eggs, and a medium-sized egg contains 240 mg cholesterol. Consequently one of the simplest ways of effecting a reduction is to bring down average egg consumption from 5 to 3 per week. Across the country this would amount to a reduction from 14 000 million to 9 000 million 1. Lewis B. 2. Stamler J.
Hypothesis into theory. J Roy Soc Med 1978; 71: 809-18. Primary prevention of coronary heart disease: the last 20 years. Am J Cardiol
1981; 47: 722-35. 3. Glueck CJ, Connor WE.
Diet-coronary heart disease relationships reconnoitered. Am J
Clin Nutr 1978; 31: 727-37
year. This is the nub of the matter for the Eggs Authority and well see it has commercial implications, but why should health come second? eggs
a
we can
DENIS BURLEY
Horsham, West Sussex
University of Edinburgh, 56 Buccleuch Street,
RICHARD TURNER
Edinburgh EH8 9LP
PROLACTIN-LOWERING EFFECT OF GROWTH-HORMONE-RELEASING FACTOR IN CHILDREN WITH GROWTH-HORMONE DEFICIENCY
SIR,-Your July 16 issue carried
two
papers
on
the effect of
pancreatic growth-hormone-releasing factor’ (hpGRF-40) on growth-hormone (GH) release in patient with GH deficiency. We can confirm the GH-releasing effect of synthetic hpGRF in children with isolated GH deficiency and have found that the peptide has an inherent prolactin-lowering action in such children. Five children with isolated GH deficiency (four boys, one girl) aged 10-17 years and one boy aged 16 years operated on 1 year previously for a craniopharyngioma were tested with an intravenous dose of 1 g/kg synthetic hpGRF-40 (Bachem, Bubendorf, Switzerland). All the GH-deficient children, whose height was below the third percentile, had had GH replacement therapy or GH human
3°
CHANGES IN PLASMA PROLACTIN IN FIVE PATIENTS WITH GH DEFICIENCY AND IN ONE PATIENT WITH CRANIOPHARYNGIOMA GIVEN
1
tg/kg hpGRF-40 AS AN INTRAVENOUS BOLUS AT TIME ZERO
ND = values lower than the sensmvity of the assay. Normal values in prepubertal children, 8 4± 1’ 5 5 ng/ml (mean±SEM).
*Craniopharyngtoma
and other target gland hormone replacement (craniopharyngioma) withdrawn for at least a week. GH deficiency was assessed using at least two stimulation tests with insulin and levodopa and was labelled "isolated" when pituitary investigations, including evaluation of gonadotropin secretion (LHRH test) and corticotropin secretion (insulin hypoglycaemia), were normal. On the day of the experiment, after an overnight fast, an intravenous forearm cannula was inserted and two basal blood samples were taken 15 min apart. 1 g/kg hpGRF-40, prepared as described by Thorner et al,4 dissolved in 1 ml of normal saline was given intravenously over 30 s. Normal saline alone was given as a control infusion to the same patients in separate experiments few days before or after hpGRF-40. Blood was then sampled every 15 min for 1 h and then every 30 min up to 150 or 180 min. Plasma was collected and stored at - 20° C until assayed for GH and prolactin by radioimmunoassay, with reagents provided by CEA-IRE Sorin (Saluggia) and Biodata (Milan), respectively. All five patients with isolated GH deficiencies showed a definite rise in plasma GH with peaks at 15 min ranging between 6’3and 14-77 ng/ml, whilst no GH rise was elicited in the subject with a craniopharyngioma. In four of the five patients there was at the 1.
Rivier J, Spiess J, Thorner M, Vale W. Characterization of a growth hormone releasing factor from a human pancreatic islet tumor. Nature 1982; 300: 276-78. 2. Borges JLC, Blizzard RM, Gelato M, et al. Effects ofhuman pancreatic tumour growth hormone releasing factor on growth hormone and somatomedin C levels in patients with idiopathic growth-hormone deficiency Lancet 1983; ii: 119-23. 3. Grossman A, Savage MO, Wass JAH, et al. Growth-hormone-releasing factor in growth hormone deficiency: Demonstration of a hypothalamic defect in growth hormone release. Lancet 1983; ii: 137-38 4. Thorner MO, Rivier J, Spiess J, et al. Human pancreatic growth hormone releasing factor selectively stimulates growth-hormone secretion in man. Lancet 1983; i: 24-28
1089 same time a striking lowering of prolactin levels with nadirs at 60-90 min post-infusion (see table). In patients C and E there was a rebound rise at 120 min. In patient D, who had a raised serum prolactin before the experiment, prolactin concentrations were not suppressed after hpGRF; nor were they in the boy with craniopharyngioma. No rise in plasma GH or suppression of prolactin was seen after saline. No serious adverse effects or changes in pulse rate or blood pressure were noted. These data strengthen the view that there,may, in some GHdeficient patients, be an absolute or relative defect in hypothalamic GRF function. They show that hpGRF-40 will usually induce a clear-cut lowering of plasma prolactin. This prolactin effect was not seen in the patient with a craniopharyngioma, who can be thought of as having impairment of the pituitary gland. The prolactinlowering effect of hpGRF seems not to be confined to children with isolated GH deficiency but appears to be present in normal prepubertal children also (unpublished).
University of Cagliari
CARLO PINTOR ROBERTO CORDA ROSA PUGGIONI
Department of Pharmacology, Chemotherapy, and Toxicology, Faculty of Medicine and Surgery, University of Milan, 20129 Milan, Italy
VITTORIO LOCATELLI SILVANO G. CELLA EUGENIO E. MULLER
Department of Paediatrics,
DISEASE SCORING SYSTEM IN INTENSIVE CARE
SIR,-Dr Le Gall and colleagues (Sept 24, p 741) suggested a simplification of APACHE, our prototype severity-of-disease scoring system for severely ill patients.’ We heartily agree with the need for simplification and are already taking steps in this direction.2 We cannot, however, support the simplified acute physiological score (SAPS) proposed by our French colleagues. For a severity-of-disease classification to be proved valid it must consistently and accurately stratify by risk of death acutely ill patients, on the basis of initial physiological data. It must do this for all the diseases that
special care units treat and it must be as independent as possible of therapeutic decisions. Le Gall’s reanalysis of data from our joint US/French study3did not test the performance of SAPS within diseases because data were insufficient. Its validity, therefore, remains uncertain. Because it includes information
on
independent of therapy.44
ventilator support, the SAPS is
not
We are now very close to completing a disease-specific validation of a shortened acute physiology score,using information from a national survey of 6000 intensive care admissions in the United States together with data from New Zealand and Denmark. It will require fifteen or fewer physiological measurements, should be as easy to use as the SAPS, and will not require therapeutic data. Most importantly, we feel certain that our score will stratify by risk more accurately than the SAPS, both for aggregate intensive care 5 populations and for individual diagnoses. The availability of a severity-of-disease classification system applicable to many diagnoses could have important implications for the evaluation of hospital practices worldwide. Such evaluations would be more precise, however, if we could agree on a single system. We suggest that physicians and researchers withhold final judgment until ours and our French colleagues’ work are complete. ICU Research Unit,
George Washington University Medical Center,
Washington, DC 20037, USA
WILLIAM A. KNAUS DOUGLAS P. WAGNER ELIZABETH A. DRAPER JACK E. ZIMMERMAN
RACE, NUTRITION, AND INFANT MORTALITY
IN
SOUTH AFRICA
SIR,-In your account (Aug 20, p 465) of Mr R. J. Fincham’s contribution to an international conference on ethnic health issues, held in Leeds last July, you reported that the South African Department of Health and Welfare had undertaken nutritional surveys in the Eastern Cape because ofa 1979 newspaper report that "One out of every 4 black babies born in Grahamstown last year died before the age of 12 months". The true situation in Grahamstown was not stated. This figure was drawn from only 396 registered Black births in Grahamstown. This city has a Black population of 40 000, and the birth rate of Black people in South Africa is 40 per 1000. The true number of Black births for this city would therefore be about 1600, giving an infant mortality rate of about 62 per 1000 which is only one-quarter of the rate given in your account. Since Grahamstown Hospital serves a population much larger than that of Grahamstown itself, the number of deaths would also have included some infants from outside the city area in instances where city addresses were recorded on admission. This would further tend to inflate the calculated infant mortality rate. This Department undertook the surveys because local authority clinic reports on malnutrition and potential undernutrition (based on routine examinations at clinics and using the Boston standards) did not correspond to newspaper reports. The Department has for many years been subsidising local authority clinics to prevent kwashiorkor. Your account refers to the high incidence of undernutrition in "resettlement" areas. There is only one resettlement area in the Eastern Cape, and this is the only instance where this Department renders a direct health service. Other services are all local authority ones subsidised by the Department. The incidence of undernutrition in this resettlement area is negligible, based on the Boston third percentile. Referring to this community a newspaper reported in 1980 that undernutrition was very common and based its findings on the Department’s own patient clinic cards: it turned out that the reporter based his results on the third decile instead of on the third centile. As to our questioning "the applicability of the United States standards", this was merely a discussion in the original report based on conflicting opinions among world authorities, some of which have appeared in The Lancet. }-3 Fincham was coauthor of the original report on the rural area survey in which this controversy was discussed. It was also categorically stated that these surveys were not intended to compare the situation with other Third World countries but solely to discover the true situation as compared with clinic reports-ie, they were: provide information about the nutritional status of specific population were at risk of malnutrition; (b) to provide an insight into factors which influenced nutritional status; (c) to give some indication of the proportion of these populations making regular use of local authority clinics; (d) to provide a foundation on which the Department could base future health strategies; and to provide feedback, surveillance, coordination with various bodies (State, semi-State, local authorities, welfare organisations, and the private sector), promotion of community involvement, and development is an accepted priority. 4 May I end by citing a WHO report from 1981:4 "The concept of community involvement has emerged as the most important key to success in nutrition programmes and health programmes. This is... the (a)
to
groups who
primary health care as a strategy for health for all. Community involvement is related to many important aspects of strategy development. First and foremost is the need to strengthen the capability of the people themselves in identifying their own problems". basis for the concept of
1 Knaus WA,
Zimmerman JE, Wagner DP, Draper EA, Lawrence DE. APACHE, acute physiology and chronic health evaluation: a physiologically based classification
system. Crit Care Med 1981; 9: 591-97. 2 Knaus WA, Wagner DP, Draper EA. APACHE. Crit Care Med 1983; 11: 316. 3 Knaus WA, Le Gall J-R, Wagner DP, et al. A comparison of intensive care in the USA and France. Lancet 1982; ii: 642-46. 4 Scheffler RM, Knaus WA, Wagner DP, Zimmerman JE. Severity of illness and the relationship between intensive care and survival. Am J Publ Health 1982; 72: 449-54.
5 Knaus WA, Wagner DP, Draper EA. The relationship betwseen severity of illness and outcome. Clin Res 1983; 31: 299 (abstr)
1. Goldstein
H, Tanner JM. Ecological considerations in the creation and the use of child standards. Lancet 1980; i. 582-85. 2. McLaren DS, Read WWC. Classification of nutritional status in early childhood. Lancet 1972, ii: 146-48. 3. Habicht JP, Martorell R, Yardrough C, Maluna RM, Klein RE. Height and weight standards for pre-school children: How relevant are ethnic differences in growth potential? Lancet 1974; i: 611-14. 4. World Health Organisation. The role of the health sector in food and nutrition. Tech Rep Ser WHO 1981; no 667: 11, 32, 33.
growth