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INFANTILE RICKETS RETURNS TO GLASGOW
Saturday
INFANTILE RICKETS RETURNS TO GLASGOW G. C. ARNEIL M.D., Ph.D. Glasg. LEONARD GOW LECTURER IN MEDICAL DISEASES OF INFANCY AND CHILDHOOD
J. C. CROSBIE M.D. Dalhousie REGISTRAR
From the Department of Child Health, University of Glasgow, and the Royal Hospital for Sick Children, Glasgow
THE Glasgow area was notorious for at least eighty years for the extent and severity of infantile rickets. Owen (1889) wrote that the disease was very prevalent " in the industrial zone between the Firths of Clyde and Forth ". The introduction of dried milk, fortified with calciferol, and subsidised in price, followed by the fortification of proprietary rusks and cereals, virtually cleared rickets from the area during the 1939-45 war. Fortified milk was complemented by provision of synthetic " cod-liver oil compound " (calciferol in arachis oil) which was widely advocated and liberally provided through child-welfare clinics and food-distribution centres, although less than half the available supplies were ever taken up. Infantile rickets is arbitrarily defined as a disease due to an intake of vitamin D insufficient and phosphorus metabolism in alimentary absorption, renal function, and alkaline-phos-
phatase activity
are
to
maintain normal calcium
a
growing child, in whom
31
Results
In the fifteen years from
Jan. 1, 1948, to Dec. 31, 1962, 85 children with infantile rickets were admitted to the Royal Hospital for Sick Children
(fig. 1). The pattern is readily divisible into three periods. The initial
or
dwindling prevalence of
During the four-year period 1959-62 32 children with florid rickets were admitted by contrast with a total of 12 in the six-year period 1953-58. The case-records of the 32 children in the 1959-62 bulge were examined in detail. In each, florid clinical signs-well described by Soranus
hypophosphatasia.
7305
the
rickets when fortification was greatest. The prevalence remained very low with no more than 2 cases being admitted in any one year until 1959, when a rise in numbers began which has continued to date.
adequate.
The Royal Hospital for Sick Children, Glasgow, cares for a high proportion of the children with medical diseases in the Glasgow conurbation. The figures from this large hospital probably reflect fairly satisfactorily the relative prevalence of a disease such as infantile rickets.
Fig. 1-Annual incidence of infantile rickets judged by admission to Royal Hospital for Sick Children, Glasgow. Indian and Pakistani cases indicated by darker areas.
period (1948-52) represents
The disease is remediable by a single massive dose of calciferol or by a supplement to the diet of moderate amounts of vitamin D2 or D3 (10003000 i.u. per day) for a short time; thereafter eutrophy may be maintained by approximately 400 i.u. daily. The term is not applied to rickets secondary to abnormal alimentary absorption, renal function, renal tubular func-
tion,
August 1963
Fig. 2-Active and healing rickets from 3 patients in present series.
424
(130) and common knowledge since the days of Glisson (1650)-were present and radiologically confirmed (fig. 2). In 31 of the children the serum-alkaline-phosphatase level exceeded 20 King-Armstrong units per 100 ml.; in 19 the serum-phosphorus level was less than 4-0 mg. per 100 ml.;
CALCIFEROL CONTENT OF VARIOUS INFANT FOODS
and in 7 the serum-calcium level was below 9 mg. per 100 ml. In 24 of the 32 children the degree of aminoaciduria was estimated and was within acceptable limits (Jonxis and Huisman 1954). In the houses in which infantile rickets arose during 1961-62 the social conditions were very poor. Thirteen of the nineteen " homes " consisted of one or two rooms. The average number of occupants was 7-6, and the average position of the rachitic child in the family was 5th. The worst overcrowding was 11 persons in two rooms, although two families had 6 persons in one room. Sixteen of these nineteen " homes " were investigated, and only four had a water closet. In the remainder the water-closet was outside and was shared with the " landing ", the " stair ", or the tenement. Before 1962 none of the fathers were " per" manently unemployed, but during that year 3 of the 13 fathers fell into this category. A striking seasonal prevalence was noted, in keeping with the observations of Underwood (1789). 22 children were admitted between March and July, and only 10 in the seven months from August to February.
patients were treated with intramuscular calciferol (300,000-600,000 i.u.), and healing took place in every child. 17 patients received oral therapy varying from 800 to 3000 i.u. daily of vitamin D2 for eight to sixteen weeks. The 32 children were supervised until satisfactory clinical, biochemical, and radiological healing was complete. The criteria of admission to this group of 32 patients were very strictly applied, and, in fact, 5 further children with presumed infantile rickets were seen in 1962 but 15 of the
excluded from the list for one reason or another. The winter 1961-62 and the spring of 1962 were each well above average for sunshine and were not exceptionally cold; thus climatic conditions were unlikely to have been the precipitating cause.
were
Discussion
13 cases of gross infantile rickets in one year is not a serious absolute increase, but, if florid diagnosed rickets is as a small proportion of the number of latent in the population, the position is disquieting. So far it has been a local, and indeed a focal, problem, since 15 of the 32 children came from one area (C.5, Gorbals) and 12 others from the C.3, C.4, or N.W. regions. Only 5 of the children lived outside these small central districts of Glasgow, and of these only 2 lived outside the city. One possible explanation lay in the increased immigration of Indians and Pakistani into the area around 1958, which resulted in the finding of cases of delayed nutritional rickets in adolescents (Dunnigan et al. 1962). This was partly true in that 8 of the 32 children were Asian (fig. 1), but these cases were seen mainly in 1959 and 1960 when the local immigrant population was expanding. The involvement of Asian children may be due to multiple factors, including habitual consumption of a racial diet, lessened exposure to sunshine, failure of immigrants to learn (or to be taught?) that supplementary intake is essential beneath the smoke pall of a northern city, and the: hypothetical possibility that a dusky skin requires more:
regarded cases
ultraviolet radiation than a white skin (Hess 1924). The problem of this racial group is circumscribed and ought to be evanescent. The solution lies in adequate education of Asian women immigrants firstly to speak English and secondly in the elements of child care in this climate. It is revealing to have an Indian child with nutritional rickets translating into English the answer of his parents toa question about the child’s diet. A second hypothesis also seems valid. Before 1958 the subsidised National dried milk and Government cod-liver oil contained larger quantities of calciferol than today (see table). If a 6-month-old baby received National dried milk (40 fl. oz.), cod-liver oil (one teaspoonful), and rusks and cereals the intake exceeded 3000 LU. of calciferol daily. By 1957 this excessive intake by a large section of the infant population was believed to contribute to the rise in infantile hypercalcaemia in the country (Morgan et al. 1956, Rhaney and Mitchell 1956), and the vitamin-D2 content of infant foods was reduced. These changes aimed at ensuring that the British infant ingested not less than 400 i.u. and not more than 800 I.U. of vitamin D daily from all sources. In retrospect one wonders whether the very high intake of calciferol by infants aged up to 9 months during 1948-58 did not provide a store of vitamin D for use later in the critical period when supplementation lessened. This could explain the virtual absence of rickets from 1952 to 1958 when squalor and overcrowding were worse in C.5 than they are today. After the reductions in vitamin-D2 fortification of infant foods, the incidence of infantile rickets at this hospital increased. It is facile to assume that the return of infantile rickets was due to a reduction of the average intake to around 400 l.u. daily; in fact, these children received adequate supplements only during the period of driedmilk feeding, and ceased to do so when the change was made to liquid milk. Only 8 of the 32 children received supplementary vitamin D2 at all after solid feeding began, and these 8 received irregular and quite inadequate amounts. The assumption that these children did not obtain adequate supplements seems to point squarely to the failure of the mother to make use of available supplementary vitamin-D2 preparations. It is significant that we are informed that in 1962 only 3’2°o of available Government cod-liver oil was taken up in
Glasgow. Confirmation of the idea that the lactiverous nursling obtains adequate calciferol intake before weaning is given by the age-distribution of these patients. The average age at diagnosis of the 24 Caucasians in the 1959-62 group was 2 years. In the group of Caucasian children admitted during 1948-52 the average age was 18 months, and in 1937 it was 17 months. This apparent delay in the
425
diagnosis of infantile rickets may indicate that adequate calciferol intake during feeding with dried-milk preparations postponed the onset of the disease. In the present Asian group the average age at diagnosis was 361/2 months. The problem now is to ensure that vitamin-D intake is adequate for all children aged 6 months to at least 3 years. This must be achieved cautiously, bearing in mind on the one hand that excessive intake may lead to infantile hypercalcaemia and, on the other hand, that for every diagnosed case of florid rickets there are almost certainly several latent milder cases. It is an illusion that the mothers in this area knowingly prevent rickets in the early months of life by giving fortified milk, dried or evaporated. It is simply that they have difficulty in giving anything else. So soon as they cease to give fortified milk and change to liquid cow’s milk they cease (in blissful ignorance) to give adequate supplements. Fortunately, most infants aged 6-12 months in higher social groups are given proprietary foods (cereals and rusks) and calciferol is given, again unknowingly. In poorer homes, however, the " run-ofthe-house diet is often inadequate in vitamin D because the popular pre-cooked infant cereals are not purchased. Too. little is known of the present diet of the child aged 6 months to 3 years in this social group. "
Exhortation through child-welfare centres will largely more informed mothers and is no solution to the present impasse. The real problem lies with the mothers of large underprivileged families who live in slums, who do not attend the child-welfare clinics, pay little heed to health visitors, and who read little-but who do watch television. Paton and Findlay (1926) noted with concern reach the
that in Glasgow 62% of the population was housed in oneroomed or two-roomed houses: in 1961 the proportion was still 42%, and with old properties crumbling rapidly the housing situation was unsatisfactory. The stricture of " Barlow that " rickets is the coeval of civilisation seems to be accepted, rather than combated, if such squalor is allowed to remain. It is really surprising that infantile rickets disappeared to the extent that it did. The existence of infantile rickets today is as unnecessary it is undesirable. We firmly believe that only the following direct measures are likely to succeed: as
(1) All girls attending school and women at antenatal clinics, maternity hospitals, and welfare clinics should be instructed in mothercraft. Emphasis should be placed on the need for all breast-fed babies and all infants not receiving fortified milk to have calciferol supplements and on the continuation of dried-milk feeding until the 1st birthday.
(2) Instead of the issue of unpopular and unpalatable codan attractive, palatable, vitamin-D preparation (400 i.u. per teaspoonful) should be cheaply marketed. This should be well advertised, attractively labelled, and sold primarily through all chemists and cooperatives in exchange for privilege vouchers. If this preparation can contain 25 mg. of ascorbic acid as well, then only one subsidised vitamin prepara-
liver oil,
"
tion should be issued. It should not be called " cod-liver oil but should be attractively named (e.g., ’Devite ’ ourSunvite ’). This preparation should also be available at all welfare clinics and food-distribution centres.
(3) The need to give this vitamin preparation should be publicised on local television to the Glasgow area, or to any area
affected in the future.
(4) The value of fortified cereal preparations for feeding children aged 6-36 months should be emphasised. An official preparation at subsidised prices might be provided. 5) The possibility of irradiating the subsidised milk
pro-
vided for children below the age of 5 to the extent of 250 i.u. of vitamin D per pint or reconstituted pint should be
explored. (6) Mothers must be made aware that children require supplements of vitamin D, and that orange juice, blackcurrant juice, or rose-hip syrup are useless in the prevention of rickets. Advertising on television and elsewhere of vitamin-C products for infants should be monitored, lest the mothers gain the impression that this alone is adequate for the growing child.
In the long term the real answer is to make all mothers that supplementary vitamin D is essential for the health of children, and that other " tonics " are not. With positive awareness achieved, half the battle would be won, but meanwhile continued latent fortification of commonly used foods is the only practical remedy. Infantile rickets is not confined to Glasgow today: the American Academy of Pediatrics (1962) pointed out that at least 843 cases of infantile rickets occurred in the U.S.A. between 1956 and 1960. Because the disease is becoming relatively uncommon, mild cases may be missed by busy medical practitioners, and only 3 of our 32 cases were diagnosed. We urge those who work in northern cities to seek for infantile rickets in the younger children of large underprivileged families. No child has been admitted from the new housing areas built to rehouse overcrowded families, which suggests that exposure to natural heliotherapy may be helpful in prevention. The hope is that measures which are now in hand to increase the use of vitamin-D2 in the affected areas of Glasgow will check the recurrence of infantile rickets. aware
Although absolute poverty was never the sole cause of rickets in these children (and free supplies of vitamins would have been available if this were the case) poverty does contribute to the squalid social background. Summary
_
The prevalence of infantile rickets in Glasgow is rising because mothers do not realise that vitamin-D supplements are essential after dried-milk feeding ceases. There are many reasons for this. A single, cheap, palatable, vitamin preparation should be provided. This should be attractively named and easily available to the public in exchange for privilege vouchers at clinics and at chemists’ shops. This preparation should be widely advertised and publicised. The consumption of fortified cereals by infants should be encouraged, as should the use of dried or evaporated milk for infants until they are a year old. We should like to thank Prof. J. H. Hutchison and Dr. Norah Wattie, principal medical officer for maternity and child welfare, Glasgow, for their advice and assistance. We should also like to thank the firms of A. & R. Scott, Glaxo Laboratories Ltd., and Farlevs Infant Food, Ltd., for supplying information. REFERENCES American Academy of Pediatrics (1962): Report of Committee on Nutrition, Infantile Scurvy, and Nutritional Rickets in the U.S.A. Pediatrics, 29, 646. Dunnigan, M. G., Paton, J. P. J., Haase, S., McNicol, G. W., Gardner, M. D., Smith, C. M. (1962) Scot. med. J. 7, 159. Glisson, F. (1650) De rachitide sive morbo puerili, qui vulgo The Rickets dicitur. London. Hess, A. F. (1924) Amer J. Dis. Child. 28, 517. Jonxis, J. H. P., Huisman, T. H J. (1954) Lancet, ii, 513. Morgan, H. G., Mitchell, R. G., Stowers, J. M., Thomson, J. (19561 ibid. i, 925. Owen, J. (1889) Brit. med. J. i, 113. Paton, D. N., Findlay, L. (1926) Studies of Child Life in Cities and Rural Districts of Scotland. Spec. Rep. Ser. med Res. Coun., Lond. no. 101. Rhaney, K , Mitchell, R. G. (1956) Lancet, i, 1028. Soranus, E. (circa 130). Translated by H. Luneberg (1894) Die Gynakologie. Munich. Underwood, M. (1789) A Treatise on The Disease of Children; vol. I, p. 313.
INFANTILE RICKETS RETURNS TO GLASGOW G. C. ARNEIL M.D., Ph.D. Glasg. LEONARD GOW LECTURER IN MEDICAL DISEASES OF INFANCY AND CHILDHOOD
J. C. CROSBIE M.D. Dalhousie REGISTRAR
From the Department of Child Health, University of Glasgow, and the Royal Hospital for Sick Children, Glasgow
THE Glasgow area was notorious for at least eighty years for the extent and severity of infantile rickets. Owen (1889) wrote that the disease was very prevalent " in the industrial zone between the Firths of Clyde and Forth ". The introduction of dried milk, fortified with calciferol, and subsidised in price, followed by the fortification of proprietary rusks and cereals, virtually cleared rickets from the area during the 1939-45 war. Fortified milk was complemented by provision of synthetic " cod-liver oil compound " (calciferol in arachis oil) which was widely advocated and liberally provided through child-welfare clinics and food-distribution centres, although less than half the available supplies were ever taken up. Infantile rickets is arbitrarily defined as a disease due to an intake of vitamin D insufficient and phosphorus metabolism in alimentary absorption, renal function, and alkaline-phos-
phatase activity
are
to
maintain normal calcium
a
growing child, in whom
31
Results
In the fifteen years from
Jan. 1, 1948, to Dec. 31, 1962, 85 children with infantile rickets were admitted to the Royal Hospital for Sick Children
(fig. 1). The pattern is readily divisible into three periods. The initial
or
dwindling prevalence of
During the four-year period 1959-62 32 children with florid rickets were admitted by contrast with a total of 12 in the six-year period 1953-58. The case-records of the 32 children in the 1959-62 bulge were examined in detail. In each, florid clinical signs-well described by Soranus
hypophosphatasia.
7305
the
rickets when fortification was greatest. The prevalence remained very low with no more than 2 cases being admitted in any one year until 1959, when a rise in numbers began which has continued to date.
adequate.
The Royal Hospital for Sick Children, Glasgow, cares for a high proportion of the children with medical diseases in the Glasgow conurbation. The figures from this large hospital probably reflect fairly satisfactorily the relative prevalence of a disease such as infantile rickets.
Fig. 1-Annual incidence of infantile rickets judged by admission to Royal Hospital for Sick Children, Glasgow. Indian and Pakistani cases indicated by darker areas.
period (1948-52) represents
The disease is remediable by a single massive dose of calciferol or by a supplement to the diet of moderate amounts of vitamin D2 or D3 (10003000 i.u. per day) for a short time; thereafter eutrophy may be maintained by approximately 400 i.u. daily. The term is not applied to rickets secondary to abnormal alimentary absorption, renal function, renal tubular func-
tion,
August 1963
Fig. 2-Active and healing rickets from 3 patients in present series.
424
(130) and common knowledge since the days of Glisson (1650)-were present and radiologically confirmed (fig. 2). In 31 of the children the serum-alkaline-phosphatase level exceeded 20 King-Armstrong units per 100 ml.; in 19 the serum-phosphorus level was less than 4-0 mg. per 100 ml.;
CALCIFEROL CONTENT OF VARIOUS INFANT FOODS
and in 7 the serum-calcium level was below 9 mg. per 100 ml. In 24 of the 32 children the degree of aminoaciduria was estimated and was within acceptable limits (Jonxis and Huisman 1954). In the houses in which infantile rickets arose during 1961-62 the social conditions were very poor. Thirteen of the nineteen " homes " consisted of one or two rooms. The average number of occupants was 7-6, and the average position of the rachitic child in the family was 5th. The worst overcrowding was 11 persons in two rooms, although two families had 6 persons in one room. Sixteen of these nineteen " homes " were investigated, and only four had a water closet. In the remainder the water-closet was outside and was shared with the " landing ", the " stair ", or the tenement. Before 1962 none of the fathers were " per" manently unemployed, but during that year 3 of the 13 fathers fell into this category. A striking seasonal prevalence was noted, in keeping with the observations of Underwood (1789). 22 children were admitted between March and July, and only 10 in the seven months from August to February.
patients were treated with intramuscular calciferol (300,000-600,000 i.u.), and healing took place in every child. 17 patients received oral therapy varying from 800 to 3000 i.u. daily of vitamin D2 for eight to sixteen weeks. The 32 children were supervised until satisfactory clinical, biochemical, and radiological healing was complete. The criteria of admission to this group of 32 patients were very strictly applied, and, in fact, 5 further children with presumed infantile rickets were seen in 1962 but 15 of the
excluded from the list for one reason or another. The winter 1961-62 and the spring of 1962 were each well above average for sunshine and were not exceptionally cold; thus climatic conditions were unlikely to have been the precipitating cause.
were
Discussion
13 cases of gross infantile rickets in one year is not a serious absolute increase, but, if florid diagnosed rickets is as a small proportion of the number of latent in the population, the position is disquieting. So far it has been a local, and indeed a focal, problem, since 15 of the 32 children came from one area (C.5, Gorbals) and 12 others from the C.3, C.4, or N.W. regions. Only 5 of the children lived outside these small central districts of Glasgow, and of these only 2 lived outside the city. One possible explanation lay in the increased immigration of Indians and Pakistani into the area around 1958, which resulted in the finding of cases of delayed nutritional rickets in adolescents (Dunnigan et al. 1962). This was partly true in that 8 of the 32 children were Asian (fig. 1), but these cases were seen mainly in 1959 and 1960 when the local immigrant population was expanding. The involvement of Asian children may be due to multiple factors, including habitual consumption of a racial diet, lessened exposure to sunshine, failure of immigrants to learn (or to be taught?) that supplementary intake is essential beneath the smoke pall of a northern city, and the: hypothetical possibility that a dusky skin requires more:
regarded cases
ultraviolet radiation than a white skin (Hess 1924). The problem of this racial group is circumscribed and ought to be evanescent. The solution lies in adequate education of Asian women immigrants firstly to speak English and secondly in the elements of child care in this climate. It is revealing to have an Indian child with nutritional rickets translating into English the answer of his parents toa question about the child’s diet. A second hypothesis also seems valid. Before 1958 the subsidised National dried milk and Government cod-liver oil contained larger quantities of calciferol than today (see table). If a 6-month-old baby received National dried milk (40 fl. oz.), cod-liver oil (one teaspoonful), and rusks and cereals the intake exceeded 3000 LU. of calciferol daily. By 1957 this excessive intake by a large section of the infant population was believed to contribute to the rise in infantile hypercalcaemia in the country (Morgan et al. 1956, Rhaney and Mitchell 1956), and the vitamin-D2 content of infant foods was reduced. These changes aimed at ensuring that the British infant ingested not less than 400 i.u. and not more than 800 I.U. of vitamin D daily from all sources. In retrospect one wonders whether the very high intake of calciferol by infants aged up to 9 months during 1948-58 did not provide a store of vitamin D for use later in the critical period when supplementation lessened. This could explain the virtual absence of rickets from 1952 to 1958 when squalor and overcrowding were worse in C.5 than they are today. After the reductions in vitamin-D2 fortification of infant foods, the incidence of infantile rickets at this hospital increased. It is facile to assume that the return of infantile rickets was due to a reduction of the average intake to around 400 l.u. daily; in fact, these children received adequate supplements only during the period of driedmilk feeding, and ceased to do so when the change was made to liquid milk. Only 8 of the 32 children received supplementary vitamin D2 at all after solid feeding began, and these 8 received irregular and quite inadequate amounts. The assumption that these children did not obtain adequate supplements seems to point squarely to the failure of the mother to make use of available supplementary vitamin-D2 preparations. It is significant that we are informed that in 1962 only 3’2°o of available Government cod-liver oil was taken up in
Glasgow. Confirmation of the idea that the lactiverous nursling obtains adequate calciferol intake before weaning is given by the age-distribution of these patients. The average age at diagnosis of the 24 Caucasians in the 1959-62 group was 2 years. In the group of Caucasian children admitted during 1948-52 the average age was 18 months, and in 1937 it was 17 months. This apparent delay in the
425
diagnosis of infantile rickets may indicate that adequate calciferol intake during feeding with dried-milk preparations postponed the onset of the disease. In the present Asian group the average age at diagnosis was 361/2 months. The problem now is to ensure that vitamin-D intake is adequate for all children aged 6 months to at least 3 years. This must be achieved cautiously, bearing in mind on the one hand that excessive intake may lead to infantile hypercalcaemia and, on the other hand, that for every diagnosed case of florid rickets there are almost certainly several latent milder cases. It is an illusion that the mothers in this area knowingly prevent rickets in the early months of life by giving fortified milk, dried or evaporated. It is simply that they have difficulty in giving anything else. So soon as they cease to give fortified milk and change to liquid cow’s milk they cease (in blissful ignorance) to give adequate supplements. Fortunately, most infants aged 6-12 months in higher social groups are given proprietary foods (cereals and rusks) and calciferol is given, again unknowingly. In poorer homes, however, the " run-ofthe-house diet is often inadequate in vitamin D because the popular pre-cooked infant cereals are not purchased. Too. little is known of the present diet of the child aged 6 months to 3 years in this social group. "
Exhortation through child-welfare centres will largely more informed mothers and is no solution to the present impasse. The real problem lies with the mothers of large underprivileged families who live in slums, who do not attend the child-welfare clinics, pay little heed to health visitors, and who read little-but who do watch television. Paton and Findlay (1926) noted with concern reach the
that in Glasgow 62% of the population was housed in oneroomed or two-roomed houses: in 1961 the proportion was still 42%, and with old properties crumbling rapidly the housing situation was unsatisfactory. The stricture of " Barlow that " rickets is the coeval of civilisation seems to be accepted, rather than combated, if such squalor is allowed to remain. It is really surprising that infantile rickets disappeared to the extent that it did. The existence of infantile rickets today is as unnecessary it is undesirable. We firmly believe that only the following direct measures are likely to succeed: as
(1) All girls attending school and women at antenatal clinics, maternity hospitals, and welfare clinics should be instructed in mothercraft. Emphasis should be placed on the need for all breast-fed babies and all infants not receiving fortified milk to have calciferol supplements and on the continuation of dried-milk feeding until the 1st birthday.
(2) Instead of the issue of unpopular and unpalatable codan attractive, palatable, vitamin-D preparation (400 i.u. per teaspoonful) should be cheaply marketed. This should be well advertised, attractively labelled, and sold primarily through all chemists and cooperatives in exchange for privilege vouchers. If this preparation can contain 25 mg. of ascorbic acid as well, then only one subsidised vitamin prepara-
liver oil,
"
tion should be issued. It should not be called " cod-liver oil but should be attractively named (e.g., ’Devite ’ ourSunvite ’). This preparation should also be available at all welfare clinics and food-distribution centres.
(3) The need to give this vitamin preparation should be publicised on local television to the Glasgow area, or to any area
affected in the future.
(4) The value of fortified cereal preparations for feeding children aged 6-36 months should be emphasised. An official preparation at subsidised prices might be provided. 5) The possibility of irradiating the subsidised milk
pro-
vided for children below the age of 5 to the extent of 250 i.u. of vitamin D per pint or reconstituted pint should be
explored. (6) Mothers must be made aware that children require supplements of vitamin D, and that orange juice, blackcurrant juice, or rose-hip syrup are useless in the prevention of rickets. Advertising on television and elsewhere of vitamin-C products for infants should be monitored, lest the mothers gain the impression that this alone is adequate for the growing child.
In the long term the real answer is to make all mothers that supplementary vitamin D is essential for the health of children, and that other " tonics " are not. With positive awareness achieved, half the battle would be won, but meanwhile continued latent fortification of commonly used foods is the only practical remedy. Infantile rickets is not confined to Glasgow today: the American Academy of Pediatrics (1962) pointed out that at least 843 cases of infantile rickets occurred in the U.S.A. between 1956 and 1960. Because the disease is becoming relatively uncommon, mild cases may be missed by busy medical practitioners, and only 3 of our 32 cases were diagnosed. We urge those who work in northern cities to seek for infantile rickets in the younger children of large underprivileged families. No child has been admitted from the new housing areas built to rehouse overcrowded families, which suggests that exposure to natural heliotherapy may be helpful in prevention. The hope is that measures which are now in hand to increase the use of vitamin-D2 in the affected areas of Glasgow will check the recurrence of infantile rickets. aware
Although absolute poverty was never the sole cause of rickets in these children (and free supplies of vitamins would have been available if this were the case) poverty does contribute to the squalid social background. Summary
_
The prevalence of infantile rickets in Glasgow is rising because mothers do not realise that vitamin-D supplements are essential after dried-milk feeding ceases. There are many reasons for this. A single, cheap, palatable, vitamin preparation should be provided. This should be attractively named and easily available to the public in exchange for privilege vouchers at clinics and at chemists’ shops. This preparation should be widely advertised and publicised. The consumption of fortified cereals by infants should be encouraged, as should the use of dried or evaporated milk for infants until they are a year old. We should like to thank Prof. J. H. Hutchison and Dr. Norah Wattie, principal medical officer for maternity and child welfare, Glasgow, for their advice and assistance. We should also like to thank the firms of A. & R. Scott, Glaxo Laboratories Ltd., and Farlevs Infant Food, Ltd., for supplying information. REFERENCES American Academy of Pediatrics (1962): Report of Committee on Nutrition, Infantile Scurvy, and Nutritional Rickets in the U.S.A. Pediatrics, 29, 646. Dunnigan, M. G., Paton, J. P. J., Haase, S., McNicol, G. W., Gardner, M. D., Smith, C. M. (1962) Scot. med. J. 7, 159. Glisson, F. (1650) De rachitide sive morbo puerili, qui vulgo The Rickets dicitur. London. Hess, A. F. (1924) Amer J. Dis. Child. 28, 517. Jonxis, J. H. P., Huisman, T. H J. (1954) Lancet, ii, 513. Morgan, H. G., Mitchell, R. G., Stowers, J. M., Thomson, J. (19561 ibid. i, 925. Owen, J. (1889) Brit. med. J. i, 113. Paton, D. N., Findlay, L. (1926) Studies of Child Life in Cities and Rural Districts of Scotland. Spec. Rep. Ser. med Res. Coun., Lond. no. 101. Rhaney, K , Mitchell, R. G. (1956) Lancet, i, 1028. Soranus, E. (circa 130). Translated by H. Luneberg (1894) Die Gynakologie. Munich. Underwood, M. (1789) A Treatise on The Disease of Children; vol. I, p. 313.