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Vitamin D concentrations in Asian children living in England

BMJ 1999; 318 doi: https://doi.org/10.1136/bmj.318.7195.1417 (Published 22 May 1999) Cite this as: BMJ 1999;318:1417

Limited vitamin D intake and use of sunscreens may lead to rickets

  1. Stanley Zlotkin (szlotkin{at}sickkids.on.ca), Professor
  1. Department of Paediatrics and of Nutritional Sciences, Hospital for Sick Children, Faculty of Medicine, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G
  2. Directorate of Biochemical Medicine, Ninewells Hospital, Dundee DD1 9SY

    EDITOR—I would like to add a sixth suggestion to Wharton's five approaches to improving children's vitamin D status to prevent rickets.1 A case of rickets was recently diagnosed in a 12 month old white infant at the Hospital for Sick Children in Toronto. He had clinical, radiological, and biochemical evidence of rickets, which responded to vitamin D treatment. Vitamin D intake seemed adequate until six months after treatment began but was sporadic after that. Although the infant spent time outdoors in the summer, his skin was protected with potent sunscreens (SPF 30).

    Rickets presumably developed because of limited vitamin D intake combined with diminished skin penetration of ultraviolet radiation. I believe that this is the first case to be diagnosed in a white infant. Although numerous previous reports have documented vitamin D deficiency rickets from inadequate oral intake of vitamin D, in most cases the infants had dark skin and had limited exposure to ultraviolet B.2

    The ultraviolet B rays that synthesise vitamin D3 in the skin from 7-dehydrocholesterol are also associated with adverse effects on the skin. Public health advice has emphasised that skin should be shielded from the sun from birth onwards, especially in light skinned individuals. Both Health Canada and the Canadian Dermatology Association advise that infants under 1 year should be kept out of direct sunlight. Infants over 6 months are advised to wear a sunscreen of SPF 15 or higher on all areas that are exposed to the sun.3

    With the increasing use of sunscreen one may justifiably ask whether infants and children are at an increased risk of vitamin D deficiency. This question is biologically plausible since sunscreens block the absorption of ultraviolet B radiation. A sunscreen with an SPF of 30, like the one used in this case, allows only a thirtieth of the ultraviolet rays to penetrate the skin. The photoisomerisation of 7-dehydrocholesterol to previtamin D3 is prevented by sunscreens.4

    Although regular use of sunscreens has been associated with low body stores of vitamin D,5 the case presented is the first to document an association between use of sunscreens and vitamin D deficiency rickets. Infants who ingest a suboptimal amount of vitamin D and whose skin is protected by potent sunscreens should receive a vitamin D supplement.

    Footnotes

    • aCompeting interests Stanley Zlotkin occasionally gives opinions, for which he receives a fee, to companies making nutritional products for children.

    References

    Concentrations found may be function of analytical methodology used

    1. Aubrey Blumsohn (ablumsohn{at}btinternet.com), Senior registrar in biochemical medicine
    1. Department of Paediatrics and of Nutritional Sciences, Hospital for Sick Children, Faculty of Medicine, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G
    2. Directorate of Biochemical Medicine, Ninewells Hospital, Dundee DD1 9SY

      EDITOR—Lawson and Thomas suggest that the serum concentration of 25-hydroxycholecalciferol is substantially lower in Asian infants than in the general population.1 Although this finding is highly plausible, their paper does not provide reliable evidence regarding the presence or magnitude of this difference. Plasma samples in Asian subjects were collected in a different year and in a different geographical area and were apparently assayed in a different laboratory from those in the external control group. Analytical methods are unspecified.

      Year to year differences in plasma 25-hydroxycholecalciferol are likely. More importantly, the North West Thames external quality assurance survey showed that serum measurements of 25-hydroxycholecalciferol differed considerably both between and within laboratories over the period of the study. 2 3 The number of subjects classified as having 25-hydroxycholecalciferol below 25 μmol/l may be as much a function of analytical methodology as of ethnic group. A similar explanation may account for the apparent absence of seasonal variation in the control data.

      Footnotes

      • bCompeting interest None declared.

      References

      View Abstract