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Introduction of solids to the infant diet
  1. G A Khakoo,
  2. G Lack
  1. Department of Paediatric Allergy, Asthma and Immunology, Imperial College London at St Mary’s Hospital, London, UK
  1. Correspondence to:
    Dr G Lack
    Department of Paediatric Allergy, Asthma and Immunology, Imperial College London at St Mary’s Hospital, Salton House, St Mary’s Hospital, Praed Street, London W2 1NY, UK;

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Commentary on the papers by Morgan et al and Zutavern et al

The Department of Health has recently supported the WHO advice for mothers to exclusively breast feed until 6 months of age.1 Furthermore, there are expert committee guidelines regarding the introduction of solids in the diet of infants at high risk of developing allergy. The joint guidelines of the European Society for Paediatric Allergology and Clinical Immunology (ESPACI) and the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) recommend that solid food introduction be delayed until 5 months of age. The American Academy of Pediatrics advice is more detailed, suggesting that solids be delayed until 6 months of age, cows’ milk to 1 year, egg to 2 years, and peanuts, tree nuts, and fish to 3 years.2 It is not surprising that these guidelines differ as they are based on the limited evidence of two studies. The first, a prospective non-randomised study in an atopic population, suggested that eczema and a history of food allergy was reduced at age 1 year in infants fed solids after 6 months of age compared with those infants with solids introduced at 3 months, but no difference was seen at 5 year follow up.3 The second study had a similar design, but was conducted in a normal population. This study showed more eczema, but not asthma, at 2–4 years of age in infants fed four or more solid foods before age 4 months compared with infants receiving no solid foods before 4 months of age. This difference was maintained until 10 years of age.4

The increased information to health professionals and the public regarding dietary interventions which are perceived to reduce allergy has resulted in the risk of recent dietary intervention studies being confounded by reverse causality. Thus, mothers who are atopic, come from atopic families, or have a baby already showing signs of allergy, for example, eczema, may take steps that they perceive will reduce the chance of their children developing allergies, or be advised by health professionals to do so.

The addition of two studies, published in this issue, looking at the effect on allergy of the timing of introduction of solids to the infant diet5,6 is most welcome in view of the limited literature to date. The study of Morgan et al prospectively followed up 257 well preterm infants from three maternity units, with follow up to 1 year of age. The introduction of four or more solid foods before 17 weeks post-term was associated with a higher risk of eczema in infants with and without a family history of allergy.5 Unfortunately no data are presented on the extent of prematurity, which may confound the results since increasing prematurity is known to be associated with a decreased risk of atopy.7 This could be due to a higher infectious burden and altered gut microbial flora in more preterm infants, with higher risks of sepsis and necrotising enterocolitis. Such infants would also be more likely to have delayed introduction of solids. Thus the observed relation between early introduction of solids and infant atopy could be confounded by the higher infectious burden in more premature infants in whom solids are delayed for medical reasons.

The study of Zutavern et al is a well conducted prospective birth cohort study involving 642 infants, with follow up to 5½ years of age.6 The dietary data were collected prospectively, the allergic phenotype was carefully documented for wheeze and eczema, and objective skin prick test data were also collected. The data were corrected for parental asthma and atopy. This study shows no evidence to support a protective effect of late introduction of solids on the development of eczema or asthma. The authors mention that the increased risk of eczema associated with the late introduction of egg is likely to be due to reverse causality.

In summary, the study of Morgan et al suggests that in preterm infants a delay in the introduction of solids may help to reduce the development of early childhood allergy. However, in the general population, the study of Zutavern et al challenges the widely held belief that delayed introduction of solids reduces the risk of allergy. These studies add to the current conflicting literature, which taken as a whole does not allow an authoritative statement to be made regarding the relation between the introduction of solids and the development of allergy. Future studies will need to take into account confounding factors such as reverse causality, and identify specific endpoints, such as food allergy, eczema, and asthma.

Commentary on the papers by Morgan et al and Zutavern et al


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