I read this article with interest and was pleased by the emphasis given to Medical Education in this journal(1, 2). There is necessity for more literature on Medical Education in frontline journals like this.

Reading the RCPCH document for Level 2 competency for Core Highest Specialist Training in Paediatrics(3), I was disappointed that Best Evidence Medical Education (BEME)was not included.

It is necessary to move from opinion-based education to evidence- based education. Since its introduction, the implementation of BEME has been slow due to lack of awareness. We hardly read literature on education, or more appropriately, are not even aware that such literature exists(4).

Whereas it was once assumed that a competent basic or clinical scientist would naturally be an effective teacher, it is now acknowledged that preparation for teaching is essential. In a review of this topic, authors conclude that the very nature of being professional in today's social and fiscal context demands that medical educators provide evidence of effectiveness and efficiency of their programs(5).

Fortunately we live in a time where ubiquitous acceptance of Evidence Based Medicine (EBM) has made the concept of Evidence- based practise irrefutable. All that is needed now is to lead Trainees into applying the equivalent principles of seeking evidence and implementing appropriate change based on the best available evidence to engender the thought process of Evidence –based education.

Specialist Trainee curriculum should therefore encompass guidance on how BEME can be applied. This may include:

1.encouraging reflection on teaching methods allowing the trainees to identify the gaps in their teaching practice

2.encouragement to seek feedback from students and the opportunity to discuss the feedback with experienced teachers to decide on the required strategy for improvement

3.facilitating the process by providing information about database such as the Campbell Collaboration (www.campbell.gse.upenn.edu) and Best Evidence Medical Education collaboration (www.bemecollaboration.org)

These are suggestions for creating a paradigm shift to encourage young doctors to look at teaching activities in the light of exsisting best evidence. Emphasis given to Medical Education in high impact journals will aid in achieving this goal.

Reference: 1.McGraw ME. Delivery of the paediatric curriculum of the Royal College of Paediatrics and Child Health (RCPCH). Arch Dis Child2009;94(4):254-7. 2.Bindal T, Wall D, Goodyear HM. Specialist registrars’ views on their teaching role. Arch Dis Child2009;94(4):311-3. 3.A Framework for Competences for Level 2 Training in Paediatrics, 2005 Royal College of Paediatrics and Child Health 4.BEME Guide No. 1: Best Evidence Medical Education. Medical Teacher, 1999 ;21 (6): 553 – 562 5.Dauphinee WD, Wood-Dauphinee S.The need for evidence in medical education: the development of best evidence medical education as an opportunity to inform, guide, and sustain medical education research. Acad Med. 2004;79(10):925-30.

Dear Editor.

Packman et al. responded to Howell et al.’s article (doi 10.1136/adc.2007.134114) on bilingualism and stuttering. We showed that speaking two languages in the preschool years increased the chances of children starting to stutter and decreased the likelihood of recovery from stuttering relative to speakers who learned English when they started school.

We do not consider, as Packman et al. suggest, that studying the general population of bilinguals would benefit the study of how speaking a second language affects stuttering. First, statistically speaking, demonstrating that bilingualism has no effect on stuttering, as the authors wish to do, is impossible. Also, investigating the general population of bilinguals is a flawed approach as bilingualism is massively heterogeneous within and between societies (including the US, Australia and Canada, where the authors work). Consequently, stringent controls (not biased sampling) have to be imposed in studies on bilingualism and stuttering. The controls we imposed excluded children who were brought up bilingual for social, educational or financial advantage. This reduced the heterogeneity in the bilingual sample. We compared bilinguals who had to use an additional language in the home with a matched sample who only spoke a language other than English in the home. The two groups of children selected for our study were directly comparable with respect to socio-economic status etc., and provided an appropriate sample on which to test the hypothesis of whether deferring learning English as a second language affected onset of stuttering and whether stuttering recovered. The same controls are appropriate for selecting similar groups for study across countries (unlike a sample from the general population of bilinguals at large).

They go on to state that our cohort is biased, and refer to a clinical study that followed up children from about age 3 to 8. 1 They say that the generally accepted age of stuttering onset is 3 years. However, the authoritative handbook in the area notes that the onset of developmental stuttering can occur at any age up to 13 years. 2 Consequently, studies that cease examination at age 8 bias estimates of age of onset to lower ages by excluding cases where onset occurs after age 8. They also incorrectly state that the gender ratio is 1:1 (there was a higher ratio of males/females in our study). All studies we are aware of (including the one they cited 1) show more males stutter than females. For example, the classic study by Andrews and Harris 3 from 2 to teenage reported a ratio of 2.4:1. A gender ratio of 1:1 suggests they are including children who do not stutter as stutterers (they have many false positives) and there is about an equal chance of misdiagnosis for each gender. The reasons for such misdiagnoses could be because they 4 use parental nominations for identifying cases and employ symptoms for diagnosing stuttering (whole word repetitions) that are excluded by several authorities. 5 6 7 The inclusion of these would lead to fluent children being classed as stutterers.

Packman et al. suggest that the Lidcombe program of therapy may be appropriate to treat bilingual children who stutter. However, the study they cited excluded children who did not have “proficiency in English” and there is no translation of the procedure into several of the languages spoken by our participants. In addition to the fact that they may be treating children who do not stutter, the statistical treatment in the study they cite has been faulted and long-term follow-up indicates that some “children [treated by Lidcombe] may start to stutter again”. 8

They state that an epidemiological study is appropriate to determine whether there is a relationship between stuttering and bilingualism. We have warned about the problems of grouping together heterogeneous bilinguals for study, as is necessary in epidemiological work. They overlook the fact that our work reported on the risk of starting to stutter and chance of recovery, using longitudinal data through to teenage. They suggest the onset age is about three years and that most recovery occurs in the first three years after onset. Conceivably, an epidemiological study at ages less than 8 could provide information about risk factors for onset of stuttering. However, it would not be informative about recovery since 50% of cases still stuttering at age 8 will recover 9 10, and recovery is not resolved until teenage. 3 9 10 Although epidemiological work does not require a longitudinal dimension, this is necessary when studying recovery, where results on the same speakers are needed in order to avoid biases. As in our study, they will need to use standardized instruments to establish persistence and recovery at teenage. If they intend to asses the impact bilingualism has on school performance, they will again need to extend examination to teenage.

In their last paragraph, they state that 4% stutter-like dysfluencies suggests our children would still be stuttering. Frequencies around this value have been used to differentiate young children who stutter from normally fluent speaking peers for English 1 and Dutch. 11 As discussed earlier, relatively high rates of supposed stuttering events may be due to inclusion of monosyllabic whole word repetitions, which are a common feature in fluent children’s and adults’ speech. 12

In summary, we consider our conclusions to be valid. Our experimental groups were matched appropriately and thoroughly documented with respect to language background and assessment for stuttering. The authors of the letter make statements that are contradicted in the literature. There are major faults in the way the authors of the letter propose to study the relationship between bilingualism and stuttering.

Acknowledgement This work was supported by grant 072639 from the Wellcome Trust to Peter Howell. Address Correspondence to: Peter Howell, Division of Psychology and Language Sciences, University College London, Gower Street, London WC1E 6BT, England. Email: p.howell@ucl.ac.uk

References

1Yairi E., Ambrose NG. Early childhood stuttering. Austin, TX: Pro- Ed, 2005.

2Bloodstein O., Bernstein Ratner N. A handbook on stuttering, 6th ed. Clifton Park, NY: Thomson, 2007.

3Andrews G., Harris M. The syndrome of stuttering. Clinics in Developmental medicine (No 17). London: Heinemann, 1964.

4Reilly S., et al. Predicting stuttering onset by the age of 3 years. Pediatrics, 2009;123:270-277.

5Conture EG. Stuttering. 2nd ed. Englewood-Cliffs: Prentice Hall; 1990.

6Ryan B. A longitudinal study of articulation, language, rate, and fluency of 22 preschool children who stutter. Journal of Fluency Disorders, 2001;26:107-127.

7Wingate ME. Foundations of stuttering. San Diego: Academic; 2002.

8Packman A., Kuhn L. Looking at stuttering through the lens of complexity. International Journal of Speech-Language Pathology, 2009;11:77– 82.

9Fritzell B. The prognosis of stuttering in schoolchildren: A 10-year longitudinal study. In Proceedings of the XVI Congress of the International Society of Logopedics and Phoniatrics, 186-187. Basel: Karger, 1976.

10Howell P, Davis S, Williams R. Late childhood stuttering. Journal of Speech Language and Hearing Research, 2008;51:669-687.

11 Boey et al., Characteristics of stuttering-like disfluencies in Dutch speaking older children, adolescents and adults. Journal of Fluency Disorders, 2007;32:310-329..

12 Levelt W. Speaking: From intention to articulation. Cambridge, MA: Bradford Books, 1989.

Peter Howell,

Stephen Davis,

Division of Psychology and Language Sciences, University College London, United Kingdom

Roberta Williams,

Department of Language and Communication Science, City University London, United Kingdom

Dear Sir, Some days ago we received a letter from colleagues in London asking us to comment on the article of Simeone and coll. reporting a lack of relationship between chronic constipation (CC) and cow’s milk allergy (CMA), recently published in ADC (1). Our English Colleagues referred that they had observed “dramatic cases” of chronic constipation unresponsive to laxative treatment which fully resolved on CM-free diet and as this is also our experience in many cases (2-5) they asked to “defend this truth”. However, we think that the study of Simeone and coll. is very different from our previous studies on CC and CMA. In their article (1) they investigated for an association between CC and atopic disease and to do this performed a series of IgE-mediated assays. It is, in part, not surprising that they did not find a more frequent association of atopy (positive assays and clinical history) in CC patients than in controls, as it is well known that the immunologic mechanisms of the majority of gastrointestinal manifestations of food allergy are not based on IgE- mediated mechanisms (6) and we ourselves have not found a higher frequency of positive IgE-based assays in patients with CC due to CMA. Thus, a lack of association between atopy or IgE-mediated assays and CC was to have been expected and does not mean that CC cannot be due to CMA. The only aspect of the Simeone study which could be compared with our and others’ previous studies (7-10), is that they placed eleven CC patients unresponsive to laxative treatment on CM-free diet. They found that none of these eleven patients improved on CM-free diet. On the basis of this very small patient sample they concluded that “the refractory constipation is not associated with CMA in the general paediatric population”. This could also be true in the general population, although we do have doubts about this, but more than eleven patients must be evaluated before a firm conclusion can be reached. What is certain is that in a tertiary gastroenterology clinic with experience in the food allergy-intolerance field – as ours is - the frequency of CC unresponsive to laxative treatments and due to food allergy is higher than one third of cases. Probably this high frequency is biased by the pre-selection of the patients referred to our clinic, but whatever the real frequency of the relationship between CC and food allergy may be, many prestigious research groups from England (7), the USA (10), Finland (11) and other centres world-wide (8,9) have reported results identical to ours and firmly confirmed that CC can be a manifestation of food allergy. Furthermore, the CC-CMA association has also been included in a review published in Gastroenterology (12). Finally, we recently suggested the possibility that the patients could be suffering from multiple food allergy and not simply from CM hypersensitivity. In fact, bowel movements normalised in some patients unresponsive to CM-free diet when they were placed on a more restricted oligoantigenic diet (5). Do paediatricians who first visit a child consider the hypothesis of CMA- related constipation? We believe they do, but this does not mean that a CM -free diet should be prescribed for every patient with CC. The first treatment approach must be a regular diet (water, fibre, etc) and laxatives. However, if the patient does not improve and especially when he/she has a previous history or a family history of CMA, the probability of a CMA diagnosis increases. In these cases a consultation with a specialist should be suggested and, after further evaluation, an elimination diet could be prescribed. We do not know how many paediatricians - or paediatric gastroenterologists - in the world use this approach, but we think there are too few. Despite the clear evidence, there are still many paediatricians who do not accept that CMA can be a cause of CC. The Naples Gastroenterology School is a medical teaching school which we have learned a great deal from and its members contribute to form opinions and guidelines in paediatric gastroenterology. Unfortunately, their experience with CC conflicts with the evidence in the literature about the relationship between CC and CMA and this certainly hinders the possibility of a correct treatment for patients with CC due to CMA. Our role can be to add further data to help better understand the problem and to offer further evidence of this relationship. Yours faithfully,

REFERENCES 1) Simeone D, Miele E, Boccia G, Marino A, Troncone R, Staiano A. Prevalence of atopy in children with chronic constipation. Arch Dis Child 2008;93;1044-1047 2) Iacono G, Carroccio A, Cavataio F, Montalto G, Cantarero MD, NotarbartoloA. Chronic constipation as a symptom of cow milk allergy. J Pediatr 1995; 126: 34–9. 3) Iacono G, Cavataio F, Montalto G, et al. Intolerance of cow’s milk and chronic constipation in children. N Engl J Med 1998; 338: 1100–4. 4) Carroccio A, Scalici C, Maresi M, et al. Chronic constipation and food intolerance: a model of proctitis causing constipation. Scand J Gastroenterol 2005; 40: 33–42 5) Iacono G, Bonventre S, Scalici C, et al. Food intolerance and chronic constipation: manometry and histology study. Eur J Gastroenterol Hepatol 2006; 18: 143–50. 6) Sampson H, Sicherer SH, Birnbaim AH. American Gastroenterological Association Medical Position Statement: guidelines for the evaluation of food allergies. Gastroenterology 2001; 120: 1023–5. 7) Shah N, Lindley K, Milla P. Cow’s milk and chronic constipation in children. N Engl J Med 1999; 340: 891–2. 8) Daher S, Sole` D, de Morais MB. Cow’s milk and chronic constipation in children. N Engl J Med 1999; 340: 891. 9) Daher S, Tahan S, Sole` D, et al. Cow’s milk protein intolerance and chronic constipation in children. Pediatr Allergy Immunol 2001; 12: 339–43. 10) Vanderhoof JA, Perry D, Hanner TL, Young RJ. Allergic constipation: association with infantile milk allergy. Clin Pediatr 2001; 40: 399–402 11) Turunen S, Karttunen TJ, Kokkonen J. Lymphoid nodular hyperplasia and cow’s milk hypersensitivity in children with chronic constipation. J Pediatr 2004; 145: 606–11. 12) Bischoff S, Crowe SE. Gastrointestinal food allergy: new insights into pathophysiology and clinical perspectives. Gastroenterology 2005; 128: 1089–113

Sir,

We understand the concerns of doctors Lin and Fu about reverse causation regarding the protective effect of fish on eczema at one year of age. We cannot, of course, be sure that reverse causation does not contribute to our results, but there are reasons that speak in favour of a real effect.

Firstly, we found no correlation between time of onset of the eczema and age at introduction of fish.

Secondly, when excluding infants with food-induced eczema, there was still a protective effect, as was the case when excluding infants with food allergy.

Thirdly, when excluding infants with onset of eczema before 4 months of age, there was still a protective effect in infants with later onset of eczema. Also, the protective effect was equal between infants with and without atopic heredity.

Furthermore, we are not the only group that has reported such effects. In the BAMSE study (1), Kull et al. found that fish consumption during the first year of life was protective against allergic disease at 4 years. In a Norwegian study (1), Øien et al. found that fish reduced the risk of having allergic disease at 2 years. Both studies excluded children with disease before one year of age to avoid reverse causation.

We are at this moment analysing the data from our follow-up when the children are 4.5 years old, and will hopefully be able to address the question further.

References:

1. Kull I, Bergström A, Lilja G, Pershagen G, Wickman M. Fish consumption during the first year of life and development of allergic diseases during childhood. Allergy. 2006;61:1009-15.

2. Øien T, Storrø O, Johnsen R. Fish and cod liver oil consumption during pregnancy and the first year of life and allergic diseases at 2 years of age. A prospective birth cohort study. XXVII Congress of the European Academy of Allergology and Clinical Immunology, Barcelona. [Abstract]. 2008.

Yours sincerely,

Bernt Alm MD PhD, Nils Åberg MD PhD, Laslo Erdes MD, Per Möllborg MD, Rolf Pettersson MD, Gunnar Norvenius MD PhD, Emma Goksör MD, and Göran Wennergren MD PhD.

Competing interests: none