ACKNOWLEDGEMENTS The research reported was supported by grants from BLISS, the preterm infant charity; the Health Foundation; and Well-Being of Women (Drs Marlow and Wolke). The EPICure Investigator Group included K Costeloe (London), A T Gibson (Sheffield), E M Hennessy (London), N Marlow (Nottingham), A R Wilkinson (Oxford), and D Wolke (Warwick).
Eating problems at age 6 years in a whole population sample of extremely preterm children
Article first published online: 13 OCT 2009
© The Authors. Journal compilation © Mac Keith Press 2009
Developmental Medicine & Child Neurology
Volume 52, Issue 2, pages e16–e22, February 2010
How to Cite
SAMARA, M., JOHNSON, S., LAMBERTS, K., MARLOW, N. and WOLKE, D. (2010), Eating problems at age 6 years in a whole population sample of extremely preterm children. Developmental Medicine & Child Neurology, 52: e16–e22. doi: 10.1111/j.1469-8749.2009.03512.x
- Issue published online: 15 JAN 2010
- Article first published online: 13 OCT 2009
- PUBLICATION DATA Accepted for publication 3rd August 2009. Published online.
Aim The aim of this study was to investigate the prevalence of eating problems and their association with neurological and behavioural disabilities and growth among children born extremely preterm (EPC) at age 6 years.
Method A standard questionnaire about eating was completed by parents of 223 children (125 males [56.1%], 98 females [43.9%]) aged 6 years who were born at 25 weeks’ gestation or earlier (mean 24.5wks, SD 0.7wks; mean birthweight 749.1g, SD 116.8g), and parents of 148 classmates born at term (66 males [44.6%], 82 females [55.4%]). All children underwent neurological, cognitive, and anthropometric assessment, and parents and teachers completed a behaviour scale.
Results Eating problems were more common among the EPC than the comparison group (odds ratio [OR] 3.6, 95% confidence interval [CI] 2.1–6.3), including oral motor (OR 5.2, 95% CI 2.8–9.9), hypersensitivity (OR 3.0, 95% CI 1.6–5.6), and behavioural (OR 3.8, 95% CI 1.9–7.6) problems. Group differences were reduced after adjustment for cognitive impairment, neuromotor disability, and other behaviour problems. EPC with eating problems were shorter, lighter, and had lower mid-arm circumference and lower body mass index (BMI) even after adjusting for disabilities, gestational age, birthweight, and feeding problems at 30 months.
Interpretation Eating problems are still frequent in EPC at school age. They are only partly related to other disabilities but make an additional contribution to continued growth failure and may require early recognition and intervention.
Body mass index
Extremely preterm children
Surviving extremely preterm infants are at significantly increased risk of long-term cognitive, motor, or behavioural impairments.1–3 Preterm infants often have feeding problems while in neonatal care, including swallowing problems, oral sensory and motor dysfunction, or fatigue during feeding. Problems experienced after discharge include delayed feeding skill development, food refusal,4 and difficulty with the transition to solid foods, often accompanied by growth faltering.5 Reasons proposed for these difficulties include immaturity and treatment related to preterm birth including parenteral or tube feeding, adverse oral motor experiences,6 and postdischarge health problems, such as neurological or cognitive disabilities. All of these could complicate the child’s eating skill development and result in increased parental distress, depression, and lack of confidence in feeding.7
There are few estimates concerning the prevalence of feeding problems of extremely preterm infants, and none at school age,4 despite eating remaining a primary concern for parents post discharge.8 Furthermore, it is unclear whether eating problems are specific or can be fully or mostly accounted for by general cognitive deficits or neuromotor or other behavioural problems often found in EPC.1,3
In this report, we describe eating behaviour at age 6 years among children born at a gestational age of 25 weeks or less in a whole-population study. We aimed to answer three questions. First, is the prevalence of clinically relevant eating problems higher in EPC than in children born at term? Second, can eating problems be accounted for by comorbidity, including cognitive deficits or other neurological or behavioural disabilities? And, third, do eating problems in the clinical range have a significant impact on attained growth (height, weight, head circumference, mid-arm circumference, and body mass index) at age 6 years?
The population comprised all surviving children in the UK and Ireland born at or before 25 weeks and 6 days of gestation during the period March to December 1995 (the EPICure study3). A total of 308 children were known to be alive at 30 months. Of these, the parents of 241 children (78%) consented to the study, of whom 223 (72%) completed the eating questionnaire. The majority of the children (204/241) were in mainstream education. For each child assessed in mainstream school, we sought an age- and sex-matched classmate as a comparison.3 The eating questionnaire was completed by the parents of 148 children in the comparison group.
This study was approved by the Trent Multicentre Research Ethics Committee and the local education authorities in Scotland.
Feeding and eating behaviour assessment
When the children were 30 months of age, their parents were asked, in a single item, whether their children had any feeding problems.9 At 6 years of age, the parents completed a specially developed eating questionnaire designed on the basis of a comprehensive review of the type of eating problems in studies of the general population.6 The scale included 19 items (see Appendix S1, supporting information published online). A principal component factor analysis with varimax rotation yielded four factors with distinct high loadings of 0.48 or higher and acceptable eigenvalues >1: refusal–faddy eating problems (seven items, e.g. refuses to eat, is a faddy eater); oral motor problems (six items, e.g. dribbles when drinking, has problems with biting crackers); oral hypersensitivity problems (two items, e.g. does not like things to be put in his/her mouth); and behavioural problems around meals (four items, e.g. makes a mess, has tantrum during meals). A total eating-difficulties score was also constructed (higher scores on each scale indicate more problems; see Appendix S1 for the Cronbach’s α of total eating problems and each subscale).
To derive clinical categories, each scale was dichotomized into normal versus clinical (score above the 90th centile or near according to the comparison group), as suggested by other standard behaviour scales.1 If the child scored below the 90th centile, the eating behaviour was considered normal (no eating difficulty). Parents were also asked whether or not they felt that their child had an eating problem (mild or severe) and if the eating difficulties upset or distressed their child (a little, quite a lot, or a great deal).
Pervasive behaviour problems
Child behaviour was reported by parents and teachers.1 Using the Strengths and Difficulties Questionnaire,10 Child behaviour was classified as follows: if the child scored below the 90th centile in both the parent and the teacher report, the behaviour was considered normal (no behaviour difficulty); mild difficulty refers to the classification of the child in the clinical range (above the 90th centile) as reported by either the parent or the teacher; and clinical pervasive behaviour problems refers to the classification of the child in the clinical range by both the parent and the teacher.1
Children were assessed with the Kaufman Assessment Battery for Children at 6 years of age.11 The Mental Processing Component provides an ‘overall cognitive score’.2 Cognitive impairment was categorized according to conventional SD-banded cut-offs using the scores of the comparison group as reference data (mild, 1–2SD below the mean; moderate, 2–3SD below the mean; severe, more than 3SD below the mean).
Disability classification (neurological assessment)
Mild disability included neurological signs with minimal functional consequences. Moderate disability included reasonable independence and ambulant CP. Severe disability included non-ambulant CP (see Table II).3
The weight of individuals was measured on identical weighing scales (Salter Housewares Ltd, Kent, UK), height using a standard stadiometer (Child Growth Foundation, London, UK), and maximum occipitofrontal head circumference and mid-arm circumference using a LASSO-O tape (Child Growth Foundation). Each measure was taken twice and the mean value computed. Body mass index (BMI) was computed as weight/height2 (kg/m2).
The children were assessed by seven experienced developmental paediatricians and eight psychologists, who received formal training. Assessment sessions of every second child were videotaped and randomly quality checked by the senior assessment paediatrician or psychologist (agreement >90%).
Analysis of variance (anova) was used to compare the EPC and comparison groups and to compare males with females in each group (with effect sizes reported as η2). Categorical outcomes were evaluated with χ2 tests for trends or Fisher’s exact test as appropriate (Statistical Package for the Social Sciences 15.0; SPSS Inc., Chicago, IL, USA). All statistical tests were two-sided. Odds ratios and 95% confidence intervals (CIs) are reported for the comparison of EPC and classmates and for the comparison of males and females in each group. The 95% CIs were obtained using bootstrapping (20 000 bootstrap samples, using the bias-corrected and accelerated method in MatLab R2009a [the Statistics Toolbox for MatLab]12,13). Odds ratios approximated risk ratios when the incidence of the outcome in the study population (comparison group) was low (<0.10%).14 Selective dropout was determined by comparing neonatal, 12-month, and 30-month follow-up data of those assessed at 6 years and those who were lost to follow-up. To test for the presence of specific eating problems, logistic regressions adjusted for cognitive disability (no/mild vs moderate/severe), neuromotor disability (no vs others), or pervasive behaviour disability (no vs mild/severe) were computed. In the EPC group logistic regressions were also performed to test whether eating difficulties predict parents’ acknowledgement of eating problems and of their child’s distress in the EPC group. Correlations and partial correlations (adjusting for disabilities, gestational age, birthweight, and feeding problems at 30mo) were performed to test the relationship between total eating problems and growth measures. Graph Pad Prism 5 software (GraphPad Software Inc., San Diego, CA, USA) was used to design the graphs.
Children lost to follow-up (dropouts)
Compared with children who were assessed, dropouts (maximum n=85) were more likely to be of non-white ethnic origin (34.1/100 vs 18.9/100; p=0.004), to have young mothers (≤21y age: 24.7/100 vs 9.4/100; p=0.001), to live in overcrowded homes (49.4/100 vs 21.5/100; p<0.001), to have experienced more than one serious life event by 30 months (48.2/100 vs 23.3/100, p<0.001), to suffer from cerebral palsy (CP) at 30 months (30.8/100 vs 15.6/100; p=0.007), to have a lower psychomotor development index score (PDI mean 78.7 vs 84.8; p=0.015), to have more feeding problems (42.4/100 vs 30.4/100; p=0.049), and to be diagnosed with overall severe disability (40/100 vs 25/100; p=0.014) at 30 months of age. No differences were found in any of the assessed nine neonatal complications (e.g. prenatal steroid treatment), five other socio-economic factors (e.g. mother is single or separated), and six developmental and growth parameters (e.g. weight, height) up to 30 months.1,3
Eating behaviour differences
Total eating problems were more common in the EPC group than in the comparison group according to the total eating problems scale (p<0.001; effect size=0.080; Table I). This was also true for the oral motor (p<0.001; effect size=0.099), refusal–faddy (p=0.026; effect size=0.016), behavioural (p<0.001; effect size=0.076), and hypersensitivity (p<0.001; effect size=0.052) subscales. Males were found to have more oral motor difficulties (p=0.001; effect size=0.124) and behavioural problems (p=0.013; effect size=0.087) than females (Table I). The interaction between group and sex was not significant.
|Eating difficulties||Comparison group||Extremely preterm group||Odds ratio for clinical range (95% CI)a|
|Number/number with information||Mean (SD)||Clinical range (%)||Number/number with information||Mean (SD)||Clinical range (%)|
|Total eating difficulties||19/148||6.1 (4.9)b||12.8b||76/218||10.0 (7.4)b||34.9b||3.6 (2.1–6.5)|
|Males||8/66||6.1 (5.1)||12.1b||43/122||10.5 (7.3)||35.2b||3.9 (1.7–9.0)|
|Females||11/82||6.1 (4.7)||13.4c||33/96||9.4 (7.5)||34.4c||3.4 (1.6–7.2)|
|Oral motor difficulties||13/148||0.4 (1.0)b||8.8b||72/215||1.8 (2.5)b||33.5b||5.2 (2.8–10.3)|
|Males||9/66||0.6 (1.3)c||13.6b||49/120||2.2 (2.7)c||40.8b||4.4 (1.9–9.6)|
|Females||4/82||0.3 (0.6)c||4.9b||23/95||1.4 (2.3)c||24.2b||6.2 (2.1–18.9)|
|Refusal–faddy problems||16/148||3.9 (3.5)d||10.8||38/223||4.9 (4.0)d||17.0||1.7 (0.9–3.3)|
|Males||7/66||3.6 (3.4)||10.6||19/125||4.8 (3.7)||15.2||1.5 (0.6–3.8)|
|Females||9/82||4.3 (3.5)||11.0||19/98||5.3 (4.3)||19.40||1.9 (0.8–4.6)|
|Behavioural problems||14/148||1.4 (1.4)b||9.5b||52/219||2.3 (1.7)b||23.7b||3.0 (1.6–5.8)|
|Males||6/66||1.6 (1.4)d||9.1c||31/123||2.5 (1.8)d||25.2c||3.4 (1.3–8.5)|
|Females||8/82||1.3 (1.4)d||9.8d||21/96||2.1 (1.7)d||21.9d||2.6 (1.1–6.2)|
|Hypersensitivity problems||11/148||0.1 (0.5)b||7.4b||50/213||0.5 (1.0)b||23.5b||3.8 (1.9–8.0)|
|Males||6/66`||0.1 (0.4)||9.1c||35/120||0.6 (1.1)||29.2c||4.1 (1.6–10.4)|
|Females||5/82||0.1 (0.5)||6.1d||15/93||0.4 (0.9)||16.1d||2.9 (1.0–8.5)|
Total eating difficulties in the clinical range were also more frequent in the EPC group than in the comparison group (odds ratio [OR] 3.6; 95% CI 2.1–6.3; p<0.001), as were oral motor problems (OR 5.2; 95% CI 2.8–9.9; p<0.001), behavioural problems (OR 3.0; 95% CI 1.6–5.6; p<0.001), and hypersensitivity problems (OR 3.8; 95% CI 1.9–7.6; p<0.001; Table I).
Both males and females in the EPC group had more total eating difficulties (males p<0.001; females p=0.001), oral motor problems (p<0.001), behavioural problems (males p=0.005; females p=0.023), and hypersensitivity problems (males p=0.001; females p=0.031) than their sex-matched counterparts in the comparison group (Table I). Within the EPC group, males were more likely than females to have oral motor problems (OR 2.2; 95% CI 1.2–3.9; p=0.007) and more often had hypersensitivity problems (OR 2.1; 95% CI 1.1–4.2; p=0.019).
Gestation, disability, and eating difficulties
In the EPC group, there were significant associations between gestation at birth and total eating difficulties (p=0.003) and hypersensitivity problems (p=0.038; Table II). Cognitive impairment and neuromotor disability were associated with an increased prevalence of clinical oral motor problems (p=0.022, p<0.001 respectively) and hypersensitivity problems (p<0.001, p<0.001 respectively). Pervasive behaviour difficulties showed significant associations with eating problems on all scales: total eating difficulties (p<0.001), oral motor problems (p=0.001), refusal–faddy problems (p=0.010), behavioural eating problems (p<0.001), and hypersensitivity problems (p=0.001) were all in the clinical range (Table II).
|Total eating difficulties (n=218)||Oral motor problems (n=215)||Refusal–faddy problems (n=223)||Behavioural problems (n=219)||Hypersensitivity problems (n=213)|
|Normal||Clinical range||Normal||Clinical range||Normal||Clinical range||Normal||Clinical range||Normal||Clinical range|
|Gestational age (wks)|
|≤23||13 (59.1)||9 (40.9)a||12 (60)||8 (40)||19 (86.4)||3 (13.6)||14 (63.6)||8 (36.4)||18 (81.8)||4 (18.2)b|
|24||34 (50)||34 (50.0)||39 (59.1)||27 (40.9)||57 (83.8)||11 (16.2)||50 (74.6)||17 (25.4)||41 (65.1)||22 (34.9)|
|25||95 (74.2)||33 (25.8)||92 (71.3)||37 (28.7)||109 (82)||24 (18)||103 (79.2)||27 (20.8)||104 (81.3)||24 (18.8)|
|No disability (score >94)||44 (68.8)||20 (31.3)||46 (71.9)||18 (28.1)b||54 (84.4)||10 (15.6)||53 (85.5)||9 (14.5)||57 (90.5)||6 (9.5)c|
|Mild disability (score 82–94)||49 (71)||20 (29)||51 (75)||17 (25)||57 (80.3)||14 (19.7)||52 (75.4)||17 (24.6)||54 (80.6)||13 (19.4)|
|Moderate disability (score 70–81)||27 (60)||18 (40)||28 (62.2)||17 (37.8)||34 (73.9)||12 (26.1)||31 (67.4)||15 (32.6)||35 (81.4)||8 (18.6)|
|Severe disability (score ≤69)||22 (55)||18 (45)||18 (47.4)||20 (52.6)||40 (95.2)||2 (4.8)||31 (73.8)||11 (26.2)||17 (42.5)||23 (57.5)|
|No disability||113 (66.1)||58 (33.9)||125 (74)||44 (26)c||141 (82)||31 (18)||134 (79.8)||34 (20.2)||135 (81.6)||30 (18.2)c|
|Abnormal signs||14 (66.7)||7 (33.3)||10 (47.6)||11 (52.4)||18 (81.8)||4 (18.2)||13 (59.1)||9 (40.9)||14 (70)||6 (30)|
|CP ambulatory||10 (66.7)||5 (33.3)||7 (50)||7 (50)||15 (100)||0 (0)||10 (66.7)||5 (33.3)||10 (66.7)||5 (33.3)|
|CP, non-ambulatory||5 (45.5)||6 (54.5)||1 (9.1)||10 (90.9)||11 (78.6)||3 (21.4)||10 (71.4)||4 (28.6)||4 (30.8)||9 (69.2)|
|Pervasive total difficulties (SDQ)|
|No disability||89 (80.9)||21 (19.1)c||85 (78.7)||23 (21.3)c||100 (90.9)||10 (9.1)b||103 (93.6)||7 (6.4)c||94 (85.5)||16 (14.5)a|
|Mild disability||36 (50.7)||35 (49.3)||40 (57.1)||30 (42.9)||56 (75.7)||18 (24.3)||43 (60.6)||28 (39.4)||49 (74.2)||17 (25.8)|
|Severe disability||17 (47.2)||19 (52.8)||18 (50)||18 (50)||28 (75.7)||9 (24.3)||20 (55.6)||16 (44.4)||20 (55.6)||16 (44.4)|
Group differences in hypersensitivity and behavioural problems between EPC and comparison children became non-significant after adjustment for cognitive abilities, neuromotor disability, and pervasive behavioural difficulties together (Table III). In contrast, even after adjustment for all variables, total eating difficulties and oral motor problems still differed between EPC and comparison children, and are thus only partly explained by these disabilities.
|Unadjusted (95% CI)||Adjusted for categorized MPCa (95% CI)||Adjusted for neuromotor (95% CI)||Adjusted for pervasive total behaviour difficulties – SDQa (95% CI)||Adjusted for all variables (95% CI)b|
|Total eating difficulties||3.6 (2.1–6.5)c||3.0 (1.6–5.5)c||3.5 (1.9–6.4)c||2.7 (1.5–5.0)d||2.5 (1.3–4.8)d|
|Oral motor problems||5.2 (2.8–10.3)c||3.7 (1.8–7.8)c||3.6 (1.8–7.4)c||4.1 (2.2–8.2)c||2.7 (1.3–5.7)d|
|Refusal–faddy problems||1.7 (0.9–3.3)||1.8 (0.9–3.6)||1.8 (0.9–3.6)||1.3 (0.7–2.6)||1.6 (0.8–3.3)|
|Behavioural problems||3.0 (1.6–5.8)d||2.4 (1.2–5.0)e||2.4 (1.2–5.0)d||1.7 (0.8–3.5)||1.6 (0.7–3.6)|
|Hypersensitivity problems||3.8 (1.9–8.0)c||2.5 (1.1–6.0)e||2.8 (1.3–6.3)d||3.0 (1.5–6.4)d||1.9 (0.8–4.7)|
Table IV shows that in the EPC group total eating difficulties and the subscales significantly predicted parents’ judgement of significant eating difficulties and their child’s distress.
|Parents’ acknowledgement of eating problems (95% CI)||Distress (95% CI)|
|Total eating difficulties||1.4 (1.3–1.6)a||1.3 (1.1–1.4)a|
|Oral motor problems||1.6 (1.3–1.9)a||1.5 (1.2–2.0)a|
|Refusal–faddy problems||1.6 (1.4–1.8)a||1.2 (1.01–1.4)b|
|Behavioural problems||1.8 (1.5–2.2)a||1.5 (1.1–2.2)b|
|Hypersensitivity problems||2.2 (1.7–3.1)a||1.8 (1.1–3.1)c|
Eating problems and growth parameters
Attained growth was significantly poorer in EPC without eating problems (normal range) than in the comparison children without eating problems in terms of weight (mean difference 2.6kg; 95% CI 1.6–3.7kg; p<0.001; Fig. 1), height (mean difference 3.1cm; 95% CI 1.6–4.6cm; p<0.001), head circumference (mean difference 1.4cm 95% CI 1.03–1.8cm; p<0.001), and mid-arm circumference (mean difference 1.2cm 95% CI 0.7–1.7cm; p<0.001). In addition, BMI was lower in the EPC group (mean difference 1.2; 95% CI 0.8–1.7; p<0.001; see appendix S2, supporting information published online). Among children with eating problems (clinical range), mean differences between EPC and comparison children were even greater for height (4.2cm; 95% CI 1.2–7.1cm; p=0.006) and head circumference (1.7cm; 95% CI 0.8–2.6cm; p<0.001; Appendix S2). In contrast, differences in weight (2.1kg; 95% CI 0.5–3.7kg; p=0.013; Fig. 1), mid-arm circumference (0.8cm; 95% CI 0.04–1.6cm; p=0.049), and BMI (0.7; 95% CI: 0.07–1.3; p=0.029) were similar between the two groups without eating problems.
Among the EPC group, children with eating problems weighed less (mean difference 1.1kg; 95% CI 0.09–2.1kg; p=0.033 Fig. 1) and had smaller heads (mean difference 0.6cm; 95% CI 0.2–1.1cm; p=0.009) and lower BMI (mean difference 0.5; 95% CI 0.04–0.96; p=0.032) than children without eating problems (Appendix S2), but no significant difference in height and mid-arm circumference was found. In contrast, among the comparison group, only BMI was lower in those with eating problems than in those without (mean difference 1.1; 95% CI 0.1–2.0; p=0.028).
Correlations of total eating problems and growth parameters amongst EPC indicated that, with increasing eating problems, EPC were lighter (Spearman’s ρ=−0.242, n=223, p<0.001) and shorter (ρ=−0.232, n=220, p<0.001) and had smaller head circumference (ρ=−0.211, n=221, p=0.002), smaller mid-arm circumference (ρ=−0.165, n=221, p=0.014), and lower BMIs (ρ=−0.164, n=220, p=0.015). The partial correlations remained significant between total eating problems and weight (r=−0.204, n=203, p=0.003), height (r=−0.149, n=203, p=0.033), mid-arm circumference (r=−0.156, n=203, p=0.025), and BMI (r=−0.162, n=203, p=0.021), even when adjusting for gestational age, birthweight, feeding problems at 30 months, and cognitive, neuromotor, and pervasive behaviour disabilities, but were no longer significant for head circumference (r=−0.087, n=213, p=0.213).
In this whole population cohort of EPC, we found a considerable excess of eating problems. These difficulties continue to cause significant distress and are perceived as significant problems by parents. Total eating problems at 6 years of age in EPC are only partly explained by other disabilities; in particular, differences with comparison children in total and oral motor problems remain after adjustment for disabilities. The eating problems in EPC significantly correlate with poorer attained growth at 6 years of age beyond the prediction afforded by disabilities, gestation, birthweight, and early feeding problems.
Among EPC, both males and females were more likely to have eating problems than their classmates. However, as previously shown,2,3 among EPC, cognitive and neurological problems were twice as frequent in males as in females, which partly explains the sex difference in oral hypersensitivity. Males in the EPC group were also more likely than females to suffer oral motor problems, an indicator of generally more delayed development in males than in females. Our findings also show that oral motor dysfunction persists beyond infancy7 in one-third of EPC. Furthermore, oral hypersensitivity and behavioural eating problems are still found in one-quarter of EPC at early school age, whereas food refusal or faddy eating is only slightly more common. Infants and toddlers with neurological impairments4,15 are more likely to experience eating problems and have more difficulty in dealing with highly textured food. Our findings indicate that EPC with neurological or cognitive disabilities, which often occur together,3 contribute to, but do not fully account for, eating problems observed.15 In particular, oral motor problems and oral hypersensitivity are increased in children with CP15 (found in 12/100 of EPC).3 Furthermore, learning disabilities,* as indicated by low cognitive scores, are associated with overall, and specifically oral motor and hypersensitivity, eating problems but do not explain them.16 Although impaired oral motor eating skills are transient and resolve in some extremely preterm infants, in others they may be early indicators of neurodevelopmental impairment17 due to brain damage,18 with both the neurodevelopmental and eating problems persisting. The more preterm the infant, the longer the dependency on tube feeding. As shown here, those infants born at extremely low gestation with neurodevelopmental problems are at greatest risk of developing tactile defensiveness and oral hypersensitivity.6,19
In contrast, refusal to eat, the most frequent problem encountered in general population samples of infants,20 was only slightly more common in EPC than in children in the comparison group. Refusal to eat is often related to difficult and irregular temperament and negative emotionality,21 and frequently leads to higher levels of conflict, non-contingency, and maternal intrusiveness during feeding interactions,22 thus resulting more often in secondary problems, including hyperactive behaviour23 or distress.24 The behavioural eating problems were explained by general behavioural problems of the children both at home and at school, rather than confined to the eating situation. This is another indicator that the pervasive and multiple problems common among EPC,1,2 rather than parenting difficulties, are a major contributor to eating problems in these children. Nevertheless, the eating and, in particular, the behavioural and oral hypersensitivity problems were perceived by parents as difficulties and as distressing. Thus, eating problems put an additional burden on the families of EPC with impairment.25
EPC (with and without eating problems) were smaller than comparison children.26 However, EPC with eating problems were significantly smaller and had less muscle mass than those without eating problems. In particular, poor weight gain and the development of muscle was lowest among EPC with eating problems, as reported previously.4,9 The relationship of eating problems to poor growth in our study was not explained by other disabilities, gestation, birthweight, or more physical activity (i.e. hyperactivity). Thus, although disabilities partly contribute to eating problems, it appears that the poor nutritional intake associated with eating problems in EPC explains some of the growth deficits in these children. Eating problems in infants are highly persistent throughout childhood27 and have been found to increase the risk of other cognitive, behavioural, and psychosocial problems28 in general population samples owing to malnutrition. Thus, even in children with significant disability, rectifying eating problems may potentially improve their growth and possibly their cognitive development.29
Overall, considering the stress caused to the child and caregiver, eating problems are not trivial for the families.30 Interventions suggested include oral motor therapy to reduce oral motor deficits and oral hypersensitivity.31 Furthermore, Fucile et al.32 have shown that intervention before the transition from tube to oral feeding may prevent some of the ‘early’ feeding difficulties in preterm children. On the other hand, behavioural therapy can be effective in treating behavioural eating problems.15 Early advice and support to parents whose preterm infants experience eating problems may reduce perceived eating difficulties33 and increase parental confidence in parenting and nurturing their children.
This study has a number of strengths, including its large sample size and the inclusion of a comparison group from the same neighbourhood. The logistic regressions before and after adjusting for disability factors included bootstrapping to determine 95% CIs, and they provided very similar values to those produced by SPSS but safer estimates of effect size ranges. Limitations are that we were unable to recruit a comparison child for each preterm child in mainstream classes.3 Previous research34 has shown that eating disorder questionnaires and interviews are highly correlated but may slightly overestimate the rate of eating problems.35 A structured feeding assessment including direct observation or structured testing of oral motor skills36 would have been desirable but was not feasible within a half-day comprehensive psychological and medical examination. Furthermore, those participants who did not attend the assessments were more likely to be from socially disadvantaged families. Although there was no difference regarding medical variables, early feeding behaviour, or growth, CP and overall disability were more frequent in those lost to follow-up than those assessed.1,3 Thus, the rate of eating problems reported here, often associated with another disability or social deprivation,15 is likely to be an underestimate of the true rate in the total EPC population.37
In conclusion, at school age, EPC still have a two to five times increased risk of eating problems, and these are only partly accounted for by coexisting neurological, developmental, or pervasive behavioural impairments. Eating problems in EPC increase the risk of growth problems. Clinicians should be aware of the distress caused to the children and families, and early intervention, identification, and referral may alleviate some of the problems for the children and caregivers.38
North American usage: mental retardation.
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- 11Kaufman Assessment Battery for Children. Circle Pines, MN: American Guidance Service, 1983., .
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- 17Developmental outcome for neonates with dysfunctional and disorganized sucking patterns: preliminary findings Infant-Toddler Intervention. Transdisciplinary J 1999; 9: 299–308., .
- 18A pilot study of oral-motor dysfunction in ‘at risk’ infants. Paediatrics 1985; 5: 13–25., .
- 20The management of infant feeding problems. In: CooperPJ, SteinA, editors. Childhood Feeding Problems and Adolescent Eating Disorders. London: Routledge, 2006: 41–91., , .
- 31The therapeutic approach to the child with feeding difficulty. II. Management and treatment. In: SullivanPB, RosenbloomL, editors. Feeding the Disabled Child. London: Mac Keith Press, 1996; pp 117–32., .
- 38Frequent problems in infancy and toddler years: excessive crying, sleeping and feeding difficulties. In: BergmannKE, BergmannRL, editors. Health Promotion and Disease Prevention in the Family. Berlin: De Gruyter, 2003: 44–88..
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