Picky eating (also known as fussy, faddy or choosy eating) is usually classified as part of a spectrum of feeding difficulties. It is characterised by an unwillingness to eat familiar foods or to try new foods, as well as strong food preferences. The consequences may include poor dietary variety during early childhood. This, in turn, can lead to concern about the nutrient composition of the diet and thus possible adverse health-related outcomes. There is no single widely accepted definition of picky eating, and therefore there is little consensus on an appropriate assessment measure and a wide range of estimates of prevalence. In this review we first examine common definitions of picky eating used in research studies, and identify the methods that have been used to assess picky eating. These methods include the use of subscales in validated questionnaires, such as the Children's Eating Behaviour Questionnaire and the Child Feeding Questionnaire as well as study-specific question(s). Second, we review data on the prevalence of picky eating in published studies. For comparison we present prevalence data from the UK Avon Longitudinal Study of Parents and Children (ALSPAC) in children at four time points (24, 38, 54 and 65 months of age) using a study-specific question. Finally, published data on the effects of picky eating on dietary intakes (both variety and nutrient composition) are reviewed, and the need for more health-related data and longitudinal data is discussed.
5 November 2018 in Proceedings of the Nutrition Society
Picky eating is a common behaviour in early childhood. There is neither a universally accepted definition of picky eating, nor is there agreement on the best tool to identify it. Causes of picky eating include early feeding difficulties, late introduction of lumpy foods at weaning, pressure to eat and early choosiness, especially if the mother is worried by this; protective factors include the provision of fresh foods and eating the same meal as the child. The consequences for the child's diet include poor dietary variety and a possible distortion of nutrient intakes, with low intakes of iron and zinc (associated with low intakes of meat, and fruit and vegetables) being of particular concern. Low intakes of dietary fibre, as a result of low intakes of fruit and vegetables, are associated with constipation in picky eaters. There may be developmental difficulties in some children with persistent picky eating. There is little evidence, however, for a consistent effect of being a picky eater on growth trajectories. There may be a small subgroup of children in whom picky eating does not resolve who might be at risk of thinness during adolescence, or of developing an eating disorder or adult picky eating: these children need to be identified at an early age to enable support, monitoring and advice to be offered to parents. Strategies for avoiding or ameliorating picky eating include repeated exposures to unfamiliar foods, parental modelling of eating fruit and vegetables and unfamiliar foods, and the creation of positive social experiences around mealtimes.
1 March 1991 in The American Journal of Clinical Nutrition
The mechanisms involved in the homeostatic regulation of zinc were studied in five male subjects by using stable 70Zn as a marker. When dietary zinc was reduced from 85 to 12 /imol/d, adaptation was achieved by a mean (±SEM) reduction in urine zinc of 48 ± 7% and in fecal zinc of 46 ± 12% over 25 d in four subjects. The latter was caused by an increase in the efficiency of zinc absorption from 38 ± 3% to 93 ± 1% after 15 d of zinic deprivation and by a reduction in intestinal endogenous losses of zinc. In a fifth subject, who had some evidence of a resolving alcohol-induced hepatitis, urine and fecal zinc were reduced by 64% and 41%, respectively, in 15 d and zinc absorption increased from 46% to 93%. More information on adaptive responses is needed to enable current dietary recommendations to be reconsidered.
Neurodevelopmental delays can interfere with children’s engagement with the world and further development, and may have negative consequences into adulthood. Mercury is highly toxic and may negatively influence neurodevelopment because it can freely cross the placenta and accumulate in the fetal brain. We searched four publication databases (Embase, PsycINFO, PubMed/MEDLINE, Scopus) for studies examining the relationship between early life mercury exposure and scores on neurodevelopmental performance measures in children aged 0 to 5 years old. Study quality was assessed using the National Institutes of Health (NIH) Quality Assessment Tool. Thirty-two prospective studies were included in the review. Neurodevelopmental performance was measured using 23 different scales, most commonly the Bayley Scales of Infant and Toddler Development (BSID). In most cases, the evidence for an association between mercury and neurodevelopment was weak. There did not appear to be exceptions for particular childhood ages, outcome scales, or mercury levels. The small number of results to the contrary were more likely to be studies which did not meet our high-quality criteria, and could be a consequence of multiple testing, selection bias, or incomplete confounder adjustment. Based on current evidence, dietary mercury exposure during pregnancy is unlikely to be a risk factor for low neurodevelopmental functioning in early childhood.
1 December 2016 in The American Journal of Clinical Nutrition
Lead is a widespread environmental toxin. The behaviour and academic performance of children can be adversely affected even at low blood lead levels (BLL) of 5–10 µg/dl. An important contribution to the infant's lead load is provided by maternal transfer during pregnancy. Our aim was to determine BLL in a large cohort of pregnant women in the UK and to identify the factors that contribute to BLL in pregnant women. Pregnant women resident in the Avon area of the UK were enrolled in the Avon Longitudinal Study of Parents and Children (ALSPAC) in 1991–1992. Whole blood samples were collected at median gestational age of 11 weeks and analysed by inductively coupled plasma dynamic reaction cell mass spectrometry (n = 4285). Self-completion postal questionnaires were used to collect data during pregnancy on lifestyle, diet and other environmental exposures. Statistical analysis was carried out with SPSS v19. The mean±SD BLL was 3.67±1.47 (median 3.41, range 0.41–19.14) µg/dl. Higher educational qualification was found to be one of the strongest independent predictor of BLL in an adjusted backwards stepwise logistic regression to predict maternal BLL <5 or ≥5 µg/dl (odds ratio 1.26, 95% confidence interval 1.12–1.42; p<0.001). Other predictive factors included cigarette smoking, alcohol and coffee drinking, and heating the home with a coal fire, with some evidence for iron and calcium intake having protective effects. The mean BLL in this group of pregnant women is higher than has been found in similar populations in developed countries. The finding that high education attainment was independently associated with higher BLL was unexpected and currently unexplained. Reduction in maternal lead levels can best be undertaken by reducing intake of the social drugs cigarettes, alcohol and caffeine, although further investigation of the effect of calcium on lead levels is needed.