Background: Dietary restriction during infancy may influence later eating behaviour. The aim of this study was to determine whether consuming a cows' milk exclusion (CME) diet during infancy affects eating habits in later childhood, once cows' milk has been reintroduced into the diet.
Methods: Children were recruited from two large birth cohort studies in the UK. A small number of participants were recruited from allergy clinic. Two groups were recruited: an experimental group of children who had consumed a CME diet during infancy and a control group, who had consumed an unrestricted diet during infancy. Parents and children completed questionnaires regarding eating behaviour and food preferences.
Results: In total, 101 children of mean age 11.5 years were recruited (28 CME and 73 controls). The CME group scored significantly higher on 'slowness of eating' and on the combined 'avoidant eating behaviour' construct (p < 0.01). The number of foods avoided and symptoms was associated with higher levels of avoidant eating behaviour (p < 0.05). The CME group rated liking for several dairy foods (butter, cream, chocolate, full fat milk and ice cream) significantly lower than the control group (p < 0.05), although there were no significant differences seen for any other category of food.
Conclusion: This study demonstrated that consuming a CME diet during infancy has persistent and long-term effects on eating habits and food preferences. To reduce future negative eating behaviours, children's exclusion diets need to be as varied as possible and reintroduction of cows' milk products closely monitored.
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http://dx.doi.org/10.1111/pai.12513 | DOI Listing |
Pediatrics
January 2025
School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland.
Objectives: Investigate associations of different family healthy lifestyle scores (HLS) during the first 1000 days with childhood overweight and obesity (OWOB).
Methods: Cohort-specific analyses were conducted on participants (n = 25 006) from 4 European birth cohorts (The study on the pre- and early postnatal determinants of child health and development [EDEN], Elfe, France; Generation R, the Netherlands; and Lifeways, Ireland). Three composite HLSs were calculated: a maternal pregnancy HLS based on prepregnancy body mass index (BMI) and diet quality, physical activity, smoking status, and alcohol consumption during pregnancy; a parental pregnancy HLS additionally considering paternal BMI and smoking status; and an infancy HLS based on breastfeeding duration, age of solid food introduction, and exposure to passive smoking.
Pediatr Allergy Immunol
January 2025
Department of Clinical Sciences, Pediatrics, Umeå University, Umeå, Sweden.
Introduction: Diet diversity (DD) in infancy may be protective for early food allergy (FA) but there is limited knowledge about how DD incorporating consumption frequency influences FA risk.
Methods: Three measures of DD were investigated in 2060 infants at 6 and/or at 9 months of age within the NorthPop Birth Cohort Study: a weighted DD score based on intake frequency, the number of introduced foods, and the number of introduced allergenic foods. In multivariable logistic regression models based on directed acyclic graphs, associations to parentally reported physician-diagnosed FA at age 9 and 18 months were estimated, including sensitivity and stratified analyses.
Nutrients
January 2025
Department of Psychiatry and Behavioral Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Background/objectives: While studies in rat pups suggest that early zinc exposure is critical for optimal brain structure and function, associations of prenatal zinc intake with measures of brain development in infants are unknown. This study aimed to assess the associations of maternal zinc intake during pregnancy with MRI measures of brain tissue microstructure and neurodevelopmental outcomes, as well as to determine whether MRI measures of the brain mediated the relationship between maternal zinc intake and neurodevelopmental indices.
Methods: Forty-one adolescent mothers were recruited for a longitudinal study during pregnancy.
Rev Med Chil
September 2024
Hospital de Niños Dr. Roberto del Río, Santiago, Chile.
Hereditary tyrosinemia type 1 (HT-1) is an inborn error of metabolism caused by a defect in tyrosine (tyr) degradation. This defect results in the accumulation of succinylacetone (SA), causing liver failure with a high risk of hepatocarcinoma and kidney injury, leading in turn to Fanconi syndrome with urine loss of phosphate and secondary hypophosphatemic rickets (HR). HT-1 diagnosis is usually made in infants with acute or chronic liver failure or by neonatal screening programs.
View Article and Find Full Text PDFBMC Med Genomics
January 2025
Department of Critical Care Medicine, Affiliated Hospital of Medical School, Nanjing Drum Tower Hospital, Nanjing University, No. 321 Zhongshan Road, Nanjing, 210008, Jiangsu Province, China.
Background: Glycerol-3-phosphate dehydrogenase 1 (GPD1) gene defect can cause hypertriglyceridemia (HTG), which usually occurs in infants. The gene defect has rarely been reported in adult HTG patients. In the present study, we described the clinical and functional analyses of a novel GPD1 missense variant in a Chinese adult patient with recurrent hypertriglyceridemia‑related acute pancreatitis (HTG-AP), consuming a high-fat diet and smoking heavily.
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