Testing the direction of effects between child body composition and restrictive feeding practices: results from a population-based cohort.

Background: Parental restrictive feeding (i.e., limiting food intake of children) has been linked to childhood overweight. However, the directionality of the causal pathway remains unknown.Objective: The objectives of this study were to examine the bidirectional association of maternal restrictive feeding with children's weight and body composition across childhood and to explore a possible mediating role of maternal concern about child weight.Design: Data were available for 4689 mother-child dyads participating in Generation R, a prospective birth cohort in the Netherlands. At ages 4 and 10 y, restrictive feeding was assessed with the parent-reported Child Feeding Questionnaire, and children's body mass index (BMI) was measured. At age 6 y, fat mass index (FMI) and fat-free mass index (FFMI) were measured with dual-energy X-ray absorptiometry. Both directions of the relation between restriction and child body composition were examined with multivariable linear regression analyses and cross-lagged modeling. Mediation analyses were performed to examine concern about child weight (mother reported at child age of 10 y) as a potential mediator.Results: Higher child sex- and age-adjusted BMI SD scores (zBMI) at age 4 y predicted more restrictive feeding at age 10 y (B = 0.15; 95% CI: 0.11, 0.18). Both sex- and age-adjusted FMI SD scores (zFMI) and sex-and age-adjusted FFMI SD scores (zFFMI) at 6 y were also positively associated with restrictive feeding at 10 y. Maternal concern about child weight partially mediated these associations from child body composition to restrictive feeding (e.g., for zBMI at 4 y: Bindirect = 0.10; 95% CI: 0.07, 0.13). There was no temporal association from restrictive feeding at age 4 y to child zBMI at age 10 y after adjustment for baseline zBMI.Conclusions: The continued use of restrictive feeding practices at age 10 y appeared to be primarily a response of mothers to an unhealthy weight of their child rather than a cause of children's overweight. Guidelines discouraging restrictive feeding for preventing childhood overweight should therefore be reconsidered.

Haplotype of the angiotensinogen gene is associated with coronary heart disease in familial hypercholesterolemia.

OBJECTIVE: Familial hypercholesterolemia is characterized by high plasma low-density lipoprotein cholesterol levels and premature coronary heart disease. Despite the monogenetic origin of familial hypercholesterolemia, the incidence of coronary heart disease varies considerably among patients, which is only partly explained by classical risk factors. Hypertension is an important risk factor for coronary heart disease that is associated with angiotensinogen levels. Therefore, we analyzed the angiotensinogen gene as a modifier gene for coronary heart disease risk in patients with familial hypercholesterolemia. METHODS: In a cohort of 1785 familial hypercholesterolemia patients, we reconstructed five frequent haplotypes of the angiotensinogen gene, based on four polymorphisms. The five haplotypes cover approximately 98% of the genetic diversity accounted for by these four polymorphisms. The associations between the haplotypes and coronary heart disease were analyzed with the haplo.stats program, adjusted for age, sex and smoking. RESULTS: Patients homozygous for the C allele of the 4072 T>C polymorphism had a 34% increased coronary heart disease risk (P = 0.017) compared to patients homozygous for the T allele. Haplotype H3, consisting of the minor allele of the 4072T>C polymorphism and the major alleles of the other polymorphisms, had a frequency of 15% and was associated with a 45% increased coronary heart disease risk (P = 0.006) compared to the wild-type haplotype H1. CONCLUSIONS: We conclude that genetic variation in the angiotensinogen gene contributes to coronary heart disease risk in patients with familial hypercholesterolemia.