Lower protein content in infant formula reduces BMI and obesity risk at school age: Follow-up of a randomized trial

American Journal of Clinical Nutrition (Impact Factor: 6.77). 03/2014; 99(5). DOI: 10.3945/ajcn.113.064071
Source: PubMed


Early nutrition is recognized as a target for the effective prevention of childhood obesity. Protein intake was associated with more rapid weight gain during infancy-a known risk factor for later obesity.
We tested whether the reduction of protein in infant formula reduces body mass index (BMI; in kg/m(2)) and the prevalence of obesity at 6 y of age.
The Childhood Obesity Project was conducted as a European multicenter, double-blind, randomized clinical trial that enrolled healthy infants born between October 2002 and July 2004. Formula-fed infants (n = 1090) were randomly assigned to receive higher protein (HP)- or lower protein (LP)-content formula (within recommended amounts) in the first year of life; breastfed infants (n = 588) were enrolled as an observational reference group. We measured the weight and height of 448 (41%) formula-fed children at 6 y of age. BMI was the primary outcome.
HP children had a significantly higher BMI (by 0.51; 95% CI: 0.13, 0.90; P = 0.009) at 6 y of age. The risk of becoming obese in the HP group was 2.43 (95% CI: 1.12, 5.27; P = 0.024) times that in the LP group. There was a tendency for a higher weight in HP children (0.67 kg; 95% CI: -0.04, 1.39; P = 0.064) but no difference in height between the intervention groups. Anthropometric measurements were similar in the LP and breastfed groups.
Infant formula with a lower protein content reduces BMI and obesity risk at school age. Avoidance of infant foods that provide excessive protein intakes could contribute to a reduction in childhood obesity. This trial was registered at as NCT00338689.

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Available from: Jean-Paul Langhendries, Jan 07, 2015
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    • "L-amino acid formulas provide a high dietary acid load [35] and chronic ingestion may have a potentially negative impact on the kidney [34] and bone health in PKU [36]. There have also been recent concerns that a higher protein intake in infancy may contribute to a higher BMI and risk of obesity in children [37]. Given that obesity has been reported in PKU, particularly in female patients [38] [39] [40], additional study is required investigating total protein intakes in infancy and its long term effect on the development of obesity. "
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    ABSTRACT: Background: There appears little consensus concerning protein requirements in phenylketonuria (PKU). Methods: A questionnaire completed by 63 European and Turkish IMD centres from 18 countries collected data on prescribed total protein intake (natural/intact protein and phenylalanine-free protein substitute [PS]) by age, administration frequency and method, monitoring, and type of protein substitute. Data were analysed by European region using descriptive statistics. Results: The amount of total protein (fromPS and natural/intact protein) varied according to the European region. Higher median amounts of total protein were prescribed in infants and children in Northern Europe (n = 24 centres) (infants b1 year, N2–3 g/kg/day; 1–3 years of age, N2–3 g/kg/day; 4–10 years of age, N1.5– 2.5 g/kg/day) and Southern Europe (n = 10 centres) (infants b1 year, 2.5 g/kg/day, 1–3 years of age, 2 g/kg/day; 4–10 years of age, 1.5–2 g/kg/day), than by Eastern Europe (n = 4 centres) (infants b1 year, 2.5 g/kg/day, 1–3 years of age, N2–2.5 g/kg/day; 4–10 years of age, N1.5–2 g/kg/day) and withWestern Europe (n = 25 centres) giving the least (infants b1 year, N2–2.5 g/kg/day, 1–3 years of age, 1.5–2 g/kg/day; 4–10 years of age, 1–1.5 g/kg/day). Total protein prescription was similar in patients aged N10 years (1–1.5 g/kg/day) and maternal patients (1–1.5 g/kg/day). Conclusions: The amounts of total protein prescribed varied between European countries and appeared to be influenced by geographical region. In PKU, all gave higher than the recommended 2007 WHO/FAO/UNU safe levels of protein intake for the general population.
    Molecular Genetics and Metabolism 01/2015; · 2.63 Impact Factor
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    • "Notably, increased postnatal catch-up growth in small for gestational age infants is associated with increased postnatal mTORC1 signalling and increased childhood asthma risk [22]. Moreover, excessive postnatal protein intake by formula feeding increases weight gain, total body fat mass and increases the risk of childhood obesity [23-25], which has been linked to increased amino acid-mediated mTORC1-signalling [26]. "
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    ABSTRACT: This article provides a new view of the cellular mechanisms that have been proposed to explain the links between infant formula feeding and the development of atopy and obesity. Epidemiological evidence points to an allergy- and obesity-preventive effect of breastfeeding. Both allergy and obesity development have been traced back to accelerated growth early in life. The nutrient-sensitive kinase mTORC1 is the master regulator of cell growth, which is predominantly activated by amino acids. In contrast to breastfeeding, artificial infant formula feeding bears the risk of uncontrolled excessive protein intake overactivating the infant's mTORC1 signalling pathways. Overactivated mTORC1 enhances S6K1-mediated adipocyte differentiation, but negatively regulates growth and differentiation of FoxP3(+) regulatory T-cells (Tregs), which are deficient in atopic individuals. Thus, the "early protein hypothesis" not only explains increased mTORC1-mediated infant growth but also the development of mTORC1-driven diseases such as allergy and obesity due to a postnatal deviation from the appropriate axis of mTORC1-driven metabolic and immunologic programming. Remarkably, intake of fresh unpasteurized cow's milk exhibits an allergy-preventive effect in farm children associated with increased FoxP3(+) Treg numbers. In contrast to unprocessed cow's milk, formula lacks bioactive immune-regulatory microRNAs, such as microRNA-155, which plays a major role in FoxP3 expression. Uncontrolled excessive protein supply by formula feeding associated with the absence of bioactive microRNAs and bifidobacteria in formula apparently in a synergistic way result in insufficient Treg maturation. Treg deficiency allows Th2-cell differentiation promoting the development of allergic diseases. Formula-induced mTORC1 overactivation is thus the critical mechanism that explains accelerated postnatal growth, allergy and obesity development on one aberrant pathway.
    Allergy Asthma and Clinical Immunology 07/2014; 10(1):37. DOI:10.1186/1710-1492-10-37 · 2.03 Impact Factor
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    ABSTRACT: AIM: Segmental body composition in children was assessed using the bioimpedance analyzer (BIA) TANITA BC-418 and compared with dual-energy X-ray absorptiometry (DXA) values. METHODS: A cross-sectional validation study in which 7-year-old children from the Spanish subsample of the EU Childhood Obesity Project were assessed through anthropometry, BIA and DXA. Main outcome measures were fat and lean masses of the trunk, left arm and left leg (in kg) assessed through BIA direct outputs (BIAoutputs) and DXA. Predictive equations for the composition of each segment were derived from raw impedance and anthropometric measurements; results obtained from these predictive equations (BIAregressions) were also compared to DXA. RESULTS: One hundred seventy-one (84 boys) 7-year-old children were studied. BIAoutputs and DXA results showed small differences for leg lean mass (6.5%) and high differences for trunk fat and trunk lean masses (>30%). BIAregressions results showed differences of about 20% for trunk fat mass, 1.5% for trunk lean mass and 3.7% for leg lean mass compared to DXA. CONCLUSIONS: Segmental body composition measures predicted by internal algorithms of the TANITA BC-418 were not valid for clinical or epidemiological use, except for leg lean mass. The assessment of segmental composition was improved using our own predictive equations combining segmental-specific anthropometric measurements with segmental impedances.
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