thesis
The branched-chain amino acid requerement in neonates
- Publication date
- 26 September 2012
- Publisher
- Growth during the earliest stages of life is an important determinant of an individual’s
later health and risk of chronic disease. Substantial evidence shows that growth in the
first 2 years of life, especially high early weight gain, is associated with adverse health
outcomes later in life, including increased blood pressure, increased weight gain
and body fat deposition and increased risk of diabetes. Higher protein intake
for infants who are formula fed may play a role with these health outcomes because
formula-fed children reach a higher body weight and weight for length at one year of
age compared to those fed breast milk. A lower protein intake in infant formula is
associated with lower weight up at 2 years of age which might be beneficial because
the slower pattern of growth in breastfed infants might be protective for the development
of the metabolic syndrome. In preterm infants, however, a higher protein
intake in the first month of life correlates with improved neurodevelopment.
Preterm infants have higher protein turnover rates and protein losses than terms and
thereby higher protein requirements. Excessive intake of amino acids has been
shown to reduce (brain) growth and to influence neurotransmitter concentrations in the
brain of rats which might put the developing brain at risk. Inadequate amino acid
intake impairs protein synthesis, which is pivotal for growth. The growth rate of the preterm
infant should mimic at least the growth rate of the intrauterine fetus at the same
gestational age. Achieving appropriate growth and nutrition accretion of preterm
neonates is often difficult during hospitalization because of metabolic and gastrointestinal
immaturity and other complicating medical conditions. Many preterm neonates
require total parental nutrition for their initial nutritional support but this is associated
with several complications, including the increased risk of infection, mucosal atrophy
and cholestatic jaundice. Therefore, transition to full enteral feeding and the cessation of
TPN are accomplished as soon as feasible and safe, taking in consideration that enteral
feeding is associated with a detrimental morbidity like necrotising enterocolitis.
Enteral nutrition can be initiated immediately after birth by introducing small amounts
to enhance the development of the gastro-intestinal tract and for this reason is referred
to as “trophic”, “priming” or “minimal enteral feeding”.