Pediatric Feeding Disorder: Consensus Definition and Conceptual Framework

Pediatric feeding disorders (PFDs) lack a universally accepted definition. Feeding disorders require comprehensive assessment and treatment of 4 closely related, complementary domains (medical, psychosocial, and feeding skill-based systems and associated nutritional complications). Previous diagnostic paradigms have, however, typically defined feeding disorders using the lens of a single professional discipline and fail to characterize associated functional limitations that are critical to plan appropriate interventions and improve quality of life. Using the framework of the World Health Organization International Classification of Functioning, Disability, and Health, a unifying diagnostic term is proposed: “Pediatric Feeding Disorder” (PFD), defined as impaired oral intake that is not age-appropriate, and is associated with medical, nutritional, feeding skill, and/or psychosocial dysfunction. By incorporating associated functional limitations, the proposed diagnostic criteria for PFD should enable practitioners and researchers to better characterize the needs of heterogeneous patient populations, facilitate inclusion of all relevant disciplines in treatment planning, and promote the use of common, precise, terminology necessary to advance clinical practice, research, and health-care policy

Association between umbilical cord glucocorticoids and blood pressure at age 3 years

<p>Abstract</p> <p>Background</p> <p>Animal data show that decreased activity of placental 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which potently inactivates glucocorticoids (e.g. cortisol) to inert forms (cortisone), allows increased access of maternal glucocorticoids to the fetus and 'programs' hypertension. Data in humans are limited. We examined in humans the association between venous umbilical cord blood glucocorticoids, a potential marker for placental 11β-HSD2 enzyme activity, and blood pressure at age 3 years.</p> <p>Methods</p> <p>Among 286 newborns in Project Viva, a prospective pre-birth cohort study based in eastern Massachusetts, we measured cortisol (<it>F</it>) and cortisone (<it>E</it>) in venous cord blood and used the ratio of <it>F/E </it>as a marker for placental 11β-HSD2 activity. We measured blood pressure (BP) when the offspring reached age 3 years. Using mixed effects regression models to control for BP measurement conditions, maternal and child characteristics, we examined the association between the <it>F/E </it>ratio and child BP.</p> <p>Results</p> <p>At age 3 years, each unit increase in the <it>F/E </it>ratio was associated with a 1.6 mm Hg increase in systolic BP (95% CI 0.0 to 3.1). The <it>F/E </it>ratio was not associated with diastolic blood pressure or birth weight for gestational age <it>z</it>-score.</p> <p>Conclusion</p> <p>A higher <it>F/E </it>ratio in umbilical venous cord blood, likely reflecting reduced placental 11β-HSD2 activity, was associated with higher systolic blood pressure at age 3 years. Our data suggest that increased fetal exposure to active maternal glucocorticoids may program later systolic blood pressure.</p

Maternal protein intake is not associated with infant blood pressure

Animal data show that low protein intake in pregnancy programs higher offspring blood pressure, but similar data in humans are limited. We examined the associations of first and second trimester maternal protein intake with offspring blood pressure (BP) at the age of six months. In a prospective US cohort study, called Project Viva, pregnant women completed validated semi-quantitative food-frequency questionnaires (FFQ) to measure gestational protein intake. Among 947 mother-offspring pairs with first trimester dietary data and 910 pairs with second trimester data, we measured systolic blood pressure (SBP) up to five times with an automated device in the offspring at the age of six months. Controlling for blood pressure measurement conditions, maternal and infant characteristics, we examined the effect of energy-adjusted maternal protein intake on infant SBP using multivariable mixed effects models. Mean daily second trimester maternal protein intake was 17.6% of energy (mean 2111 kcal/day). First trimester nutrient intakes were similar. Mean SBP at age 6 months was 90.0 mm Hg (SD 12.9). Consistent with prior reports, adjusted SBP was 1.94 mm Hg lower [95% confidence interval (CI) -3.45 to -0.42] for each kg increase in birth weight. However, we did not find an association between maternal protein intake and infant SBP. After adjusting for covariates, the effect estimates were 0.14 mm Hg (95% CI 20.12 to 20.40) for a 1% increase in energy from protein during the second trimester, and 20.01 mm Hg (95% CI 20.24 to -0.23) for a 1% increase in energy from protein in the first trimester. Variation in maternal total protein intake during pregnancy does not appear to program offspring blood pressure