Poor Childhood Growth Research Articles

The Influence of Vitamin D on Bone Health Across the Life Cycle1-3

Vitamin D is often looked upon only as that fat-soluble vitamin found in cod liver oil fatty fish (salmon mackerel) fortified milk and fortified breads and cereals and which is associated with sun exposure and preventing rickets in children. However in the Nutrition and Bone Health Working Group of the American Society for Bone and Mineral Research we learned that vitamin D has important ramifications for health not only throughout life but even during fetal development. Dr. Cooper reviewed the important factors that are related to normal patterns of skeletal growth. He noted that many factors influence the accumulation of bone mineral during childhood and adolescence including heredity gender diet physical activity endocrine status and a wide variety of risk factors. He also emphasized that maternal vitamin D deficiency as well as other factors modulated bone mineral acquisition during intrauterine life and was associated with low birth size and poor childhood growth that were directly linked to increased risk of hip fracture later in life. Children born to mothers who had suboptimal vitamin D status had significantly reduced whole body bone mineral content at age 9 y. This deficit in skeletal growth remained significant even after adjustment for childhood weight and bone area. (excerpt)

Developmental Origins of Osteoporotic Fracture: the Role of Maternal Vitamin D Insufficiency1-4

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most efforts in fracture prevention have been directed at retarding the rate of age-related bone loss and reducing the frequency and the severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone-mineral content, but not volumetric bone density, than girls. Furthermore, there is a disassociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors (e.g., cigarette smoking). In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of endocrine systems such as the GH/IGF-1 and parathyroid hormone/vitamin D axes. Maternal vitamin D insufficiency is associated with reduced bone mineral acquisition during intrauterine and early postnatal life. Furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Bone Mineral Density and Markers of Bone Turnover in Boys with Constitutional Delay of Growth and Puberty

It has been suggested that poor growth in childhood or puberty might be a correctable determinant of osteoporosis. To assess the effect of the growth and puberty delay on bone metabolism, we measured bone mineral density (BMD) and markers of bone turnover in 41 boys with constitutional delay of growth and puberty. Total body (TB) and lumbar spine (LS) BMD were measured by dual-energy x-ray absorptiometry. Serum osteocalcin, total alkaline phosphatase, and urinary deoxypyridinoline cross-links as markers of bone turnover were evaluated. BMD was decreased by at least 1 sd in TB in 23 boys (56%) and in LS in 27 boys (66%). After adjustment of BMD for bone age, TB was decreased in 11 boys (27%) and LS in 13 boys (32%). Bone age and chronological age significantly correlated with areal and volumetric BMD. The significant increments of height, weight, TB, and LS BMD between the consecutive pubertal stages were reported. Mean alkaline phosphatase, osteocalcin, and deoxypyridinoline were within reference ranges and showed no differences between pubertal stages. In conclusion, in boys with constitutional delay of growth and puberty, bone turnover is normal, and BMD increases in a manner similar to healthy children.

Chronic T cell-mediated enteropathy in rural west African children: relationship with nutritional status and small bowel function.

Previous studies from The Gambia have shown that poor childhood growth is resistant to all but the most intense nutritional intervention and highly dependent on small bowel permeability related to enteropathy. We thus aimed to characterize the mucosal inflammatory response in rural Gambian children in relation to intestinal permeability and nutritional status. Small bowel biopsies were taken from 38 rural Gambian children (age, 0.5-3 y) with a range of nutritional and clinical states (median weight z score, -4.6; range, 0.5 to -6.4), 75% of whom had diarrhea. Morphometry was performed with immunohistochemical analysis for a range of lineage and activation markers, including proinflammatory and regulatory cytokines, and related to current clinical status and gut permeability. Comparison was made with 19 age-matched U.K. controls. All Gambian children, regardless of nutritional status, had evidence of chronic cell-mediated enteropathy with crypt hyperplasia, villous stunting, and high numbers of intraepithelial lymphocytes. CD25+ cells were 20-fold higher than in U.K. controls. Although small bowel architecture was independent of nutritional status, T cell numbers rose and B cell numbers fell with worsening nutrition, and mucosal cytokine production became biased toward a proinflammatory response, with progressive decrease of transforming growth factor-beta expression. Tropical enteropathy predates the onset of marasmus and is characterized by a cell-mediated TH1 response. Protein-energy malnutrition is associated with reduction of regulatory immune responses in the mucosal microenvironment, potentially impairing the mechanisms of oral tolerance.

Prenatal and childhood influences on osteoporosis.

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss, and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content, but not volumetric bone density, than girls. Furthermore, in both genders there is a dissociation between the peak velocities for height gain and bone mineral accrual. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status and sporadic risk factors such as cigarette smoking. Measures for maximizing bone mineral acquisition, particularly through encouraging physical activity and adequate dietary calcium intake, are likely to affect the risk of fracture in later generations. In addition to these modifiable factors during childhood, evidence has also accrued that the risk of fracture might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the hypothalamic - pitutiary - adrenal (HPA) and growth hormone/insulin-like growth factor I (GH/IGF-I) axes. Maternal smoking, diet and physical activity levels appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Perinatal predictors of growth at six months in small for gestational age babies.

Poor growth in childhood is associated with a number of later complications and early recognition may enable early intervention to improve outcomes. Approximately 20% of small for gestational age (SGA) babies remain small at two years. Most catch up growth occurs in the first 6 months and smallness at 6 months predicts later small size in the majority of cases. There are no previous reports of perinatal predictors of size at 6 months in SGA babies. The aim of this study was to identify the perinatal factors associated with small size at 6 months in infants who were SGA at birth (birthweight < 10th%). SGA infants had assessments of length, weight, and head circumference performed at three monthly intervals by the same researcher. Detailed perinatal data was collected in all cases. Abnormal size was defined as a length, weight or head circumference measurement < 10th% for 6 months corrected age. Infants were considered to show failure of catch-up growth if measurements at 6 months were further below the population mean than birth measurements. Two hundred and forty eight babies were recruited of whom 203 (82%) completed followup at 6 months. Forty (20%) babies were short, and in logistic regression shortness at 6 months was predicted by shortness at birth and male sex. Thirty one (16%) had weight < 10th% and low weight was predicted in logistic regression by early gestation at diagnosis of SGA (median 30.8 weeks in those who were under weight and 33.9 weeks in those of normal weight p < 0.0001). Thirty seven (18%) had a low head circumference which was predicted by small head size at birth. Three quarters of the babies who were short, underweight, or had low head circumference at 6 months also showed failure of catch-up growth. Shortness and small head circumference at 6 months were predicted by shortness and small head circumference at birth, especially in boys. Underweight was predicted by early detection of SGA antenatally. Most SGA babies who remained small at 6 months failed to show catch up growth after birth.

Recommendations for protein and energy intakes by patients with phenylketonuria.

Recent reports describe poor growth in treated children with phenylketonuria (PKU). That poor growth is not a concomitant of the disorder and need not result from therapy is demonstrated by data from the U.S.A. PKU Collaborative Study and from recent data from the U.S.A. In these studies, sufficient protein equivalent was supplied by medical food containing either a low phenylalanine (Phe) casein hydrolysate or Phe-free L-amino acids. Protein and energy intakes of infants and children with PKU who grew well are compared to intakes of normal North American children. Factors that influence nitrogen (N) requirements include: state of health, energy intake, the form in which N is administered and the size of the dose. Failure to prevent poor growth in childhood may lead to a stunted adult [13] who is at risk for obesity. The use of actual body weight as a basis for calculating protein and energy requirements is appropriate only when the child is growing normally. Based on experience with PKU in the U.S.A., the following are recommended: (1) a protocol that prescribes a range for Phe, protein, and energy for infants and children should be developed; (2) adequate protein equivalent to cover N losses due to poor utilization of amino acids and protein hydrolysates should be prescribed; (3) medical food should be administered in several doses throughout the day; (4) a source of Phe should be fed with the medical food; (5) adequate energy should be prescribed to prevent excess use of amino acid for energy purposes; (6) nutrition support during illness should be appropriate to help prevent muscle protein catabolism with attendant elevated plasma Phe.

Lesson of the week: Spontaneous fractures in children and adolescents with cerebral palsy

Children and adolescents with cerebral palsy, in addition to the motor disability, have other, associated disabilities: hearing and visual impairment, learning disabilities, failure to thrive in infancy and poor growth in childhood, and scoliosis. They are prone to dislocations, particularly dislocation of the hips. They also develop other contractures and deformities, which may need surgery. * Children and adolescents with cerebral palsy have a tendency to sustain spontaneous fractures We report on five children and adolescents who developed spontaneous fractures of long bones, an association which, as far as we are aware, is not recognised. The five subjects, aged 10 to 19 years (four male and one female) with various types of cerebral palsy, were resident pupils at Meldreth Manor School, …

Growth of Children with Hypochondroplasia Treated with Growth Hormone for up to Three Years

Hypochondroplasia is a skeletal dysplasia characterised by poor childhood growth and an inadequate pubertal growth spurt. 31 children with a radiological diagnosis of hypochondroplasia have been treated for up to 3 years with recombinant human growth hormone, mean dose 17.9 U/m2/week as daily subcutaneous injections. Mean pre-treatment height velocity standard deviation score (SDS) was -0.51; this increased to +1.58 after 1 year of treatment. This improvement diminishes over the next 2 years. The effect on final height remains unknown. There was a considerable variation in clinical response within the group treated.