Aim
Children with cerebral palsy (CP) have reduced levels of physical activity compared with children without physical disability and experience risk factors for becoming overweight or obese. In the ...Australian CP population, there is little information available about the weight status of children with CP. The aims of this study were to compare the distribution of body mass index (BMI) in a cohort of ambulant children with CP with the BMI distribution of Australian children and explore the relationship between BMI and gross motor function.
Methods
A retrospective cohort study of 587 children with CP Gross Motor Function Classification System (GMFCS) levels I–III who attended a Gait Laboratory between July 1995 and January 2012 was carried out. The BMI and Z‐score were calculated at each assessment. Data were grouped into the categories of underweight, healthy, overweight and obese according to age‐specific and sex‐specific percentiles.
Results
There were 348 boys and 240 girls with a mean age 11.2 (standard deviation 3.2) years. Mean BMI Z‐score was 0.11 (standard deviation 1.33). Seven percent of children were underweight, 73.6% healthy, 7.3% overweight and 12.1% obese. This was similar to the distribution of children without disability. The largest percentage of children in the healthy group were classified GMFCS I. The largest percentage of children in the obese group were classified GMFCS III.
Conclusions
In this cohort, 19.4% of ambulant children with CP were overweight or obese. This is of concern as BMI may impact on the outcomes of surgical intervention and rehabilitation. Further research is needed to determine the consequences of obesity for children with CP.
Elevated non-high-density lipoprotein cholesterol (HDL-C) levels are used to identify children at increased cardiovascular risk, but the use of non-HDL-C in childhood to predict atherosclerosis is ...unclear. We examined whether the National Heart, Lung, and Blood Institute classification of youth non-HDL-C status predicts high common carotid artery intima-media thickness in adulthood.
We analyzed data from 4 prospective cohorts among 4582 children aged 3 to 19 years who were remeasured as adults (mean follow-up of 26 years). Non-HDL-C status in youth and adulthood was classified according to cut points of the National Heart, Lung, and Blood Institute and the National Cholesterol Education Program Adult Treatment Panel III. High carotid intima-media thickness (cIMT) in adulthood was defined as at or above the study visit-, age-, sex-, race-, and cohort-specific 90th percentile of intima-media thickness.
In a log-binomial regression analysis adjusted with age at baseline, sex, cohort, length of follow-up, baseline BMI, and systolic blood pressure, children with dyslipidemic non-HDL-C were at increased risk of high cIMT in adulthood (relative risk RR, 1.29; 95% confidence interval CI, 1.07-1.55). Compared with the persistent normal group, the persistent dyslipidemia group (RR, 1.80; 95% CI, 1.37-2.37) and incident dyslipidemia (normal to dyslipidemia) groups (RR, 1.45; 95% CI, 1.07-1.96) had increased risk of high cIMT in adulthood, but the risk was attenuated for the resolution (dyslipidemia to normal) group (RR, 1.17; 95% CI, 0.97-1.41).
Dyslipidemic non-HDL-C levels predict youth at risk for developing high cIMT in adulthood. Those who resolve their non-HDL-C dyslipidemia by adulthood have normalized risk of developing high cIMT in adulthood.
Obesity in childhood is associated with metabolic dysfunction, adverse subclinical cardiovascular phenotypes and adult cardiovascular disease. Longitudinal studies of youth with obesity investigating ...changes in severity of obesity with metabolomic profiles are sparse. We investigated associations between (i) baseline body mass index (BMI) and follow-up metabolomic profiles; (ii) change in BMI with follow-up metabolomic profiles; and (iii) change in BMI with change in metabolomic profiles (mean interval 5.5 years).
Participants (n = 98, 52% males) were recruited from the Childhood Overweight Biorepository of Australia study. At baseline and follow-up, BMI and the % >95th BMI-centile (percentage above the age-, and sex-specific 95th BMI-centile) indicate severity of obesity, and nuclear magnetic resonance spectroscopy profiling of 72 metabolites/ratios, log-transformed and scaled to standard deviations (SD), was performed in fasting serum. Fully adjusted linear regression analyses were performed.
Mean (SD) age and % >95th BMI-centile were 10.3 (SD 3.5) years and 134.6% (19.0) at baseline, 15.8 (3.7) years and 130.7% (26.2) at follow-up. Change in BMI over time, but not baseline BMI, was associated with metabolites at follow-up. Each unit (kg/m
) decrease in sex- and age-adjusted BMI was associated with change (SD; 95% CI; p value) in metabolites of: alanine (-0.07; -0.11 to -0.04; p < 0.001), phenylalanine (-0.07; -0.10 to -0.04; p < 0.001), tyrosine (-0.07; -0.10 to -0.04; p < 0.001), glycoprotein acetyls (-0.06; -0.09 to -0.04; p < 0.001), degree of fatty acid unsaturation (0.06; 0.02 to 0.10; p = 0.003), monounsaturated fatty acids (-0.04; -0.07 to -0.01; p = 0.004), ratio of ApoB/ApoA1 (-0.05; -0.07 to -0.02; p = 0.001), VLDL-cholesterol (-0.04; -0.06 to -0.01; p = 0.01), HDL cholesterol (0.05; 0.08 to 0.1; p = 0.01), pyruvate (-0.08; -0.11 to -0.04; p < 0.001), acetoacetate (0.07; 0.02 to 0.11; p = 0.005) and 3-hydroxybuturate (0.07; 0.02 to 0.11; p = 0.01). Results using the % >95th BMI-centile were largely consistent with age- and sex-adjusted BMI measures.
In children and young adults with obesity, decreasing the severity of obesity was associated with changes in metabolomic profiles consistent with lower cardiovascular and metabolic disease risk in adults.
We prospectively examined whether family socioeconomic status (SES) in childhood is associated with metabolic syndrome (MetS), impaired fasting glucose (IFG), or type 2 diabetes in adulthood.
The ...sample comprised 2,250 participants from the longitudinal Cardiovascular Risk in Young Finns Study cohort. Participants were 3-18 years old at baseline (mean age 10.6 years), and they were followed for 31 years. SES was characterized as reported annual income of the family and classified on an 8-point scale.
For each 1-unit increase in family SES in childhood, the risk for adult MetS decreased (risk ratio 95% confidence interval 0.94 0.90-0.98; P = 0.003) when adjusted for age, sex, childhood cardiometabolic risk factors (lipids, systolic blood pressure, insulin, and BMI), childhood physical activity, and fruit and vegetable consumption. The association remained after adjustment for participants' own SES in adulthood (0.95 0.91-0.99; P = 0.005). A similar association was seen between childhood SES and the risk of having either adult IFG or type 2 diabetes (0.96 0.92-0.99; P = 0.01, age and sex adjusted). This association became nonsignificant after adjustment for childhood risk factors (P = 0.08). Of the individual components of MetS, lower SES in childhood predicted large waist circumference (0.96 0.93-0.99; P = 0.003) and a high triglycerides concentration (0.96 0.92-1.00; P = 0.04) after adjustment for the aforementioned risk factors.
Lower SES in childhood may be associated with an increased risk for MetS, IFG, and type 2 diabetes in adulthood. Special attention could be paid to children of low SES families to decrease the prevalence of MetS in adulthood.
The impact of contemporary chemotherapy treatment for childhood acute lymphoblastic leukemia on central nervous system activity is not fully appreciated.
Neurocognitive testing and functional ...magnetic resonance imaging (fMRI) were obtained in 165 survivors five or more years postdiagnosis (average age = 14.4 years, 7.7 years from diagnosis, 51.5% males). Chemotherapy exposure was measured as serum concentration of methotrexate following high-dose intravenous injection. Neurocognitive testing included measures of attention and executive function. fMRI was obtained during completion of two tasks, the continuous performance task (CPT) and the attention network task (ANT). Image analysis was performed using Statistical Parametric Mapping software, with contrasts targeting sustained attention, alerting, orienting, and conflict. All statistical tests were two-sided.
Compared with population norms, survivors demonstrated impairment on number-letter switching (P < .001, a measure of cognitive flexibility), which was associated with treatment intensity (P = .048). Task performance during fMRI was associated with neurocognitive dysfunction across multiple tasks. Regional brain activation was lower in survivors diagnosed at younger ages for the CPT (bilateral parietal and temporal lobes) and the ANT (left parietal and right hippocampus). With higher serum methotrexate exposure, CPT activation decreased in the right temporal and bilateral frontal and parietal lobes, but ANT alerting activation increased in the ventral frontal, insula, caudate, and anterior cingulate.
Brain activation during attention and executive function tasks was associated with serum methotrexate exposure and age at diagnosis. These findings provide evidence for compromised and compensatory changes in regional brain function that may help clarify the neural substrates of cognitive deficits in acute lymphoblastic leukemia survivors.
Childhood obesity is associated with cardiovascular risk factors (CVRF), subclinical cardiovascular phenotypes (carotid intima-media thickness, cIMT; pulse-wave velocity, PWV; and carotid ...elasticity), and adult cardiovascular disease (CVD) mortality. In youth with obesity (body mass index, BMI ≥95th centile), we investigated associations between changes in adiposity and CVRF in early adolescence and subclinical cardiovascular phenotypes in late adolescence.
Participants had adiposity measures (the severity of obesity in percentage >95th BMI-centile (%>95th BMI-centile)), waist circumference (WC), percentage total body fat (%BF) and CVRF (systolic blood pressure, SBP; glycoprotein acetyls, GlycA; and low-density lipoprotein cholesterol) assessed in early (mean age 10.2 ± 3.5y) and late (15.7 ± 3.7y) adolescence. Subclinical cardiovascular phenotypes were assessed in late adolescence. Multivariable regression analysis was performed.
Decreasing the %>95th BMI-centile was associated with carotid elasticity (0.945%/10 mmHg, p = 0.002) in females, and with PWV in males (−0.75 m/s, p < 0.001). Changes in all adiposity measures (per 1-unit increase) were associated with carotid elasticity (−0.020 to −0.063%/10 mmHg, p < 0.005), and PWV (0.011–0.045 m/s, p < 0.005). Changes in GlycA (per 50μmol-increase) were associated with elasticity (−0.162%/10 mmHg, p = 0.042), and changes in SBP (per 10 mmHg-increase) were associated with PWV (0.260 m/s, p < 0.001). Adjusted for change in BMI, the coefficient for GlycA was reduced by 46% and for SBP by 12%. Only male sex was associated with cIMT (+34 μm, p = 0.006).
In youth with obesity, decreasing or maintaining the severity of obesity, and decreasing the levels of SBP and GlycA from early to late adolescence was associated with low arterial stiffness.
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•Small declines in adiposity associate with lower arterial stiffness in adolescence.•Changes in glycoprotein acetyls (GlycA) associate with carotid elasticity in adolescents with obesity.•Changes in blood pressure associate with pulse-wave velocity in adolescents with obesity.•In adolescents with obesity, males had higher carotid intima-media thickness (cIMT) than females.•Male sex was the only cardiovascular risk factor associated with arterial injury.
Both fetal growth restriction and prematurity have been associated with elevated blood pressure (BP). However, their combined effects on adult BP are unclear.
Our analyses were based on 1756 ...participants in the population-based Cardiovascular Risk in Young Finns Study who had information on birth weight and gestational age, together with longitudinal data on cardiovascular risk markers from age 3-18 years in 1980 to age 34-49 years in 2011. Three groups were defined by birth data: those born at term (term); those born preterm (<37 weeks) with an appropriate birth weight (>-1 SD z score according to national sex and gestational week-stratified data) for gestational age (preterm appropriate birth weight for gestational age); and those born preterm with low birth weight (≤-1 SD z score) for gestational age preterm small birth weight for gestational age (SGA).
There were no differences between the three groups in BP at baseline, but at the 31-year follow-up (mean age 41 years), mean SBP in the preterm SGA group was 7.2 mmHg (95% confidence interval = 2.3-12.1 mmHg, P = 0.004) higher than the preterm appropriate birth weight for gestational age group and 7.3 mmHg (95% confidence interval = 5.2-9.4 mmHg, P < 0.0001) higher than the term group, adjusted for age and sex. In addition, preterm SGA individuals had a higher prevalence of adult hypertension compared with those born at term (36.9 vs. 25.4%; age, sex, and risk factors adjusted P = 0.006).
These longitudinal data suggest that elevated BP levels associated with prematurity are more likely to be present in those with fetal growth restriction.
The activity of the Insulin-like Growth Factors (IGFs) ligands elicited via their receptors and transduced by various intracellular signal pathways is modulated by the IGF Binding Proteins (IGFBPs). ...Among all the IGFBPs, IGFBP-2 has been implicated in the regulation of IGF activity in most tissue and organs. Besides binding to IGFs in the circulation these IGF-regulatory activities of IGFBP-2 involve interactions with components of the extracellular matrix, cell surface proteoglycans and integrin receptors. In addition to these local peri-cellular activities, IGFBP-2 exerts other key functions within the nucleus, where IGFBP-2 directly or indirectly promotes transcriptional activation of specific genes. All of these IGFBP-2 activities, intrinsic or dependent on IGFs, contribute to its functional roles in growth/development, metabolism and malignancy as evidenced by studies in IGFBP-2 animal models and also by many in vitro studies. Finally, preclinical studies have demonstrated that IGFBP-2 administration can be beneficial in improving metabolic responses (inhibition of adipogenesis and enhanced insulin sensitivity), while blockade of IGFBP-2 appears to be an effective approach to inhibiting tumour growth and metastasis.
In high-income countries, cancer is the leading cause of death among middle-aged adults. Prospective data on the effects of childhood risk exposures on subsequent cancer mortality are scarce.
We ...examined whether childhood body mass index (BMI), blood pressure, glucose and lipid levels were associated with adult cancer mortality, using data from 21,012 children enrolled aged 3-19 years in seven prospective cohort studies from the U.S., Australia, and Finland that have followed participants from childhood into adulthood. Cancer mortality (cancer as a primary or secondary cause of death) was captured using registries.
354 cancer deaths occurred over the follow-up. In age-, sex, and cohort-adjusted analyses, childhood BMI (Hazard ratio HR, 1.13; 95% confidence interval CI 1.03-1.24 per 1-SD increase) and childhood glucose (HR 1.22; 95%CI 1.01-1.47 per 1-SD increase), were associated with subsequent cancer mortality. In a multivariable analysis adjusted for age, sex, cohort, and childhood measures of fasting glucose, total cholesterol, triglycerides, and systolic blood pressure, childhood BMI remained as an independent predictor of subsequent cancer mortality (HR, 1.24; 95%CI, 1.03-1.49). The association of childhood BMI and subsequent cancer mortality persisted after adjustment for adulthood BMI (HR for childhood BMI, 1.35; 95%CI 1.12-1.63).
Higher childhood BMI was independently associated with increased overall cancer mortality.
This study evaluated the effects of heat stress (HS) and dietary nano chromium picolinate (nCrPic) on metabolic responses of sheep to an intravenous glucose tolerance test (IVGTT), an intravenous ...insulin tolerance test (ITT) and an intramuscular adrenocorticotropin hormone (ACTH) challenge in sheep. Thirty-six sheep housed in metabolic cages were randomly allocated within 3 dietary groups (0, 400 and 800 μg/kg supplemental nCrPic) to either thermoneutral (22 °C) or cyclic HS (22 to 40 °C) conditions for 3 wk. Basal plasma glucose tended to be increased during HS (P = 0.052) and decreased by dietary nCrPic (P = 0.013) while plasma non-esterified fatty acid concentrations were decreased (P = 0.010) by HS. Dietary nCrPic reduced the plasma glucose area under the curve (P = 0.012) while there were no significant effects of HS on plasma glucose area under the curve in response to the IVGTT. The plasma insulin response over the first 60 min after the IVGTT was decreased by HS (P = 0.013) and dietary nCrPic (P = 0.022) with the effects being additive. In response to the ITT plasma glucose reached a nadir sooner (P = 0.005) in sheep exposed to HS, although there was no effect on the depth of the nadir. Dietary nCrPic decreased (P = 0.007) the plasma glucose nadir after ITT. Over the duration of the ITT plasma insulin concentrations were lower in sheep exposed to HS (P = 0.013) whereas there was no significant effect of supplemental nCrPic. There was no effect of either HS or nCrPic on cortisol response to ACTH. Dietary nCrPic supplementation decreased (P = 0.013) mitogen-activated protein kinase-8 (JNK) and increased (P = 0.050) carnitine palmitoyltransferase 1B (CPT1B) mRNA expression in skeletal muscle. Results of this experiment demonstrated that animals under HS and supplemented with nCrPic had greater insulin sensitivity.
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