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Objective To examine the relationship between brown adipose tissue (BAT) and muscle development, two tissues that derive from a common cell lineage, during the first 6 months of postnatal life. Study design Thirty healthy term infants (15 males and females) underwent whole-body magnetic resonance imaging examinations. Measurements of BAT in the supraclavicular area as well as measures of trunk musculature and subcutaneous adiposity were obtained at birth and at 6 months of age. Results Paraspinous musculature and subcutaneous white adipose tissue (WAT) increased, and the proportion of BAT in the supraclavicular area decreased during infancy. Although measures of BAT did not correlate with paraspinous musculature through the first 6 months of life ( r = −0.35; P = .09), BAT was a significant predictor of paraspinous musculature after adjusting for weight, body length, and WAT ( P = .002); infants with the smallest decreases in BAT had the greatest gains in musculature. In contrast, changes in BAT did not predict increases in subcutaneous WAT ( P = .25) during infancy, which were primarily determined by body weight. Conclusions Changes in BAT are associated with muscle development but not WAT accumulation in healthy infants. Studies are needed to determine the mechanism(s) by which BAT could facilitate muscle growth, and the degree to which decreased muscle mass, such as in preterm and low birth weight infants, is related to a deficiency of BAT.

To examine whether anthropometric measurements, blood pressure (BP), fasting total cholesterol, and low-density lipoprotein are related to ultrasound measures of carotid intima-media thickness (CIMT) in children and teenagers with no known risk factors for cardiovascular disease.This cross-sectional study included 599 subjects, 6 to 20 years of age (292 males, 307 females; 224 Hispanics, 210 European-Americans, 126 African-Americans, and 39 Asian-Americans) whose body mass index, waist circumference, BP, lipid profiles, and values for CIMT were determined.Measures of CIMT were significantly greater in males than females (P=.006) and in African-Americans when compared with other ethnic groups (all P.05). There were no relations between age, diastolic BP, or fasting levels of triglycerides, total cholesterol, or low-density lipoprotein values and CIMT measures, regardless of sex or ethnic background. Stratified multiple regression analysis indicated that body mass index and waist circumference independently predicted CIMT in both males and females, even after controlling for age, weight, BP, fasting lipid levels, and ethnic background.Increased body mass and adiposity are associated with increased intima-media thickness in children and teenagers. This association is present in children not considered overweight, underscoring the need for the continued promotion of adequate nutritional and physical exercise behavior during childhood.

To determine whether increased thyroid hormones levels have an effect on various bone components (cortical vs cancellous bone).The anthropometric and 3-dimensional quantitative computed tomography (CT) bone measurements, including bone density (BD), cross-sectional area (CSA) of the lumbar spine and femur, and cortical bone area (CBA) of the femur, of 18 children and adolescents with untreated hyperthyroidism were reviewed and compared with those of age-, sex-, and ethnicity-matched historical controls.No significant differences in height, weight, body mass index (BMI), or pubertal staging between patients and controls were found. Cortical BD was significantly lower (P.001) in children and adolescents with hyperthyroidism compared with historical controls. After adjusting for weight and height, no difference in femur CSA between hyperthyroid children and historical controls was evident. No significant correlations among thyroid hormone levels, antithyroid antibody levels, and cortical BD values were found.As determined by CT, cortical bone is the preferential site of bone loss in children and adolescents with untreated hyperthyroidism.

A prospective study was conducted to investigate the possibility of osteoporosis after treatment for childhood acute lymphoblastic leukemia (ALL). Forty-two survivors of ALL had the trabecular bone density of the spine evaluated by quantitative computed tomography, 6 to 98 months (mean 42 months) after completion of chemotherapy. The ALL survivors had significantly lower bone density than age-, gender-, and race-matched nonleukemic control subjects had (10% less, p less than 0.001); this decrease was accounted for solely by the subset of patients who had received cranial irradiation (n = 30; p less than 0.001). The relative reduction in bone density in ALL survivors was unrelated to age at the time of diagnosis or time without therapy. The effects on bone density of 18 Gy and of 22.5 to 25.2 Gy were indistinguishable. We conclude that survivors of ALL commonly have reduced bone density in the lumbar spine and suggest that the diminution is related to nervous system irradiation, not to the disease or to chemotherapy.

We have observed the development of chronic inflammatory bowel disease, indistinguishable from Crohn disease, in two boys with glycogen storage disease type Ib (GSD-Ib). A chance association of these diseases in two patients is unlikely. Studies of their neutrophils showed severe chronic neutropenia (mean absolute granulocyte counts of less than 500 cells/microliter) and markedly deficient chemotactic response (less than 5% of reference values) in the patients with GSD-Ib and normal neutrophil values in four patients with glycogen storage disease type Ia (GSD-Ia). Monocyte counts and responses to chemotactic stimulation were normal in both GSD-Ia and GSD-Ib. Chronic inflammatory bowel disease appears to be associated with GSD-Ib, and neutrophil abnormalities may be involved in the pathogenesis of the bowel inflammation.

To determine if osteoporosis is prevalent among patients with cystic fibrosis, we compared the vertebral bone density measured by quantitative computed tomography in 57 such patients (29 male, 28 female, aged 3 to 21 years) with those of an age-, race-, and sex-matched control group of 57 healthy subjects. Patients with cystic fibrosis had significantly lower bone density (10% lower, p less than 0.001) than in controls. The decrease in bone density in patients with cystic fibrosis was unrelated to age. Shwachman clinical evaluation scores (based on case history, pulmonary physical findings, growth, and x-ray findings) correlated positively with age-standardized bone density values (p less than 0.01). Male patients had substantially lower bone density than did female patients (p less than 0.02), but bone density differences related to gender were not significant when effects of disease severity were controlled for. Decreased bone density was more common in patients with poor nutritional status as determined by anthropometric measurements (p less than 0.05). We conclude that osteoporosis is a frequent complication in children with cystic fibrosis regardless of their age and is more prevalent in patients with greater disease severity.