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1.  Pubertal Height Velocity and Associations with Pre-pubertal and Adult Heights in Cystic Fibrosis 
The Journal of pediatrics  2013;163(2):376-382.e1.
To test the hypothesis that pubertal peak height velocity (PHV) in cystic fibrosis (CF) has improved and is influenced by pre-pubertal growth and genetic potential.
Study design
PHV from 1862 children born in 1984–87 and documented in the 1986–2008 US CF Foundation Registry was determined by statistical modeling and classified into normal, delayed (2-SD > average age), attenuated (magnitude < 5th percentile), or both (D&A). Genetic potential for height was estimated by parental stature.
PHV averaged 8.4 cm/y at age 14.0 y in boys and 7.0 cm/y at age 12.1 y in girls, ~6 mo delay and ~15% reduction compared with healthy children. PHV was normal in 60%, delayed in 9%, attenuated in 21% and D&A in 5%. Patients with delayed PHV reached similar adult height percentile (boys: 34th, girls: 46th) to those with normal PHV (boys: 33rd, girls: 34th); both were significantly taller than the attenuated (boys: 11th, girls: 19th) and D&A PHV subgroups (boys: 8th, girls: 14th). Pancreatic sufficient patients had taller pre-pubertal and adult heights but similar PHV compared with pancreatic insufficient or meconium ileus patients. Adjusting for genetic potential reduced adult height percentiles more in boys (25th to 16th) than girls (28th to 24th). Height at age 7 y, PHV age and magnitude, and parental stature significantly predicted adult height.
Pubertal PHV has improved in children with CF born after mid 1980s compared with older cohorts but remains below normal. Suboptimal pre-pubertal and pubertal growth led to adult height below genetic potential in CF.
PMCID: PMC3700583  PMID: 23535012
growth; linear growth; nutritional status; puberty; adolescents; height; height velocity; peak height velocity; genetic potential
2.  Early childhood weight status in relation to asthma development in high-risk children 
Obesity has been proposed to be a risk factor for the development of childhood asthma.
To examine weight status from birth to age 5 years in relation to the occurrence of asthma at age 6 and 8 years.
285 full-term high-risk newborns with at least one asthmatic/atopic parent, enrolled in the Childhood Origin of Asthma (COAST) project, were studied from birth to age 8 years. Overweight was defined by weight-for-length percentiles > 85th prior to age 2 years and body mass index percentile > 85th at ages 2–5 years.
No significant concurrent association was found between overweight and wheezing/asthma occurrence at each year of age. In contrast, longitudinal analyses revealed complex relationships between overweight and asthma. Being overweight at age 1 year was associated with a decreased risk of asthma at age 6 (OR=0.32, p=0.02) and 8 years (OR=0.35, p=0.04) as well as better lung function. However, being overweight beyond infancy was not associated with asthma occurrences. In fact, only children who were overweight at age 5 but not at age 1 year had an increased risk of asthma at age 6 years (OR=5.78, p=0.05).
In children genetically at high risk of developing asthma, overweight at age 1 year was associated with a decreased risk of asthma and better lung function at age 6 and 8 years. However, being overweight beyond infancy did not have any protective effect and even could confer a higher risk for asthma.
PMCID: PMC2998556  PMID: 21051081
Asthma; overweight; children; high risk birth cohort
3.  Incorporating Genetic Potential When Evaluating Stature In Children With Cystic Fibrosis 
The 2002 Cystic Fibrosis Foundation (CFF) practice guidelines recommend adjusting for genetic potential when evaluating height status in children with CF. However, there is paucity of data to support this recommendation. We compared three methods of classifying short stature: unadjusted height percentile < 10th, Himes adjusted height percentile < 10th, and unadjusted height below the CFF target height lower bound.
Patients and Methods
Data from 3306 children with parental heights documented in the 1986–2005 CFF Patient Registry were analyzed.
Mean height percentile of CF children (33rd) was lower than their parents’ (mothers’ 53rd, fathers’ 57th), and 80% of CF children were below the average of their parental height percentiles. In children with short parents, Himes adjusted height percentile was significantly higher than unadjusted height percentile (27th vs. 8th), whereas the opposite was found in children with tall parents (Himes adjusted at 18th vs. unadjusted at 49th). Consequently, the prevalence of short stature decreased from 52% to 22% in children with short parents and increased from 8% to 34% in children with tall parents after Himes adjustment. In children with discrepant classification on short stature before and after Himes adjustment, percent predicted forced expiratory volume in one second was negatively associated with unadjusted height percentile but positively associated with Himes adjusted height percentile. In children with short parents, the CFF method underestimated the prevalence of short stature (9%) compared to the Himes method (22%).
Without adjustment of genetic potential, the prevalence of short stature is underestimated and the association between height and lung function is biased.
PMCID: PMC2834199  PMID: 20138592
cystic fibrosis; height; parent-child relationship; short stature; lung function
4.  Effect of smoking status on total energy expenditure 
Individuals who smoke generally have a lower body mass index (BMI) than nonsmokers. The relative roles of energy expenditure and energy intake in maintaining the lower BMI, however, remain controversial. We tested the hypothesis that current smokers have higher total energy expenditure than never smokers in 308 adults aged 40-69 years old of which 47 were current smokers. Energy expenditure was measured by doubly labeled water during a two week period in which the subjects lived at home and performed their normal activities. Smoking status was determined by questionnaire. There were no significant differences in mean BMI (mean ± SD) between smokers and never smokers for either males (27.8+5.1 kg/m2 vs. 27.5+4.0 kg/m2) or females (26.5+5.3 kg/m2 vs. 28.1+6.6 kg/m2), although the difference in females was of similar magnitude to previous reports. Similarly, total energy expenditure of male smokers (3069+764 kcal/d) was not significantly different from that of never smokers (2854+468 kcal/d), and that of female smokers (2266+387 kcal/d) was not different from that of never smokers (2330+415 kcal/d). These findings did not change after adjustment for age, fat-free mass and self-reported physical activity. Using doubly labeled water, we found no evidence of increased energy expenditure among smokers, however, it should be noted that BMI differences in this cohort also did not differ by smoking status.
PMCID: PMC2989978  PMID: 21040542
5.  Classification tree for detection of single-nucleotide polymorphism (SNP)-by-SNP interactions related to heart disease: Framingham Heart Study 
BMC Proceedings  2009;3(Suppl 7):S83.
The aim of this study was to detect the effect of interactions between single-nucleotide polymorphisms (SNPs) on incidence of heart diseases. For this purpose, 2912 subjects with 350,160 SNPs from the Framingham Heart Study (FHS) were analyzed. PLINK was used to control quality and to select the 10,000 most significant SNPs. A classification tree algorithm, Generalized, Unbiased, Interaction Detection and Estimation (GUIDE), was employed to build a classification tree to detect SNP-by-SNP interactions for the selected 10 k SNPs. The classes generated by GUIDE were reexamined by a generalized estimating equations (GEE) model with the empirical variance after accounting for potential familial correlation. Overall, 17 classes were generated based on the splitting criteria in GUIDE. The prevalence of coronary heart disease (CHD) in class 16 (determined by SNPs rs1894035, rs7955732, rs2212596, and rs1417507) was the lowest (0.23%). Compared to class 16, all other classes except for class 288 (prevalence of 1.2%) had a significantly greater risk when analyzed using GEE model. This suggests the interactions of SNPs on these node paths are significant.
PMCID: PMC2795986  PMID: 20018079
6.  Serum Carotenoid Concentrations in Postmenopausal Women from the United States with and without Osteoporosis 
Antioxidant defenses may be compromised in osteoporotic women. Little is known about fruit and vegetable or carotenoid consumption among postmenopausal women. The primary carotenoids in human serum are α- and β-carotene, lycopene, β-cryptoxanthin, lutein, and zeaxanthin. This study investigated the interrelationships among serum carotenoid concentrations, fruit and vegetable intake, and osteoporosis in postmenopausal women (n = 59, 62.7 ± 8.8 y). Bone density was assessed by dual energy x-ray absorptiometry and osteoporosis diagnosis was based upon T-scores. Serum samples (n = 53) and 3-day diet records (n = 49) were analyzed. Logistic regression analyzed differences between carotenoids after adjusting for serum retinol; supplement usage; milk, yogurt, fruit, and vegetable intake; and BMI. Pearson statistics correlated carotenoids with specific fruit or vegetable intake. Serum lycopene concentrations were lower in the osteoporosis group than controls (p = 0.03). β-Cryptoxanthin intake was higher in the osteoporosis group (p = 0.0046). Total fruit and vegetable intakes were correlated with serum lycopene and β-cryptoxanthin (p = 0.03, 0.006, respectively). Serum α-carotene concentration was associated with carrot intake, and zeaxanthin and β-cryptoxanthin with lettuce intake. Carotenoids that may have beneficial skeletal effects are lower in women with osteoporosis. Research is needed to identify potential protective mechanisms or utilization of carotenoids during osteoporosis.
PMCID: PMC2692339  PMID: 19003732
β-cryptoxanthin; carotenoids; lycopene; osteoporosis; postmenopausal women

Results 1-6 (6)