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Featured researches published by Molly M. Lamb.


JAMA | 2010

Prevalence of High Body Mass Index in US Children and Adolescents, 2007-2008

Cynthia L. Ogden; Margaret D. Carroll; Lester R. Curtin; Molly M. Lamb; Katherine M. Flegal

CONTEXT The prevalence of high body mass index (BMI) among children and adolescents in the United States appeared to plateau between 1999 and 2006. OBJECTIVES To provide the most recent estimates of high BMI among children and adolescents and high weight for recumbent length among infants and toddlers and to analyze trends in prevalence between 1999 and 2008. DESIGN, SETTING, AND PARTICIPANTS The National Health and Nutrition Examination Survey 2007-2008, a representative sample of the US population with measured heights and weights on 3281 children and adolescents (2 through 19 years of age) and 719 infants and toddlers (birth to 2 years of age). MAIN OUTCOME MEASURES Prevalence of high weight for recumbent length (> or = 95th percentile of the Centers for Disease Control and Prevention growth charts) among infants and toddlers. Prevalence of high BMI among children and adolescents defined at 3 levels: BMI for age at or above the 97th percentile, at or above the 95th percentile, and at or above the 85th percentile of the BMI-for-age growth charts. Analyses of trends by age, sex, and race/ethnicity from 1999-2000 to 2007-2008. RESULTS In 2007-2008, 9.5% of infants and toddlers (95% confidence interval [CI], 7.3%-11.7%) were at or above the 95th percentile of the weight-for-recumbent-length growth charts. Among children and adolescents aged 2 through 19 years, 11.9% (95% CI, 9.8%-13.9%) were at or above the 97th percentile of the BMI-for-age growth charts; 16.9% (95% CI, 14.1%-19.6%) were at or above the 95th percentile; and 31.7% (95% CI, 29.2%-34.1%) were at or above the 85th percentile of BMI for age. Prevalence estimates differed by age and by race/ethnic group. Trend analyses indicate no significant trend between 1999-2000 and 2007-2008 except at the highest BMI cut point (BMI for age > or = 97th percentile) among all 6- through 19-year-old boys (odds ratio [OR], 1.52; 95% CI, 1.17-2.01) and among non-Hispanic white boys of the same age (OR, 1.87; 95% CI, 1.22-2.94). CONCLUSION No statistically significant linear trends in high weight for recumbent length or high BMI were found over the time periods 1999-2000, 2001-2002, 2003-2004, 2005-2006, and 2007-2008 among girls and boys except among the very heaviest 6- through 19-year-old boys.


Annals of Nutrition and Metabolism | 2010

Early-life predictors of higher body mass index in healthy children.

Molly M. Lamb; Dana Dabelea; Xiang Yin; Lorraine G. Ogden; Georgeanna J. Klingensmith; Marian Rewers; Jill M. Norris

Background/Aims: Childhood obesity tracks into adulthood, and may increase diabetes and cardiovascular disease risk in adulthood. Prospective analyses may better define the pathways between early life factors and greater childhood body mass index (BMI), a measure of obesity. Methods: The Diabetes Autoimmunity Study in the Young (DAISY) prospectively follows children from birth that are at increased genetic risk for type 1 diabetes. We examined longitudinal data for 1,178 DAISY subjects (mean age at last follow-up: 6.59 years (range: 2.0–11.5 years). Birth size and diabetes exposure in utero were collected in the enrollment interview. Infant diet information was collected via interviews throughout infancy. Infant weight gain and childhood BMI were measured at clinic visits. Results: Female gender, diabetes exposure in utero, larger size for gestational age, shorter breastfeeding duration, and more rapid infant weight gain predicted higher childhood BMI. Formal mediation analysis suggests the effect of shorter breastfeeding duration on childhood BMI may be mediated by more rapid infant weight gain. Also, the effect of diabetes exposure in utero on childhood BMI may be mediated by larger size for gestational age. Conclusion: We identified strong interrelationships between early life factors and childhood BMI. Understanding these pathways may aid childhood obesity prevention efforts.


JAMA Pediatrics | 2013

Infant Exposures and Development of Type 1 Diabetes Mellitus The Diabetes Autoimmunity Study in the Young (DAISY)

Brittni Frederiksen; Miranda Kroehl; Molly M. Lamb; Jennifer Seifert; Katherine Barriga; George S. Eisenbarth; Marian Rewers; Jill M. Norris

IMPORTANCE The incidence of type 1 diabetes mellitus (T1DM) is increasing worldwide, with the most rapid increase among children younger than 5 years of age. OBJECTIVE To examine the associations between perinatal and infant exposures, especially early infant diet, and the development of T1DM. DESIGN The Diabetes Autoimmunity Study in the Young (DAISY) is a longitudinal, observational study. SETTING Newborn screening for human leukocyte antigen (HLA) was done at St. Josephs Hospital in Denver, Colorado. First-degree relatives of individuals with T1DM were recruited from the Denver metropolitan area. PARTICIPANTS A total of 1835 children at increased genetic risk for T1DM followed up from birth with complete prospective assessment of infant diet. Fifty-three children developed T1DM. EXPOSURES Early (<4 months of age) and late (≥6 months of age) first exposure to solid foods compared with first exposures at 4 to 5 months of age (referent). MAIN OUTCOME AND MEASURE Risk for T1DM diagnosed by a physician. RESULTS Both early and late first exposure to any solid food predicted development of T1DM (hazard ratio [HR], 1.91; 95% CI, 1.04-3.51, and HR, 3.02; 95% CI, 1.26-7.24, respectively), adjusting for the HLA-DR genotype, first-degree relative with T1DM, maternal education, and delivery type. Specifically, early exposure to fruit and late exposure to rice/oat predicted T1DM (HR, 2.23; 95% CI, 1.14-4.39, and HR, 2.88; 95% CI, 1.36-6.11, respectively), while breastfeeding at the time of introduction to wheat/barley conferred protection (HR, 0.47; 95% CI, 0.26-0.86). Complicated vaginal delivery was also a predictor of T1DM (HR, 1.93; 95% CI, 1.03-3.61). CONCLUSIONS AND RELEVANCE These results suggest the safest age to introduce solid foods in children at increased genetic risk for T1DM is between 4 and 5 months of age. Breastfeeding while introducing new foods may reduce T1DM risk.


Journal of the Academy of Nutrition and Dietetics | 2015

The Association between Food Insecurity and Obesity in Children—The National Health and Nutrition Examination Survey

Jasbir Kaur; Molly M. Lamb; Cynthia L. Ogden

BACKGROUND Food insecurity can put children at greater risk of obesity because of altered food choices and nonuniform consumption patterns. OBJECTIVE We examined the association between obesity and both child-level food insecurity and personal food insecurity in US children. DESIGN Data from 9,701 participants in the National Health and Nutrition Examination Survey, 2001-2010, aged 2 to 11 years were analyzed. Child-level food insecurity was assessed with the US Department of Agricultures Food Security Survey Module based on eight child-specific questions. Personal food insecurity was assessed with five additional questions. Obesity was defined, using physical measurements, as body mass index (calculated as kg/m²) greater than or equal to the age- and sex-specific 95th percentile of the Centers for Disease Control and Prevention growth charts. Logistic regressions adjusted for sex, race/ethnic group, poverty level, and survey year were conducted to describe associations between obesity and food insecurity. RESULTS Obesity was significantly associated with personal food insecurity for children aged 6 to 11 years (odds ratio=1.81; 95% CI 1.33 to 2.48), but not in children aged 2 to 5 years (odds ratio=0.88; 95% CI 0.51 to 1.51). Child-level food insecurity was not associated with obesity among 2- to 5-year-olds or 6- to 11-year-olds. CONCLUSIONS Personal food insecurity is associated with an increased risk of obesity only in children aged 6 to 11 years. Personal food-insecurity measures may give different results than aggregate food-insecurity measures in children.


Pediatric Diabetes | 2008

Maternal diet during pregnancy and islet autoimmunity in offspring

Molly M. Lamb; Mark A. Myers; Katherine Barriga; Paul Zimmet; Marian Rewers; Jill M. Norris

Background:  Recent studies on the etiology of type 1 diabetes mellitus (T1DM) suggest that the components of the infant diet are associated with islet autoimmunity (IA), a precursor of T1DM. The role of prenatal nutritional exposures has not been thoroughly investigated.


Pediatric Diabetes | 2015

The effect of childhood cow's milk intake and HLA-DR genotype on risk of islet autoimmunity and type 1 diabetes: The Diabetes Autoimmunity Study in the Young

Molly M. Lamb; Melissa R. Miller; Jennifer Seifert; Brittni Frederiksen; Miranda Kroehl; Marian Rewers; Jill M. Norris

Cows milk intake has been inconsistently associated with islet autoimmunity (IA) and type 1 diabetes (T1D) development. Genetic and environmental factors may modify the effect of cows milk on IA and T1D risk.


Public Health Nutrition | 2007

Plasma micronutrients are associated with dietary intake and environmental tobacco smoke exposure in a paediatric population

Heather L Brady; Molly M. Lamb; Ronald J. Sokol; Colleen A Ross; Jennifer Seifert; Marian Rewers; Jill M. Norris

BACKGROUND While adult populations have been well described in terms of nutritional status, such as the concentration of nutrient biomarkers, little work has been done in healthy paediatric populations. OBJECTIVE The primary objective of this analysis was to explore the determinants of plasma micronutrients in a group of healthy infants and children. DESIGN The Diabetes Autoimmunity Study in the Young (DAISY) has enrolled 1433 newborns at increased risk for type 1 diabetes in Denver, Colorado. A representative random sample of 257 children from the DAISY cohort between the ages of 9 months and 8 years with a total of 815 clinic visits over time was used in this analysis. Annual dietary intake was assessed over time with Willett food-frequency questionnaires that were validated in this population. Environmental tobacco smoke (ETS) was assessed using a validated survey. Plasma samples were tested for vitamins, carotenoids and total lipids. Predictors of plasma micronutrients were evaluated using mixed models for longitudinal data, while adjusting for age, human leukocyte antigen genotype, type 1 diabetes family history and other potential confounders and covariates. RESULTS Increased micronutrient intake was associated with increased levels of their respective plasma nutrient, with the exception of gamma-tocopherol. Independent of dietary intake, levels of alpha- and beta-carotene and beta-cryptoxanthin were significantly lower, and gamma-tocopherol was significantly higher, in children who were exposed to ETS. CONCLUSION Dietary intake predicts plasma micronutrient levels. Exposure to ETS potentially could have negative health effects in this young population.


Clinical & Developmental Immunology | 2013

Evidence of stage- and age-related heterogeneity of non-HLA SNPs and risk of islet autoimmunity and type 1 diabetes: the diabetes autoimmunity study in the young.

Brittni N. Frederiksen; Andrea K. Steck; Miranda Kroehl; Molly M. Lamb; Randall Wong; Marian Rewers; Jill M. Norris

Previously, we examined 20 non-HLA SNPs for association with islet autoimmunity (IA) and/or progression to type 1 diabetes (T1D). Our objective was to investigate fourteen additional non-HLA T1D candidate SNPs for stage- and age-related heterogeneity in the etiology of T1D. Of 1634 non-Hispanic white DAISY children genotyped, 132 developed IA (positive for GAD, insulin, or IA-2 autoantibodies at two or more consecutive visits); 50 IA positive children progressed to T1D. Cox regression was used to analyze risk of IA and progression to T1D in IA positive children. Restricted cubic splines were used to model SNPs when there was evidence that risk was not constant with age. C1QTNF6 (rs229541) predicted increased IA risk (HR: 1.57, CI: 1.20–2.05) but not progression to T1D (HR: 1.13, CI: 0.75–1.71). SNP (rs10517086) appears to exhibit an age-related effect on risk of IA, with increased risk before age 2 years (age 2 HR: 1.67, CI: 1.08–2.56) but not older ages (age 4 HR: 0.84, CI: 0.43–1.62). C1QTNF6 (rs229541), SNP (rs10517086), and UBASH3A (rs3788013) were associated with development of T1D. This prospective investigation of non-HLA T1D candidate loci shows that some SNPs may exhibit stage- and age-related heterogeneity in the etiology of T1D.


Public Health Nutrition | 2007

Comparison of children's diets as reported by the child via the Youth/Adolescent Questionnaire and the parent via the Willett food-frequency questionnaire

Molly M. Lamb; Colleen A Ross; Heather L Brady; Jill M. Norris

OBJECTIVE A comparison of a parent-completed Willett food-frequency questionnaire (FFQ) and a self-completed Youth/Adolescent Questionnaire (YAQ) has not yet been conducted. SETTING In the Diabetes Autoimmunity Study in the Young (DAISY), parents report their childs diet on the FFQ annually from birth until age 10 years, when the child begins to report their own diet using the YAQ. SUBJECTS To determine the comparability of these collection methods, 89 children aged 10-17 years and their parents completed the YAQ and FFQ, respectively, for the childs previous years diet. DESIGN We compared reported intakes for energy, the macronutrients and a variety of micronutrients of interest to the DAISY study. RESULTS Bland-Altman plots of energy-adjusted differences between questionnaire responses against their means suggested that the two collection methods gave similar results. The average Spearman correlation coefficient of all energy-adjusted nutrient intakes was 0.50, and did not differ significantly by gender (males, r=0.48; females, r=0.46) or age (10-11 years, r=0.49; 12-17 years, r=0.51). While correlated, the nutrient values from the FFQ were higher than the nutrient values from the YAQ. CONCLUSIONS While reported nutrient intakes are correlated, an indicator variable defining which survey method a nutrient was collected with should be included in any longitudinal data analyses examining nutrient intakes collected with the YAQ and the FFQ as independent predictors of a disease outcome.


The Journal of Clinical Endocrinology and Metabolism | 2008

Dietary Glycemic Index, Development of Islet Autoimmunity, and Subsequent Progression to Type 1 Diabetes in Young Children

Molly M. Lamb; Xiang Yin; Katherine Barriga; Michelle Hoffman; Anna E. Barón; George S. Eisenbarth; Marian Rewers; Jill M. Norris

CONTEXT Dietary factors may trigger or exacerbate the autoimmune disease process. OBJECTIVE Our objective was to examine dietary glycemic index (GI) and glycemic load (GL) for association with islet autoimmunity (IA) development, and progression from IA to type 1 diabetes. DESIGN The Diabetes Autoimmunity Study in the Young follows children at increased genetic type 1 diabetes risk. Diet is collected prospectively via a parent-reported food frequency questionnaire. SETTING This was an observational study of children in the Denver area. PATIENTS A total of 1776 Diabetes Autoimmunity Study in the Young children younger than 11.5 yr was included in the study. INTERVENTIONS There were no interventions. MAIN OUTCOME MEASURES IA, defined as the presence of autoantibodies to insulin, glutamic acid decarboxylase, or protein tyrosine phosphatase at two consecutive visits, or the presence of autoantibodies at one visit and diabetic on the next consecutive visit was determined. Type 1 diabetes was diagnosed by a physician. A total of 89 subjects developed IA, and 17 subsequently developed type 1 diabetes during follow-up. Our hypothesis was formulated after data collection. RESULTS GI and GL were not associated with IA development. More rapid progression to type 1 diabetes in children with IA was associated with higher dietary GI (hazard ratio: 2.20; 95% confidence interval: 1.17-4.15) and marginally associated with GL (hazard ratio: 1.59; 95% confidence interval: 0.96-2.64) at the first IA-positive visit. CONCLUSIONS Higher dietary GI and GL are not associated with IA development, but higher GI is associated with more rapid progression to type 1 diabetes in children with IA, perhaps due to increased demand on the beta-cell to release insulin. Further study is needed to confirm this finding and identify the underlying biological mechanism.

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Edwin J. Asturias

University of Colorado Denver

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Jill M. Norris

Colorado School of Public Health

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Marian Rewers

University of Colorado Denver

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Daniel Olson

University of Colorado Denver

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Stephen Berman

Colorado School of Public Health

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Jennifer Seifert

University of Colorado Denver

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Miranda Kroehl

Colorado School of Public Health

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Samuel R. Dominguez

University of Colorado Denver

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Alma Zacarias

Centers for Disease Control and Prevention

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Anne-Marie Rick

University of Colorado Denver

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