Prevalence and Trends in Obesity and Severe Obesity Among Children in the United States, 1999-2012

IMPORTANCE: Childhood obesity is the focus of public health efforts and accurate estimates of the prevalence and severity of obesity are needed for policy decisions and directions for future research. OBJECTIVE: To examine the prevalence of obesity and severe obesity over time for 14 years of the continuous National Health and Nutrition Examination Survey, 1999 to 2012, and to examine differences in the trends by age, race/ethnicity, and sex. DESIGN, SETTING, AND PARTICIPANTS: Representative sample (N = 26 690) of children in the United States, ages 2 to 19 years, in repeated cross-sections of the National Health and Nutrition Examination Survey, 1999 to 2012. MAIN OUTCOMES AND MEASURES: Prevalence of overweight (body mass index [BMI] ≥ 85th percentile), obesity (BMI ≥ 95th percentile for age and sex), class 2 obesity (BMI ≥ 120% of the 95th percentile or BMI ≥ 35), and class 3 obesity (BMI ≥ 140% of the 95th percentile or BMI ≥ 40). RESULTS: From 2011 to 2012, 17.3% (95% CI, 15.3-19.3) of children in the United States aged 2 to 19 years were obese. Additionally, 5.9% (95% CI, 4.4-7.4) of children met criteria for class 2 obesity and 2.1% (95% CI, 1.6-2.7) met criteria for class 3 obesity. Although these rates were not significantly different from 2009 to 2010, all classes of obesity have increased over the last 14 years. CONCLUSIONS AND RELEVANCE: Nationally representative data do not show any significant changes in obesity prevalence in the most recently available years, although the prevalence of obesity may be stabilizing. Continuing research is needed to determine which, if any, public health interventions can be credited with this stability. Unfortunately, there is an upward trend of more severe forms of obesity and further investigations into the causes of and solutions to this problem are needed

Behaviors and motivations for weight loss in children and adolescents: Weight Loss Behaviors and Motivations in Children

Examine the association between weight loss behaviors and motivations for weight loss in children and adolescents and the association of weight status with these behaviors and motivations in a nationally representative sample

Urban Park Development and Pediatric Obesity Rates: A Quasi-Experiment Using Electronic Health Record Data

INTRODUCTION: Childhood obesity affects ~20% of children in the United States. Environmental influences, such as parks, are linked with increased physical activity (PA). OBJECTIVE: To examine whether changes in Body Mass Index (BMI) z-score were associated with construction of a new park. METHODS: A quasi-experimental design was used to determine whether living in proximity of a park was associated with a reduction in BMI z-score. Children were selected from health clinics within an 11 mile radius of the park. A repeated-measure ANOVA was employed for analysis of the relationship between exposure (new park) and BMI z-score. RESULTS: Participants were 1443 (median age 10.3 range (2-17.9 years), BMI: z-score 0.84 ± 1.09) African American (77.4%) adolescents. Change in BMI z-score was not statistically different for children living at different distances from the park after controlling for age, gender, race, ethnicity, or payer type (p = 0.4482). We did observe a small 0.03 increase in BMI z-score from pre- to post-park (p = 0.0007). There was a significant positive association between child's baseline age and BMI z-score (p < 0.001). CONCLUSIONS: This study found proximity to a park was not associated with reductions in BMI z-score. Additional efforts to understand the complex relationship between park proximity, access, and PA are warranted

Effects of insurance status on children's access to specialty care: a systematic review of the literature

<p>Abstract</p> <p>Background</p> <p>The current climate of rising health care costs has led many health insurance programs to limit benefits, which may be problematic for children needing specialty care. Findings from pediatric primary care may not transfer to pediatric specialty care because pediatric specialists are often located in academic medical centers where institutional rules determine accepted insurance. Furthermore, coverage for pediatric specialty care may vary more widely due to systematic differences in inclusion on preferred provider lists, lack of availability in staff model HMOs, and requirements for referral. Our objective was to review the literature on the effects of insurance status on children's access to specialty care.</p> <p>Methods</p> <p>We conducted a systematic review of original research published between January 1, 1992 and July 31, 2006. Searches were performed using Pubmed.</p> <p>Results</p> <p>Of 30 articles identified, the majority use number of specialty visits or referrals to measure access. Uninsured children have poorer access to specialty care than insured children. Children with public coverage have better access to specialty care than uninsured children, but poorer access compared to privately insured children. Findings on the effects of managed care are mixed.</p> <p>Conclusion</p> <p>Insurance coverage is clearly an important factor in children's access to specialty care. However, we cannot determine the structure of insurance that leads to the best use of appropriate, quality care by children. Research about specific characteristics of health plans and effects on health outcomes is needed to determine a structure of insurance coverage that provides optimal access to specialty care for children.</p

Restoration of Regenerative Osteoblastogenesis in Aged Mice: Modulation of TNF

Skeletal changes accompanying aging are associated with both increased risk of fractures and impaired fracture healing, which, in turn, is due to compromised bone regeneration potential. These changes are associated with increased serum levels of selected proinflammatory cytokines, e.g., tumor necrosis factor α (TNF-α). We have used a unique model of bone regeneration to demonstrate (1) that aged-related deficits in direct bone formation can be restored to young mice by treatment with TNF blockers and (2) that the cyclin-dependent kinase inhibitor p21 is a candidate for mediation of the osteoinhibitory effects of TNF. It has been hypothesized recently that TNF antagonists may represent novel anabolic agents, and we believe that the data presented here represent a successful test of this hypothesis. © 2010 American Society for Bone and Mineral Researc

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570