ライフサイエンスコーパス: childhood obesity

1 re prevalent in conjunction with the rise in childhood obesity.

2 ironmental toxicant can be a risk factor for childhood obesity.

3 ancy is unlikely to be a main contributor to childhood obesity.

4 ectronic tool to predict an infant's risk of childhood obesity.

5 loci associated with the pathophysiology of childhood obesity.

6 magnetic fields (MFs) increases the risk of childhood obesity.

7 the scope and potency of PAC treatments for childhood obesity.

8 asthma medication use on the development of childhood obesity.

9 ected because of the increased prevalence of childhood obesity.

10 hanges may have influenced the prevalence of childhood obesity.

11 and obesity, particularly as they relate to childhood obesity.

12 eview focuses on the genetic contribution to childhood obesity.

13 xamine the perinatal risk factors related to childhood obesity.

14 s and plant-based diets in the prevention of childhood obesity.

15 birth weight, was the strongest predictor of childhood obesity.

16 heavy smoking was positively associated with childhood obesity.

17 infant feeding method, and for their link to childhood obesity.

18 ciation between smoking during pregnancy and childhood obesity.

19 e physical and mental health consequences of childhood obesity.

20 ity plays a critical role in the increase in childhood obesity.

21 c Islanders, smoking was not associated with childhood obesity.

22 Television viewing is associated with childhood obesity.

23 ategies that promote fetal growth and reduce childhood obesity.

24 e, during infancy is associated with risk of childhood obesity.

25 ntial in battling the increasing epidemic of childhood obesity.

26 olemia is associated with the development of childhood obesity.

27 e of early intervention in the prevention of childhood obesity.

28 mising, population-based approach to prevent childhood obesity.

29 d as weight/height, is often used to monitor childhood obesity.

30 that of underlying infection on the risk of childhood obesity.

31 rum antibiotics were associated with risk of childhood obesity.

32 ion of metabolic homeostasis contributing to childhood obesity.

33 ncreased risk of rapid growth in infancy and childhood obesity.

34 ests that air pollution is a risk factor for childhood obesity.

35 influence risk for chronic disease including childhood obesity.

36 e, during infancy is associated with risk of childhood obesity.

37 FM4 associated with adult body mass index or childhood obesity.

38 s associated with an increased risk of early childhood obesity.

39 hild health and decreasing the prevalence of childhood obesity.

40 s a first step towards primary prevention of childhood obesity.

41 dered when implementing strategies to combat childhood obesity.

42 s has been associated with increased risk of childhood obesity.

43 terventions improved the quality of care for childhood obesity.

44 forcers may have a protective effect against childhood obesity.

45 ignificant contribution to the prevention of childhood obesity.

46 disorder, to attention deficit disorder and childhood obesity.

47 pathways involved in the pathophysiology of childhood obesity.

48 ental media monitoring in efforts to prevent childhood obesity.

49 nments to make them more walkable may reduce childhood obesity.

50 ention delivery and training initiatives for childhood obesity.

51 is potentially a modifiable risk factor for childhood obesity.

52 tervening on multiple levels of influence on childhood obesity.

53 as a target for the effective prevention of childhood obesity.

54 strogens, flame retardants, heavy metals and childhood obesity.

55 n intakes could contribute to a reduction in childhood obesity.

56 ages 0 to 23 months is associated with early childhood obesity.

57 ic disparities exist across risk factors for childhood obesity.

58 phthalate concentrations and prevalences of childhood obesity.

59 od has a potential for primary prevention of childhood obesity.

60 ring infancy was not associated with risk of childhood obesity (1.01, 0.98-1.04).

61 Childhood obesity, a major public health problem, can le

62 ciation between smoking during pregnancy and childhood obesity across race/ethnicity categories merit

63 ohort of 172 patients presenting with severe childhood obesity and a family history of obesity.

64 AMILIA Study was designed to genetically map childhood obesity and associated biological processes in

65 of measures to reduce the global epidemic of childhood obesity and encourage mechanistic studies.

66 t previous studies have focused primarily on childhood obesity and have been hampered by limited cont

67 have attempted to elucidate the etiology of childhood obesity and have increased our understanding o

68 ios (ORs) (95% confidence intervals [CI]) of childhood obesity and hyperglycemia associated with diff

69 ted in improved family-centered outcomes for childhood obesity and improvements in child BMI.

70 hite matter (WM) damage has been reported in childhood obesity and in metabolic syndrome (MetS) but m

71 and validate equations for the prediction of childhood obesity and integrate them into a mobile phone

72 s considered the gold-standard treatment for childhood obesity and is provided to the parent and chil

73 be implemented to decrease the prevalence of childhood obesity and its cardiovascular consequences in

74 amilia Study was designed to genetically map childhood obesity and its comorbidities in the Hispanic

75 micals may play a role in the development of childhood obesity and metabolic disorders, especially wh

76 ue to rise with the increasing prevalence of childhood obesity and metabolic syndrome.

77 pporting the role of neighborhood factors on childhood obesity and obesity-related behaviors, much wo

78 On the basis of our simulation models, childhood obesity and overweight will continue to be a m

79 le studies now confirm relationships between childhood obesity and specific morbidities.

80 The etiology of the development of childhood obesity and subsequent disease is poorly under

81 o smoke and NRP contribute to development of childhood obesity and suggest that combined exposures ma

82 regarding the prevention of infant and early childhood obesity and to identify research gaps and oppo

83 Given the current epidemic of childhood obesity and widespread use of artificial sweet

84 The incidence of obesity (especially childhood obesity) and its associated health-related pro

85 at IL-17(+) MAIT cells are also increased in childhood obesity, and altered MAIT cell frequencies in

86 der of importance, the main risk factors for childhood obesity are being unfit, having an obese fathe

87 emographic-socioeconomic characteristics and childhood obesity are complex in the United States.

88 mon, studies examining these same factors on childhood obesity are far fewer.

89 The prevalence and magnitude of childhood obesity are increasing dramatically.

90 Many early life risk factors for childhood obesity are more prevalent among blacks and Hi

91 Genetic and environmental contributions to childhood obesity are poorly delineated.

92 of adipokines and inflammatory molecules in childhood obesity are well documented, the contribution

93 recessive disorder that is characterized by childhood obesity associated with hyperinsulinemia, chro

94 We demonstrate that 81.3% of childhood obesity-associated heterozygous MC4R mutations

95 l surface expression of all the 14 described childhood obesity-associated MC4R missense mutations.

96 ns for the potential pharmacologic rescue of childhood obesity-associated MC4R mutations and for the

97 se mutant receptors, in addition to 11 other childhood obesity-associated MC4R mutations, indicates t

98 her examine the functional defects caused by childhood obesity-associated MC4R mutations, we develope

99 As more epidemiologic data on childhood obesity become available, researchers are face

100 9 +/- 1.5 and 12 +/- 1.5 months) for risk of childhood obesity (BMI at 2 years >91(st) centile and we

101 BPA exposure is plausibly linked to childhood obesity, but evidence is lacking to date.

102 revious studies, we addressed CNVs in common childhood obesity by examining children with a BMI in th

103 pendent African American (AA) cohort of 1479 childhood obesity cases and 1575 lean controls.

104 ohort of 1080 defined European American (EA) childhood obesity cases and 2500 lean controls (< 50(th)

105 About 5% of childhood obesity cases are caused by a defect that impa

106 ns are implicated in a significant number of childhood obesity cases.

107 ntinued to show association when two extreme childhood obesity cohorts were included (2,214 cases and

108 Childhood obesity coincides with increased numbers of ci

109 ncy was associated with an increased risk of childhood obesity compared with controls without infecti

110 The high prevalence of childhood obesity continues to persist, especially in ch

111 he question as to whether the monocytosis in childhood obesity contributes to atherogenesis over the

112 an association between plant-based diets and childhood obesity does not mean that such diets should n

113 isorder characterized by neonatal hypotonia, childhood obesity, dysmorphic features, hypogonadism, me

114 ated for decades, the emerging links between childhood obesity, early onset puberty, and adult metabo

115 been one of the most robust risk factors for childhood obesity, effects of specific parenting influen

116 Reducing the burden of childhood obesity, eliminating health disparities, and p

117 In conclusion, childhood obesity entails monocyte gene expression alter

118 pment in genetically stable populations, the childhood obesity epidemic can be primarily attributed t

119 Addressing the childhood obesity epidemic continues to be a challenge.

120 Despite the worsening childhood obesity epidemic, the rate of inpatient bariat

121 increasingly examined for their role in the childhood obesity epidemic.

122 is unknown whether asthma contributes to the childhood obesity epidemic.

123 Childhood obesity, epidemic in the United States, has be

124 t drop stems from the concurrent increase in childhood obesity, few longitudinal studies of growth an

125 ve previously described a women with extreme childhood obesity (Fig. 1), abnormal glucose homeostasis

126 Severe childhood obesity has become a major health problem, and

127 Concurrently, childhood obesity has become an epidemic in the United S

128 Childhood obesity has been attributed to a decline in to

129 The study of childhood obesity has continued to grow exponentially in

130 In the past 2 decades, the prevalence of childhood obesity has increased dramatically.

131 Worldwide prevalence of childhood obesity has increased greatly during the past

132 Childhood obesity has increased significantly in recent

133 Childhood obesity has risen by more than 50% in the last

134 Prediction equations for risk of childhood obesity have been developed and incorporated i

135 The prevalence and severity of childhood obesity have increased steadily over the past

136 e found substantially greater achievement of childhood obesity HEDIS measures in the CDS arm (adjuste

137 findings advance etiologic understanding of childhood obesity, highlighting complex effects of SES o

138 deficits and by metabolic defects including childhood obesity, hyperinsulinemia and Type 2 diabetes.

139 Given the long-term adverse sequelae of childhood obesity, identification of early life factors

140 y of smoking were positively associated with childhood obesity in a dose-response manner.

141 city-specific association of phthalates with childhood obesity in a nationally representative sample.

142 ents of pentaBDE mixture was associated with childhood obesity in a population of Latino children par

143 ion would be a promising strategy to prevent childhood obesity in humans, but more research is clearl

144 n that among adults, the rate of increase in childhood obesity in many countries has been greater tha

145 Health initiatives address childhood obesity in part by encouraging good nutrition

146 Evidence of effective treatment of childhood obesity in primary care settings is limited.

147 bute to the genetic susceptibility of common childhood obesity in subjects of both European and Afric

148 Although the increased prevalence of childhood obesity in the United States has been document

149 tly needed to tackle the growing epidemic of childhood obesity in the US.

150 The prevalence of childhood obesity increased in the 1980s and 1990s but t

151 Childhood obesity increases the risk of obesity in adult

152 during the past year in the following areas: childhood obesity, insulin resistance, dyslipidemia, hyp

153 These results indicate that childhood obesity is a powerful predictor of development

154 Childhood obesity is a silent epidemic in America.

155 Childhood obesity is also growing in frequency, and the

156 Childhood obesity is an important public health problem

157 Childhood obesity is associated with a number of metabol

158 To assess whether childhood obesity is associated with airway dysanapsis (

159 Childhood obesity is associated with increased risk of b

160 Childhood obesity is associated with type 2 diabetes mel

161 Childhood obesity is currently at its highest: recent st

162 tions, causes, evaluation, and management of childhood obesity is discussed.

163 breastfeeding to reduced risk of developing childhood obesity is inconclusive, yet previous studies

164 It is possible that the prevalence of childhood obesity is increasing across generations as a

165 Childhood obesity is increasing and is associated with a

166 The prevalence of childhood obesity is increasing and the causes of this a

167 The prevalence of childhood obesity is increasing rapidly in low- and midd

168 Childhood obesity is increasing worldwide, and all previ

169 In addition, childhood obesity is more prevalent among minority subgr

170 ere is now growing evidence that the risk of childhood obesity is strongly influenced by perinatal de

171 Childhood obesity is the focus of public health efforts

172 rly life factors related to fetal growth and childhood obesity is warranted.

173 helps to understand why, particularly during childhood, obesity is a risk factor for the development

174 acid signature significantly associated with childhood obesity, is an independent risk factor of futu

175 The increase in childhood obesity mainly reflects increased energy intak

176 Childhood obesity may be a risk factor for higher mortal

177 In the context of other options for treating childhood obesity, metformin has not been shown to be cl

178 al degeneration, sensorineural hearing loss, childhood obesity, non-insulin-dependent diabetes mellit

179 mong children may partly explain the rise in childhood obesity observed in the past few years.

180 Studies of the effect of childhood obesity on bone accrual during growth have yie

181 of this study was to determine the effect of childhood obesity on skeletal mass and dimensions relati

182 ng or nicotine exposure during pregnancy and childhood obesity or metabolic disorders at any age.

183 etween maternal smoking during pregnancy and childhood obesity or whether this association varies by

184 r contributing to the world-wide epidemic of childhood obesity/overweight.

185 NPs being associated with common early-onset childhood obesity (P = 0.0003) and common adult morbid o

186 App, thereby providing proof of concept that childhood obesity prediction research can be integrated

187 gh extensive descriptive research shows that childhood obesity predisposes a person to adult obesity,

188 data suggest that the spiralling increase in childhood obesity prevalence might be abating; increased

189 Childhood obesity prevention strategies aimed at reducin

190 mponents suggests that they hold promise for childhood obesity prevention worldwide.

191 t can be replicated in their communities for childhood obesity prevention.

192 The Childhood Obesity Project was conducted as a European mu

193 seen between infection episodes and risk of childhood obesity (ptrend <0.0001).

194 ios for obesity in adulthood associated with childhood obesity ranged from 1.3 (95 percent confidence

195 One hypothesis is that increasing childhood obesity rates may explain part of this increas

196 Childhood obesity rates remain high, especially among ad

197 l analyses (n = 10,583), the odds for severe childhood obesity reached 1.30 (P = 8.0 x 10(-11)).

198 Childhood obesity remains a prominent public health prob

199 However, treatment for childhood obesity remains largely ineffective.

200 lues in women free of disease could mitigate childhood obesity remains unknown.

201 Lung, and Blood Institute (NHLBI)-initiated childhood obesity research.

202 ure to secondhand smoke on the prevalence of childhood obesity: results from NHANES, 2007-2010.

203 Anthropometry and childhood obesity risk data were obtained for 1868 UK-bo

204 e exposure to bisphenol A (BPA) may increase childhood obesity risk, but few prospective epidemiologi

205 astfeeding is associated with a reduction in childhood obesity risk.

206 However, the common forms of childhood obesity seem to result from a predisposition t

207 lic function in the potential development of childhood obesity should be further explored.

208 een PCSK1 rs6232 and obesity is stronger for childhood obesity than for adult obesity.

209 Given the current level of childhood obesity, the models predicted that a majority

210 revalence, health consequences, and costs of childhood obesity, there has been substantial interest i

211 adolescents, the IOTF convened a workshop on childhood obesity to determine the most appropriate meas

212 ssociation have released recommendations for childhood obesity treatment and prevention which include

213 tudy and 3 European cohort studies (European Childhood Obesity Trial, Norwegian Human Milk Study, and

214 cted the monocyte gene expression profile in childhood obesity using an Illumina microarray platform

215 regulation of monocyte IMPDH2 and TMEM134 in childhood obesity was also observed in obese adults.

216 Childhood obesity was based on a body mass index greater

217 Childhood obesity was defined as a body-mass index at or

218 our ongoing genome-wide association study on childhood obesity, we demonstrate that ATOM increases th

219 In light of the worldwide increase in childhood obesity, we examined the association between b

220 The familial risk ratio for childhood obesity when a parent is obese reaches >2.5.

221 Rapid infancy weight gain is associated with childhood obesity, whereas low infancy weight is associa

222 aring an RP intervention designed to prevent childhood obesity with a safety control.

223 5 differentially regulated monocyte genes in childhood obesity with obesity and complexity of coronar

224 etween antibiotic use in infancy and risk of childhood obesity, with implications for health-care del

225 dvise reduced milk-fat consumption to reduce childhood obesity, yet the relation between lower milk f