ライフサイエンスコーパス: adversity

1 ysical abuse during childhood, socioeconomic adversity).

2 ilience (defined as the ability to cope with adversity).

3 key to mental health outcomes in the face of adversity.

4 y are particularly susceptible to early-life adversity.

5 tment option in human sufferers of childhood adversity.

6 o form patterns of psychosocial advantage or adversity.

7 e and how best to model the effects of early adversity.

8 t responding resulting from early adolescent adversity.

9 asure the existence and timing of early-life adversity.

10 ain the diversity of individual responses to adversity.

11 riety of adverse events, including childhood adversity.

12 o depression and anxiety following childhood adversity.

13 lcohol use disorder relapsing in the face of adversity.

14 houghts and prayers from strangers following adversity.

15 early, severe and/or prolonged psychosocial adversity.

16 ated at 7 years of age following exposure to adversity.

17 nt of the juvenile's own experience of early adversity.

18 internalizing symptoms following exposure to adversity.

19 accessibility in the PVN following pubertal adversity.

20 lity to depression among children exposed to adversity.

21 etrimental health consequences of early life adversity.

22 , mental abilities that are enhanced through adversity.

23 uals who experience some forms of early-life adversity.

24 er circumstances of structural and political adversity.

25 effects were specific to different types of adversity.

26 rs at the cost of atom economy and synthetic adversity.

27 cial risks, such as poverty and psychosocial adversity.

28 x, intrauterine complications, and postnatal adversity.

29 Early life adversity.

30 iorate the broad and costly effects of early adversity.

31 ulating aspects of the consequences of early adversity.

32 as the conserved transcriptional response to adversity.

33 range of poor outcomes associated with early adversity.

34 g disease by mitigating the effects of early adversity.

35 y to psychological consequences of childhood adversity.

36 he context of parent-infant interactions and adversity.

37 tionalization is a significant form of early adversity.

38 erson-dependent variables such as early-life adversity.

39 2-month-old rats that experienced early-life adversity.

40 the rodent limited bedding paradigm of early adversity.

41 ons and stress granule responses to cellular adversity.

42 anisms of altered development in response to adversity.

43 ay a key role in the biological embedding of adversity.

44 ecific to females who experienced early-life adversity.

45 for significant benefit versus threshold for adversity.

46 ared with those who did not experience early adversity.

47 fied five distinct trajectories of childhood adversities.

48 BPD and link this neural phenotype to early adversity, a well-established social environmental risk

49 hese, a small group of children had multiple adversities across social, health, and family-related di

50 including 42 exposed to chronic war-related adversity, across the first decade of life, and assessed

51 ons in Kenya to test the links between early adversity, adult social bonds, and adult fecal glucocort

52 Given that childhood adversities affect cardiometabolic health and multiple h

53 Early-life adversity affects nearly half of all youths in the Unite

54 ne the conserved transcriptional response to adversity alongside other proposed measurements of biolo

55 Whether early life adversity also imposes intergenerational effects on the

56 nonhuman animal research suggests that early adversity alters aversive learning and associated neuroc

57 r humans as well as for other species, early adversity alters the neurobiology of aversive learning b

58 djustment for sociodemographic and perinatal adversities and IQ, psychotic experiences at ages 11-12

59 designs that include detailed measurement of adversities and outcomes.

60 jectively qualifies as exposure to childhood adversity and a dearth of prospective studies, substanti

61 ses partially explain the link between early adversity and adult survival.

62 e documents an association between childhood adversity and cardiometabolic outcomes across the life c

63 tween exposure to any prenatal environmental adversity and child neurodevelopmental delay.

64 onsider further the importance of early-life adversity and continue to explore how different biologic

65 ive evidence of an association between early adversity and enduring neural changes that impact socioe

66 eractive pathway between maternal early-life adversity and infant TL that predicts emerging behaviora

67 Childhood adversity and lifetime psychopathology were each associa

68 h new neuroscientific evidence linking early adversity and nurturing care with brain development and

69 The relationship between early adversity and outcomes across the lifespan is apparent i

70 7), mediated the relationship between social adversity and poor glycemic control specially in urban a

71 o meet the urgent need for new biomarkers of adversity and psychiatric outcomes.

72 to test the relationship between early life adversity and sleep quality across the life span.

73 ompleted measures of social adversity (early adversity and social discrimination), and underwent fMRI

74 stress and reward networks after early-life adversity and suggest mechanistic roles for Crh-expressi

75 e and indicate that close ties between early adversity and survival arise even in the absence of heal

76 Early adversity and telomere length were significantly associa

77 ed to clarify the relationship between early adversity and telomere length while exploring factors af

78 ave evaluated the relationship between early adversity and telomere length, a marker of cellular sene

79 tency among studies investigating early-life adversity and the effect of parental stress, even if the

80 ed upon the presence or absence of childhood adversity and the presence or absence of lifetime psycho

81 port the well-established notions that early adversity and weak social bonds both predict poor adult

82 ironments with exposures to poverty, chronic adversities, and acutely stressful events have been link

83 lts (n=30) with a history of early childhood adversity, and a control group (n=30) without trauma exp

84 confer psychological health, buffer against adversity, and facilitate performance.

85 to children experiencing more environmental adversity, and further understanding of the factors asso

86 grief symptoms, did not experience childhood adversity, and had better quality of life and positive m

87 ty, and the interaction of genes, early-life adversity, and the epigenome in influencing gene express

88 employed by males and females in response to adversity, and the possible evolutionary and development

89 dren in our study experienced some degree of adversity, and this was associated with a moderately hig

90 Females who experience the most adversity are also socially isolated in adulthood, sugge

91 ividual differences in impulsivity and early adversity are known to be strong predictors of adolescen

92 evelopment, the detrimental effects of early adversity are likely to be long lasting.

93 nd their relation to antisocial behavior and adversity are poorly understood.

94 We previously established that chronic adversity around puberty in female mice significantly al

95 chment figures among infants who experienced adversity as a benchmark, we assessed rat pup cortical l

96 or the conserved transcriptional response to adversity as a marker of biological embedding of social

97 The detected adversities at exposures close to the levels detected in

98 Here we discuss the various ways adversity becomes neurobiologically embedded, and how th

99 ion (p=0.03, d = 0.80) and that psychosocial adversity blunted physiological yet potentiated subjecti

100 ker of the health risks linked to early-life adversity both within and across generations.

101 Early life adversity can affect an individual's health, survival, a

102 Maltreatment risk and home adversity can affect indicators of middle childhood brai

103 rain imaging in children suggests that early adversity can interfere with white matter development in

104 resonance, reactive temperament, and chronic adversity combine across early development to shape the

105 o be a mechanism for how early environmental adversity compromises health.

106 specific biological mechanism through which adversity contributes to altered brain function, which i

107 fferential gene methylation as a function of adversity contributes to the emergence of individual ris

108 d to a conserved transcriptional response to adversity (CTRA) in circulating leukocytes that may cont

109 Comprehensive evaluations of adversity demonstrated more extensive telomere length ch

110 lifespans, individuals who experienced early adversity did not accelerate their reproduction compared

111 Females who experience >/=3 sources of early adversity die a median of 10 years earlier than females

112 In rodent models, early-life adversity directly impacts hippocampal neuron structure

113 employment history), social (e.g., childhood adversity, divorce history), and psychological (e.g., ne

114 ntal health outcomes, many people exposed to adversity do not develop such outcomes.

115 nditions in birds, but in our system current adversity dominated over early life experiences with res

116 gest that cognitive deficits attributable to adversity during early-life-sensitive periods are at lea

117 lish a potential molecular mechanism whereby adversity during puberty can enact lasting transcription

118 the context of other indicators of childhood adversity (e.g., traumatic life events, socioeconomic st

119 Children exposed to various forms of adversity early in life are at increased risk for a broa

120 South Africans completed measures of social adversity (early adversity and social discrimination), a

121 f evidence supports the role of psychosocial adversities (eg, stressful life events, interpersonal di

122 cent conceptual models argue that early life adversity (ELA) accelerates development, which may contr

123 Individuals with history of early life adversity (ELA) are disproportionately prone to opioid a

124 Early life adversity (ELA) has been associated with an increased ri

125 Early life adversity (ELA) increases major depressive disorder (MDD

126 Exposure to early-life adversity (ELA) increases the risk for psychopathologies

127 Early life adversity (ELA) is a risk factor for major depressive di

128 Early life adversity (ELA) is associated with increased risk for st

129 Early life adversity (ELA) paradigms in rodents produce lasting inc

130 is, recent treatment history, and early life adversity (ELA) were determined by psychological autopsy

131 l, and behavioral consequences of early life adversity(ELA).

132 l mechanisms through which the experience of adversity emerges as individual risk for mental illness

133 These discoveries suggest that early-life adversity, especially in the perinatal period, influence

134 veniles whose mothers experienced early life adversity exhibit high mortality before age 4, independe

135 rogramming that had occurred during pubertal adversity experience.

136 Adversities experienced by female baboons early in life

137 Adversity experienced during gestation is a predictor of

138 middle school can exacerbate the stress and adversity experienced during this critical life stage.

139 During reunion, adversity-experiencing pups showed aberrant interactions

140 Neither the accumulation nor recency of the adversity explained considerable variability in DNAm.

141 The developmental timing of adversity explains more variability in DNAm than the acc

142 death by 1 to 2 years, indicating that high adversity females decline in their ability to raise offs

143 entially at risk for dementia, and childhood adversity further impacts estradiol effects on neural fu

144 ion of conserved transcriptional response to adversity genes and distinct patterns of proinflammatory

145 How does adversity get under the skin of the developing child?

146 This introduced an adversity gradient along one specific dimension, while t

147 The early adversity group showed altered hypothalamus-pituitary-ad

148 inflammatory upstream signaling in the early adversity group.

149 wever, few studies have investigated whether adversity has time-dependent effects based on the age at

150 life, an indicator of exposure to early-life adversity, has been consistently associated with poor me

151 In animal models, similar variants of early adversity have been shown to modify amygdala-hippocampal

152 s of interventions for young children facing adversity have demonstrated multiple, positive effects b

153 ernal genotype, and indices of socioeconomic adversity (housing, employment, education, electricity,

154 Although non-cardiac adversity, identifiable from additional in vivo studies,

155 ional and psychosocial sources of early-life adversity in baboons and other long-lived species.

156 than single events, it is also possible that adversity in childhood has larger effects on later life

157 Adversity in early childhood exerts an enduring impact o

158 are elucidating principles of adaptation to adversity in early childhood with molecular, cellular, a

159 iple sources of nutritional and psychosocial adversity in early life; reproductive pace; and lifetime

160 aning (MSEW) to model accumulated early life adversity in mouse offspring and studied the underlying

161 d potentials (LFPs) and behaviors exposed to adversity in response to maternal rough and nurturing ha

162 bly, CRF is strongly modulated by early-life adversity in several of these brain regions.

163 ith knowledge about the role of psychosocial adversity in shaping psychopathology risk to present a w

164 Early adversity, in the form of abuse, neglect, socioeconomic

165 Prenatal exposure to environmental adversities, including maternal overweight/obesity, diab

166 w this system can be perturbed by early-life adversity, including reduced efficacy of the caregiver a

167 Early adolescent adversity increases adult risk for anxiety disorders.

168 Early-life adversity increases hippocampal CRH expression, and bloc

169 Although exposure to adversity increases risk for poor mental health outcomes

170 umulation hypothesis, in which the effect of adversity increases with the number of occasions exposed

171 eurobiological outcomes following caregiving adversity, indicating that these pathways are probabilis

172 Evidence shows that similar early life adversities induce sex-dependent epigenetic reprogrammin

173 Early life adversity induced age-dependent disruptions in sleep and

174 n 2-month-old male rats prevented early-life adversity-induced deficits in object recognition memory

175 the intervention did not mitigate early-life adversity-induced spatial memory losses at 4 and 8 month

176 thesis that there are sensitive periods when adversity induces greater DNAm changes.

177 Chronic psychosocial adversity induces vulnerability to mental illnesses.

178 However, whether early-life adversity influences the maturation and operations of th

179 ent-related (for which there was no recorded adversity) injury.

180 n which genetic vulnerability and early-life adversity interact remains obscure.

181 Early-life adversity is a common antecedent of adolescent and adult

182 al processing of reward following early life adversity is a highly promising depressive intermediate

183 Early adversity is a risk factor for the development of adult

184 Early-life adversity is associated with accelerated cellular ageing

185 Socioeconomic adversity is associated with accelerated epigenetic agin

186 In humans, early-life adversity is associated with impairments in learning and

187 Early-life adversity is associated with increased vulnerability to

188 Childhood adversity is associated with telomere shortening, and se

189 Early adversity is correlated with increased risk for negative

190 ommon across multiple rodent models of early adversity is increased signaling via forebrain Gq-couple

191 Exposure to early-life adversity is known to predict DNA methylation (DNAm) pat

192 and a recency model, in which the effect of adversity is stronger for more proximal events.

193 Childhood adversity is strongly linked to negative mental health o

194 ce, the process of adaptation in the face of adversity, is an important concept that is enabling the

195 elated risks, partially due to socioeconomic adversity later in life.

196 celerating reproduction following early-life adversity leads to higher lifetime reproductive success.

197 We suggest that childhood adversity leads to persistent alterations in transcripti

198 at experiencing one or more sources of early adversity led to a 9 to 14% increase in females' glucoco

199 We find that while early-life adversity led to dramatically shorter lifespans, individ

200 ty of cortisol as a biomarker for stress and adversity, little is known about whether cortisol output

201 icularly during sensitive periods when these adversities may have even more enduring effects.

202 The biological fingerprint of environmental adversity may be key to understanding health and disease

203 sting that a threshold of socioenvironmental adversity may be necessary to increase incidence.

204 ls as exposed versus unexposed to early-life adversity may dilute observed effects.

205 ether, these results suggest that early life adversity may have a lasting impact on serotonergic circ

206 These results suggest that early adversity may have long-lasting physiological consequenc

207 aging, offering one mechanism through which adversity may increase risk for age-related disease.

208 That is, early life adversity may inhibit the formation of supportive social

209 t can be used to examine how additional life adversity may provoke disease risk or resilience.

210 study suggests that the shadow of childhood adversity may reach far into later adulthood in part thr

211 Childhood adversity may sensitize certain individuals to later str

212 ve emotional and/or behavioral adaptation to adversity, may be influenced by genetic factors that hav

213 dams exposed during infancy to the scarcity-adversity model of low nesting resources, and then chara

214 oci (n = 35) were predicted by the timing of adversity, namely exposures before 3 years of age.

215 were admitted with injury related to neither adversity nor accidents.

216 Neither early-life adversity nor CRHR1 blockade in the adult influenced anx

217 umulative effects of childhood and adulthood adversities on adult telomere length.

218 ak social bonds: The direct effects of early adversity on adult glucocorticoid concentrations were 11

219 that might help mitigate the impact of early adversity on brain development.

220 fic literature on the influence of childhood adversity on cardiometabolic outcomes that constitute th

221 ted the effect of any prenatal environmental adversity on child neurodevelopmental delay.

222 mediate the effect of prenatal environmental adversity on child neurodevelopmental delay.

223 e not enough to explain the effects of early adversity on glucocorticoid concentrations.

224 ak compared to the powerful effects of early adversity on glucocorticoid levels in adulthood.

225 ute to the deleterious effects of early-life adversity on hippocampal dendritic arborization, synapse

226 tcomes can be traced to the impacts of early adversity on multiple and integrated biological systems

227 e full range of reported effects of prenatal adversity on offspring growth, we propose an integrative

228 rature suggests latent effects of early life adversity on serotonin function may play a role in this

229 to understand potential influences of social adversity on the aging process.

230 the mechanisms of the effects of early-life adversity on the brain and the body.

231 probe the protean consequences of early-life adversity on the developing brain.

232 pment, which propose that antenatal maternal adversity operates through the biological pathways assoc

233 Blocking pup stress hormone during either adversity or reunion restored typical behavior, LFP powe

234 ess capable of working against many forms of adversity; organisms do not need to hope as a subjective

235 rventions toward children who are exposed to adversity, particularly during sensitive periods when th

236 y reactive young children growing in chronic adversity, particularly those who later develop anxiety

237 gically embedded, and how the timing of such adversity plays an important role in determining outcome

238 the most common causes of death in this high adversity population.

239 ween three different dimensions of childhood adversities: poverty and material deprivation, loss or t

240 In adjusted models, lifetime cumulative adversity predicted 6% greater odds of shorter telomere

241 rs to be a sensitive period when exposure to adversity predicts differential DNAm patterns.

242 female baboons to show that cumulative early adversity predicts natural adult lifespan.

243 e-1 (CRHR1) immediately following early-life adversity prevented the consequent memory and LTP defect

244 CRHR1 in young adults ameliorates early-life adversity-provoked memory deficits later in life.

245 ssect out the mechanisms by which early-life adversity provokes dysregulation of the complex interact

246 We show that during adversity, pup cortical LFP dynamic range decreased duri

247 This translational approach suggests adversity-rearing produces a stress-induced aberrant neu

248 Mothers experiencing adversity reduce maternal investment leading to stunted

249 Even more, early adversity reduced flexible, threat probability signaling

250 10 years after hospital discharge following adversity-related (self-inflicted, drug-related or alcoh

251 fter discharge, and to compare risks between adversity-related and accident-related index injury afte

252 micides in our estimates of 10-year risks of adversity-related deaths, we did not explicitly present

253 nged scanning patterns selectively along the adversity-related dimension, but not the orthogonal dime

254 Emergency hospital admission with adversity-related injury (ie, self-inflicted, drug-relat

255 e significantly increased after all types of adversity-related injury except for girls who had violen

256 Adolescents discharged after adversity-related injury had higher risks of suicide (ad

257 ficient evidence that girls discharged after adversity-related injury had increased risks of accident

258 years) who were admitted as an emergency for adversity-related or accident-related injury between Apr

259 We identified admissions for adversity-related or accident-related injury to the Nati

260 of reproductive acceleration following early adversity remain untested.

261 dies and 70% of animal studies of early-life adversity reported increased methylation at this exon va

262 tested the hypothesis that early adolescent adversity reshapes vlPAG/DR threat-related cue activity

263 Early adolescent adversity resulted in a greater proportion of cue-respon

264 may contribute to the exposure to childhood adversity, resulting in potential genetic confounding of

265 Research focused on early-life adversity revealed that early-life experiences have a pe

266 Rat pups were exposed to an Adversity-Scarcity model from postnatal day 8-12, where

267 Although cumulative lifespan adversity should have bigger impacts than single events,

268 ches alter multiple components of early-life adversity simultaneously.

269 ale rats that experienced chronic early-life adversity/stress (CES).

270 atal period is a window of vulnerability for adversities such as maternal depressive symptoms.

271 was significantly associated with childhood adversity (T = 2.3; P = .03).

272 Single adversities tended to have nonsignificant relations with

273 Living in poverty increases exposure to adversities that undermine healthy development, impeding

274 In adjusted models for cumulative childhood adversity, the occurrence of each additional childhood e

275 While often considered an adversity to be ignored, chronic stress has important pa

276 also conceptually outlines pathways linking adversity to cardiometabolic health, identifies evidence

277 4.07-5.06) than that of children with a low adversity trajectory, corresponding to 10.30 (95% CI 9.0

278 Compared with children with a low adversity trajectory, those who had early-life material

279 ng and nature of such experiences (including adversity, trauma, and enrichment) govern their influenc

280 is better adapted than the male to maternal adversity (Trivers-Willard hypothesis).

281 Adversity type and timing significantly impacted the ass

282 factors affecting the association, including adversity type, timing and study design.

283 ther this pattern emerges following specific adversity types.

284 phenotype and measures of social environment adversity varied among studies.

285 tablished prospective birth cohort (Maternal Adversity, Vulnerability, and Neurodevelopment) were use

286 Exposure to early life adversity was assessed at baseline using a cumulative ri

287 Long-term exposure to psychosocial adversity was associated with dampened striatal dopamine

288 d whether long-term exposure to psychosocial adversity was associated with dopamine dysfunction and i

289 Higher early home adversity was associated with electrophysiological profi

290 r than affective empathy, and greater social adversity was associated with reduced reported compassio

291 Parenting and home adversity was measured at baseline.

292 of health problems associated with childhood adversity, we argue that the field needs a second genera

293 logistic regression models of developmental adversities were used to adjust for potential confounder

294 cal susceptibility interacts with early life adversity, where FND can be precipitated by traumatic ev

295 ntal signals comprise a novel potent type of adversity, which contributes to subsequent vulnerabiliti

296 index the neurobiological embedding of early adversity, which in turn may impact children's cognitive

297 enoAge (9.2%), closely followed by adulthood adversity, which was suggested to contribute 9.0% of the

298 saster-related stressors that predict health adversity will help officials prepare for the coronaviru

299 ith high cumulative exposure to psychosocial adversity with n = 17 age- and sex-matched participants

300 rtion of children (36 081 [3%]) had multiple adversities within all dimensions and throughout the ent