青春期前压力与健康研究
目标 1:表征低收入早期青少年样本 (N = 225) 中的非稳态负荷 (AL) 生物标志物。 有多少生活在低收入家庭的儿童具有非典型或超出范围的生物标志物水平,哪些生物标志物以及以何种组合(目标 1a)? AL 生物标志物升高是否可以预测青春期早期的身心健康问题(目标 1b)? 11 岁和 14 岁之间 AL 生物标志物发生了多少变化和什么类型的变化(目标 1c)?
目标 2:在暴露于不同早期生活压力 (ELS) 水平的早期青少年的同一样本中,研究 ELS、近期(过去一年)和累积(自 5 岁起)压力暴露对初始 AL 水平的相对贡献在 T1(目标 2a),以及两年研究期间 AL 的变化(目标 2b)。
目标 3:探索应对资源(包括儿童的应对技能、儿童的生理自我调节和父母的应对社会化)在多大程度上独特且协同地影响这些早期青少年的 AL 水平和积累。
研究概览
详细说明
童年逆境与过早衰老疾病、大多数形式的精神病理学和早逝有关,而慢性压力是这一现象的关键机制。 迫切需要以生物学为依据的干预措施来打破这种恶性循环,但很少有研究检查可用于干预措施的童年时期潜在的可塑性心理生物学风险和保护过程。 Allostatic Load (AL)——身体在面对慢性压力时试图维持体内平衡而导致的生物损伤的累积——被认为是这样一种风险过程。 迄今为止,大多数 AL 研究都是针对成年人进行的,但针对青少年的新兴研究表明,对青春期早期 AL 积累过程的深入研究可能会产生重要的见解,以制定有效的心理生物学干预措施。 应对和自我调节是潜在的可塑性保护过程,但迄今为止,它们在 AL 研究中并未受到太多关注。 因此,该 R01 项目将检查青春期早期 AL 生物标志物的积累,并将测试压力(早年、累积、最近)和应对资源(应对技巧、父母应对社会化、生理调节)对 AL 积累的贡献。 此外,我们将研究 AL 与青春期中期出现的过早衰老疾病(例如 II 型糖尿病、代谢综合征)之间的关联。
在弱势青春期前的样本中检测到升高的 AL 生物标志物(例如,Evans,2003 年;Keller 等人,2012 年;Rogosch 等人,2011 年),并且与该人群的健康问题相关。 然而,我们对青年 AL 过程的理解仍然存在许多重要差距。 首先,AL 在儿童或青少年样本中的特征不明确。 大多数涉及儿童的现有研究仅关注 AL 指数的特定方面(如皮质醇),缺乏对高危儿童 AL 中指示的主要生物标志物类别(代谢、心血管、免疫、神经内分泌)的综合评估。 其次,缺乏将 AL 与儿童疾病联系起来的临床基准是一个主要的限制因素,再加上儿童 AL 相关疾病的较低基础率,使人们质疑使用成人阈值计算 AL 指数的典型做法(即,范围的上四分位数)。 第三,尚不清楚生命早期(出生到 5 岁)后经历的近期和累积压力在多大程度上导致任何年龄组的 AL 超过早期生命压力 (ELS) 的发展,许多 AL 研究没有包括对生活压力的深入评估。 第四,关于应对资源(青少年应对技能、应对社会化)在多大程度上可以缓冲儿童 AL 随着时间的发展和/或恶化,我们知之甚少。 这是一个关键问题,因为首席 PI 的研究表明,应对技能和资源可以缓冲高危儿童(例如,贫困儿童)免受常见压力源的影响,并且应对对 AL 的主要神经内分泌介质(例如 HPA)有影响(Wadsworth 等等人,2016 年;本德祖和沃兹沃斯,2017 年)。
本项目将以两位 PI 及其合作研究者的独特优势和能力为基础,并将包括对压力、应对资源和 AL 的最新评估,以在多个分析层次上充分捕捉这些过程。 经验丰富的儿科研究护士将在宾夕法尼亚州立大学 Hershey Hope Drive 儿科招募 200 名 11-12 岁的医疗补助登记患者。 另外 25 名家庭不符合医疗补助资格的 11-12 岁患者将作为生物标志物基准测试的中产阶级比较组。 这项研究附属的儿科实践每年进行 40,000 次患者就诊,并招收来自宾夕法尼亚州中部农村和城市社区的患者。 青年将被跟踪两年并参加三个年度评估。 生物样本将包括抽血、夜间尿液和在每个时间点采集的唾液样本。 评估将进一步包括 (a) 父母和孩子青少年生活压力访谈,以获得早期、最近和累积的生活压力指数,以及 (b) 特里尔社会压力测试,以衡量青少年 SAM 和 HPA 激活模式和父母应对社会化。 还将获得亲子副交感神经共同调节和心理症状、养育方式、亲子依恋和应对技巧的报告。 我们将检查 T1 时 AL 生物标志物的水平和相关性,以及 T1、T2 和 T3 之间发生的变化(AL 积累)的预测因子。 研究目的如下:
目标 1:表征低收入青春期前儿童 (N = 200) 样本中的 AL 生物标志物。 有多少生活在低收入家庭的儿童具有非典型或超出范围的生物标志物水平(与中产阶级比较组相比)(目标 1a)? 先前的 AL 生物标志物升高是否可以预测 13-14 岁时的身心健康问题(目标 1b)? 11 岁和 14 岁之间 AL 生物标志物发生了多少变化和什么类型的变化(目标 1c)?
目标 2:在暴露于不同水平 ELS 的青春期前儿童的同一样本中,调查 ELS、最近(过去一年)和累积(从 5 岁起)压力暴露对 T1 初始 AL 水平的相对贡献(目标 2a) ,以及两年研究期间 AL 的变化(目标 2b)。
目标 3:研究应对资源,包括儿童的应对技巧、儿童的生理自我调节、亲子依恋和父母应对社会化,如何独特且协同地影响青春期早期的 AL 水平和积累。
研究类型
参与标准
资格标准
适合学习的年龄
接受健康志愿者
有资格学习的性别
取样方法
研究人群
描述
纳入标准:
孩子
- 年龄:入学时11-12岁(含)
- 性别:男或女
- 流利的书面和口头英语
家长监护人
- 年龄:≥18岁
- 性别:男或女
- 流利的书面和口头英语
- 根据下表,家庭收入≤ 2018 年联邦贫困线的 200%:
排除标准:
孩子
- 年龄:入学时<11岁或≥13岁
- 认知障碍
- 怀孕(如果是女性)
- 慢性疾病(例如 精神障碍、癌症或心脏病)或研究者认为使受试者无法参与研究的任何其他医学状况。
家长监护人
- 年龄:≥18岁
- 认知障碍
- 囚犯
学习计划
研究是如何设计的?
设计细节
- 观测模型:队列
- 时间观点:预期
队列和干预
团体/队列 |
干预/治疗 |
---|---|
参加者
该队列将由 11-12 岁的男性和女性儿童组成,并由 18 岁以上的参与父母陪同。
该队列参与者的家庭收入不能超过 2018 年制定的联邦贫困线的 200%。
|
暴露于慢性压力
|
研究衡量的是什么?
主要结果指标
结果测量 |
措施说明 |
大体时间 |
---|---|---|
静负荷
大体时间:2年
|
代表来自高风险、农村贫困环境的青年在神经内分泌、自主神经、免疫学和代谢组学水平上的个体变化
|
2年
|
次要结果测量
结果测量 |
措施说明 |
大体时间 |
---|---|---|
儿童健康状况
大体时间:2年
|
儿童健康状况由受非静负荷影响的行为、心理、医疗和身体健康结果表示。
|
2年
|
合作者和调查者
调查人员
- 首席研究员:Martha E Wadsworth, PhD、Penn State
出版物和有用的链接
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