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Am J Psychiatry:围产期补充胆碱或减少孩子患精神分裂症风险

2013-03-19 文馨 编译 医学论坛网

  日前,《美国精神病学杂志》(Am J Psychiatry)上发表的一项随机安慰剂对照研究发现,新生儿的(大脑)抑制发育延迟与随着孩子发育成熟而发生的注意力问题有关。即使存在延迟大脑抑制发育的基因变异,围产期补充胆碱也能激活大脑抑制的及时发育。   大脑抑制不足是一种病理生理性大脑缺陷,这种缺陷与精神分裂症和其他精神障碍患者感觉门控和注意力较差有关。大脑抑制发育于围

  日前,《美国精神病学杂志》(Am J Psychiatry)上发表的一项随机安慰剂对照研究发现,新生儿的(大脑)抑制发育延迟与随着孩子发育成熟而发生的注意力问题有关。即使存在延迟大脑抑制发育的基因变异,围产期补充胆碱也能激活大脑抑制的及时发育。

  大脑抑制不足是一种病理生理性大脑缺陷,这种缺陷与精神分裂症和其他精神障碍患者感觉门控和注意力较差有关。大脑抑制发育于围产期,并受遗传和子宫内因素的影响。羊膜中的胆碱激活胎儿的α7-烟碱乙酰胆碱受体并促进大脑抑制的发育。通过促进正常的大脑发育来增加这种激活可能保护婴儿,防止今后发生疾病。研究人员研究了围产期补充胆碱对于人类婴儿大脑抑制发育的影响。

  研究人员进行了一项随机安慰剂对照的临床试验,研究入选了100名健康的孕妇,从妊娠中期开始通过饮食对她们补充磷脂酰胆碱。对孕妇或新生儿补充正常饮食剂量两倍的磷脂酰胆碱直至新生儿出生后3个月。所有女性无论接受磷脂酰胆碱治疗与否,都接受了饮食建议。分析配对声音对婴儿大脑诱发反应的P50成分的抑制的电生理记录。抑制的标准为与第一次反应相比,第二次P50反应幅度下降至少一半。

  结果,未观察到胆碱对产妇的健康、分娩、婴儿的出生或发育(造成)不良影响。出生后第五周,与安慰剂治疗组婴儿相比,胆碱治疗组婴儿的P50反应更多地受到了抑制(76%VS. 43%)(疗效值=0.7)。产后第13周时两组间无差异。在安慰剂治疗组而非胆碱治疗组中,与精神分裂症相关的CHRNA7基因型与P50抑制减少有关。

精神分裂相关的拓展阅读:


Perinatal Choline Effects on Neonatal Pathophysiology Related to Later Schizophrenia Risk

Objective  

Deficient cerebral inhibition is a pathophysiological brain deficit related to poor sensory gating and attention in schizophrenia and other disorders. Cerebral inhibition develops perinatally, influenced by genetic and in utero factors. Amniotic choline activates fetal α7-nicotinic acetylcholine receptors and facilitates development of cerebral inhibition. Increasing this activation may protect infants from future illness by promoting normal brain development. The authors investigated the effects of perinatal choline supplementation on the development of cerebral inhibition in human infants.

Method  

A randomized placebo-controlled clinical trial of dietary phosphatidylcholine supplementation was conducted with 100 healthy pregnant women, starting in the second trimester. Supplementation to twice normal dietary levels for mother or newborn continued through the third postnatal month. All women received dietary advice regardless of treatment. Infants’ electrophysiological recordings of inhibition of the P50 component of the cerebral evoked response to paired sounds were analyzed. The criterion for inhibition was suppression of the amplitude of the second P50 response by at least half, compared with the first response.

Results  

No adverse effects of choline were observed in maternal health and delivery, birth, or infant development. At the fifth postnatal week, the P50 response was suppressed in more choline-treated infants (76%) compared with placebo-treated infants (43%) (effect size=0.7). There was no difference at the 13th week. A CHRNA7 genotype associated with schizophrenia was correlated with diminished P50 inhibition in the placebo-treated infants, but not in the choline-treated infants.

Conclusions  

Neonatal developmental delay in inhibition is associated with attentional problems as the child matures. Perinatal choline activates timely development of cerebral inhibition, even in the presence of gene mutations that otherwise delay it.

    

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