Commentary: smoking during pregnancy--genes and environment weigh in.
Commentary: smoking during pregnancy--genes and environment weigh in.
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评论：怀孕期间吸烟——基因和环境的影响。
DOI：
10.1093/ije/dyq125
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发表时间：
2010
影响因子：
7.7
通讯作者：
Knopik,ValerieS
中科院分区：
文献类型：
--
作者：
Knopik,ValerieS
Iliadou等人在他们的文章中说，家庭因素混淆了母亲怀孕期间吸烟和子女超重之间的联系。1报告三个关键信息：(1)孕妇怀孕期间吸烟(SDP)与成年后子女超重的风险增加有关；(2)这种联系在一定程度上被家庭因素混淆；(3)需要确定SDP和子女超重的共同特定家庭因素。这些信息为关于SDP的作用和后来的后代结局的文献提供了重要的贡献。首先，这项研究证明了使用遗传信息设计来解决这个复杂问题的价值得到了额外的支持。其次，提醒我们注意人类状况的复杂性，在推断因果关系时要谨慎行事。在人类研究的世界里，我们很少考虑简单的关于先天和后天的科学问题，或者基因和环境是否相等。相反，我们正在处理的是多方面的问题，或许并不令人意外的是，这些问题的答案是多方面的。当人们开始研究SDP对人类群体的影响时，这种产前接触是否预示着以后的结果的问题变得相当混乱。实验室环境的控制或产前尼古丁暴露的受控交付已经不复存在，就像在动物研究中一样。遗传背景(近亲繁殖的动物品系)的控制也不复存在。当一个人开始研究人类的SDP时，他是在一个高度可变的人群中这样做的--遗传水平、环境水平以及自变量和因变量的水平上的变量。此外，在人类中，SDP不仅会导致胎儿接触尼古丁，还会导致大量其他有毒成分，如一氧化碳、氨、氮氧化物、铅和其他金属。2因此，人们不应将SDP对人类的影响仅限于尼古丁。此外，如果一名女性在怀孕期间吸烟，她在怀孕后吸烟是否也有可能不仅提供了产前的暴露，也提供了出生后的暴露？直到几年前，关于DSP是否预测未来结局的问题涉及两个独立样本的比较：那些在怀孕期间吸烟的女性和那些没有吸烟的女性，并对母亲和/或父亲的特征进行某种统计控制。毫不奇怪，两个这样的女性样本之间存在固有的差异，这就提出了一个问题：我们真的能比较她们吗？例如，怀孕期间吸烟的母亲倾向于依赖物质，3人患有其他共病精神病，3人有刑事犯罪史，4人有依赖物质的伴侣5，而且更有可能受教育程度较低。4考虑到这一点：如果患有ADHD的母亲在怀孕期间更经常吸烟，并通过基因传播增加孩子患ADHD的风险，那么所观察到的SDP与儿童ADHD之间的相关性将在很大程度上是虚假的，病因学上的相关性有限。最近已经作出努力，试图在可持续发展方案的范围内解决这一问题，取得各种成果--通过使用准试验性遗传信息方法。4、6如本报告所示，这种做法的一个例子是，1考察与社会发展计划意见不一致的兄弟姐妹对。1，4，6-9也就是说，母亲在一次怀孕期间吸烟，但在另一次怀孕期间没有吸烟。这种准实验性的遗传信息设计可以开始克服这样一个事实，即绝大多数现有研究只提供了对产前暴露可能是…的有限控制。
In their article,‘Familial factors confound the association between maternal smoking during pregnancy and offspring overweight’, Iliadou et al. 1 report three key messages:(i) maternal smoking during pregnancy (SDP) is associated with increased risk for offspring overweight in young adulthood;(ii) this association is partly confounded by familial factors; and (iii) specific familial factors common to both SDP and offspring overweight need to be identified. These messages offer important contributions to the literature on the role of SDP and later offspring outcome. First, this research demonstrates additional support for the value of using genetically informative designs to address this complex question. Secondly, we are reminded of the complexity surrounding the human condition and to tread carefully when making inferences of causation. Rarely, in the world of human research, are we considering scientific inquiries that are simple questions of nature vs nurture, or whether genes plus environment equal outcome. Rather, we are dealing with multifaceted questions that, perhaps unsurprisingly, have multifaceted answers. When one sets out to study the effects of SDP in human populations, the question of whether this pre-natal exposure predicts later outcome becomes considerably messy. Gone is the control of the laboratory environment or the controlled delivery of prenatal nicotine exposure, as in animal studies. Gone also is the control of genetic background (ie inbred animal strains). When one sets out to examine SDP in humans, one is doing so in a highly variable population—variable on the genetic level, the environmental level and the level of the independent and dependent variables. Moreover, in humans, SDP results in fetal exposure not only to nicotine but also to a large amount of other toxic components, such as carbon monoxide, ammonia, nitrogen oxide and lead and other metals. 2 Thus, one should not limit the effects of SDP in humans to nicotine alone. Further, if a woman smokes during her pregnancy, is it not also likely that she smoked after pregnancy providing not only pre-natal, but also post-natal, exposure?Up until a few years ago, this question of whether DSP predicted later outcome involved the comparison of two independent samples of women: those who smoked during pregnancy and those who did not, with some kind of statistical control for maternal and/or paternal characteristics. Unsurprisingly, there are inherent differences between two such samples of women, which begged the question: can we really compare them? For example, mothers who smoke during pregnancy tend to be substance dependent, 3 have other comorbid psychopathology, 3 have a history of criminal conviction, 4 have substance-dependent partners5 and are more likely to have less education. 4 Consider this: if mothers with ADHD more commonly smoke during pregnancy, and also confer increased child risk of ADHD via genetic transmission, the observed correlation between SDP and childhood ADHD would be largely spurious, with limited aetiological relevance. Recent efforts have been made to try to address this issue within the context of SDP across a variety of outcomes—by using quasi-experimental genetically informative approaches. 4, 6 One example of such an approach, as exemplified in the current report, 1 is to look at sibling pairs who are discordant for SDP. 1, 4, 6–9 That is, mothers have smoked during one pregnancy but not during another. Such a quasi-experimental genetically informative design can begin to overcome the fact that the vast majority of existing studies provide only limited control for the fact that pre-natal exposures may be …