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Article summary:

1. Individual differences in infants' attachment behavior are associated with a polymorphism of the oxytocin receptor gene (OXTR).

2. Oxytocin plays an important role in social behavior and has been linked to mental health outcomes, stress reactivity, and shyness.

3. Recent studies have examined associations between attachment-related phenomena in adults and single nucleotide polymorphisms (SNPs) within OXTR, with some findings suggesting a link between certain alleles and insecure attachment or reduced social support seeking.

Article analysis:

The article "Oxytocin Receptor (OXTR) Polymorphisms and Attachment in Human Infants" presents evidence from molecular genetics that suggests a link between the oxytocin receptor gene (OXTR) and the quality of infants' attachment behavior. The article provides a comprehensive overview of the role of environmental and genetic factors in infant attachment, with a focus on the potential influence of OXTR polymorphisms.

One potential bias in this article is its heavy reliance on studies that support the association between OXTR polymorphisms and attachment-related phenomena. While the article acknowledges some studies that have found no association between OXTR polymorphisms and adult attachment, it does not explore these findings in depth or consider alternative explanations for why some studies may not find an association.

Another potential bias is the article's emphasis on the positive effects of oxytocin on social behavior, without acknowledging any potential risks or negative effects. While oxytocin has been shown to improve social cognition in patients with autism, for example, it is important to note that there may be risks associated with administering oxytocin to individuals who do not have a clinical need for it.

Overall, while this article provides valuable insights into the potential role of OXTR polymorphisms in infant attachment, readers should approach its claims with caution and consider alternative explanations for any associations found.