Battaglia Marco
Department of Psychiatry and Neurosciences, Laval University, Québec, Canada; Centre de Recherche Institut Universitaire en Santé Mentale de Québec, Canada.
Dialogues Clin Neurosci. 2015 Sep;17(3):277-85. doi: 10.31887/DCNS.2015.17.3/mbattaglia.
Physiological and adaptive separation anxiety (SA) is intimately connected with the evolutionary emergence of new brain structures specific of paleomammalians, the growth of neomammalian--and later hominid--brain and skull size, and the appearance of bipedalism. All these evolutionary milestones have contributed to expanding the behavioral repertoire and plasticity of prehuman and human beings, at the cost of more prolonged dependency of the infant and of the child on parental care. Separation anxiety disorder (SAD) can be seen as an exaggerated/inappropriate manifestation of SA that constitutes a gateway to poorer mental and physical health. By blending epidemiological, genetic-epidemiological, endophenotypic, and animal laboratory approaches, it is possible to delineate some of the mechanisms that link childhood-adolescence SA and SAD to health problems later in life. Causal mechanisms include gene-environment interplays and likely differential regulation of genes and functional net-works that simultaneously affect multiple behavioral and physical phenotypes after exposure to early-life adversity, including parental separation/loss.
生理性和适应性分离焦虑(SA)与古哺乳动物特有的新脑结构的进化出现、新哺乳动物(以及后来的原始人类)脑和颅骨大小的增长以及两足行走的出现密切相关。所有这些进化里程碑都有助于扩展前人类和人类的行为技能和可塑性,但代价是婴儿和儿童对父母照顾的依赖时间更长。分离焦虑症(SAD)可被视为SA的一种过度/不适当表现,它是通往更差身心健康的一个入口。通过整合流行病学、遗传流行病学、内表型和动物实验室方法,有可能描绘出一些将儿童期至青少年期的SA和SAD与生命后期健康问题联系起来的机制。因果机制包括基因-环境相互作用,以及在暴露于早期逆境(包括父母分离/丧失)后可能对基因和功能网络进行的差异调节,这些调节会同时影响多种行为和身体表型。