Marks I M
Br J Psychiatry. 1986 Oct;149:406-18. doi: 10.1192/bjp.149.4.406.
From protozoa to mammals, organisms have been selectively bred for genetic differences in defensive behaviour which are accompanied by differences in brain and other biological functions. Studies of twins indicate some genetic control of normal human fear from infancy onwards, of anxiety as a symptom and as a syndrome, and of phobic and obsessive-compulsive phenomena. Anxiety disorders are more common among the relatives of affected probands than of controls, especially among female and first-degree relatives; alcoholism and secondary depression may also be over-represented. Familial influences have been found for panic disorder, agoraphobia, and obsessive-compulsive problems. Panic disorder in depressed probands increases the risk to their relatives of phobia as well as of panic disorder, major depression, and alcoholism. The strongest family history of all anxiety disorders is seen in blood-injury phobia; even though it can be successfully treated by exposure, its roots may lie in a genetically determined specific autonomic susceptibility. Some genetic effects can be modified by environmental means.
从原生动物到哺乳动物，生物体一直在被选择性培育，以获取防御行为方面的基因差异，这些差异伴随着大脑和其他生物学功能的差异。对双胞胎的研究表明，从婴儿期开始，正常人类的恐惧、作为症状和综合征的焦虑以及恐惧和强迫现象都受到一定的基因控制。焦虑症在受影响先证者的亲属中比在对照组亲属中更常见，尤其是在女性和一级亲属中；酗酒和继发性抑郁症在亲属中也可能更为常见。已发现惊恐障碍、广场恐惧症和强迫问题存在家族影响。抑郁先证者中的惊恐障碍会增加其亲属患恐惧症、惊恐障碍、重度抑郁症和酗酒的风险。在血液-损伤恐惧症中可看到所有焦虑症中最强的家族病史；尽管它可以通过暴露疗法成功治疗，但其根源可能在于基因决定的特定自主易感性。一些基因效应可以通过环境手段加以改变。
