第二节MDD的遗传度及其抑郁症状
一项关于双生子（和家庭）研究的荟萃分析估计成人重度抑郁症（MDD）的遗传度约为40%[16]，而且在不同的国家这一估计惊人的稳定[17,18]。如果将不可靠的测量误差考虑在内，并通过两次评估分析MDD，则遗传度估计增加至66%[19]。儿童双生子研究进一步表明，在青少年中，遗传对抑郁症状的贡献巨大，遗传度估计介于50-80%[20-22]。从童年直至至少20周岁，影响焦虑和抑郁症状的遗传因素似乎在一定程度上稳定，虽然新的遗传因素可能会在成年早期出现[23,24]。通过各种工具测量的成人抑郁症状，其遗传度约为40%，而且这一估计在各国之间差异不大[11,25,26]。这些成年抑郁症状的稳定性几乎可以完全归因于同一套遗传因素[27-29]。
第三节CAD的遗传度和CAD危险因素
双生子样本的心血管研究提出了一个明确的基因对于高血压（h2=61%）[30]、致命性卒中（h2=32%）[31]和CAD（男性h2=57%，女性h2=38%）[32]的贡献。
遗传对于这些疾病终点的贡献，源自于风险基因对于许多生物和行为危险因素的联合作用并进而影响动脉粥样硬化进程。
遗传因素已被证明对吸烟[33,34]、缺乏体力活动[35,36]、体重指数[37]、2型糖尿病[38]、收缩压和舒张压[30,39]和血浆低密度脂蛋白胆固醇（LDL-C）和高密度脂蛋白胆固醇（HDL-C）水平[40]做出重大贡献。在大多数成年双生子样本中，这些确诊的危险因素的遗传度估计为50%或更高，而且在整个成人寿命期，这些估计仍然非常相似[41-43]。其他一些可疑的危险因素的总体方差，包括葡萄糖耐受不良[44-46]、胰岛素抵抗[47]、C-反应蛋白（CRP）[48]、促炎性细胞因子[49,50]、止血[51,52]、静息心脏自主神经控制[53-55]和自主神经系统对应激反应[56]，也显示了遗传的重大贡献，遗传度估计至少为30%。
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