Morris J A
Royal Lancaster Infirmary, Lancaster LA1 4RP, UK.
FEMS Immunol Med Microbiol. 2004 Sep 1;42(1):42-7. doi: 10.1016/j.femsim.2004.06.016.
The common bacterial toxin hypothesis of sudden infant death syndrome (SIDS) is consistent with the epidemiological features of the condition including the age distribution, seasonal incidence, association with prone sleeping and with exposure to tobacco smoke. The hypothesis is supported by experimental evidence but there are two barriers to its acceptance: the speed of onset does not fit with conventional concepts of an infective process; furthermore, the hypothesis appears to offer a single explanation for what is regarded as a multifactorial disease. Concepts from information theory are used to explore these objections. Complex physiological systems process information and need a high level of redundancy to minimise error. Models show that deleterious mutations in such a system will interact synergistically. Environmental perturbations are most likely to cause failure (sudden death) in systems with several mutations. Models also indicate that mutation rates will pose a limit to the size of the functioning genome and, therefore, increased complexity in evolution depends on using old genes in new combinations rather than the chance appearance of new genes. The idea that we share our genes with the rest of creation (same genes but different combinations) leads to the following conjecture: for every receptor controlling the flow of information across a cell membrane there will be a bacterially coded molecule that can switch it off or on. Based on this premise, bacterial toxaemia could cause sudden death, merely the time it takes for a molecule to associate with or dissociate from its receptor. Regardless of the number of physiological systems involved in SIDS, the age distribution will have a unimodal peak corresponding to the age range during which infant serum IgG reaches its nadir. In this way, the two barriers to the common bacterial toxin hypothesis can be overcome: one explanation but multiple bacteria and toxins acting with variable speed on multiple target systems.
婴儿猝死综合征（SIDS）的常见细菌毒素假说与该病症的流行病学特征相符，包括年龄分布、季节性发病率、与俯卧睡眠及接触烟草烟雾的关联。该假说得到了实验证据的支持，但存在两个阻碍其被接受的因素：发病速度不符合感染过程的传统概念；此外，该假说似乎为一种被认为是多因素疾病的情况提供了单一解释。信息论的概念被用于探讨这些异议。复杂的生理系统处理信息，需要高度的冗余以将误差最小化。模型表明，此类系统中的有害突变将协同作用。环境扰动最有可能在具有多种突变的系统中导致故障（猝死）。模型还表明，突变率将对功能基因组的大小构成限制，因此，进化中复杂性的增加取决于以新的组合使用旧基因，而非新基因的偶然出现。我们与其他生物共享基因（相同的基因但不同的组合）这一观点引出了以下推测：对于每一个控制跨细胞膜信息流的受体，都会有一种细菌编码的分子能够将其关闭或开启。基于这一前提，细菌血症可能导致猝死，仅仅是一个分子与其受体结合或解离所需的时间。无论SIDS涉及多少生理系统，年龄分布都会有一个单峰峰值，对应于婴儿血清IgG达到最低点的年龄范围。通过这种方式，可以克服常见细菌毒素假说的两个障碍：一种解释，但多种细菌和毒素以可变速度作用于多个靶系统。
