本文以逻辑推理的方法,推导了克山病的初始发病机制。希图揭示出克山病的病因的征结所在。设想为求得克山病的防治工作得到基本解决。我们认为在地方病研究中,逻辑推理方法是与观察实验同样重要的方法,它们之间的关系是相辅相成的,互相促进的,我们据此推导了克山病的初始病因。一、我们在探讨克山病的初始病因中,发现乏硒说有其“真值内容”,但它尚有与事实相矛盾和不可克服或无法解释的缺陷。然而在我们探讨其“真值”时,研究了其缺陷,发现其缺陷为我们推导克山病的初始病因却提供了重要的线索。乏硒说所认为的环境乏硒和食物乏硒与克山病有直接平行的关系。但却忽略了硒对含硫氨基酸的依赖性和进入人体的同步特点,以及硒在人体内的生理作用与含硫氨基酸及其代谢产物的协同性。亚硒酸盐在体内只能充当还原剂的角色。硒在人体内可部分的取代硫而构成硒蛋氨酸、硒半胱氨酸、硒胱氨酸进一步组成蛋白质,包括结构蛋白和酶。将亚硒酸盐作为还原剂使用时可能破坏体内其它还原剂的还原能力。乏硒说由含硒酶—谷胱甘肽过氧化酶含量与活性偏低,而推导出身体的硒不足是不周密的,而恰恰影响谷胱甘肽过氧化酶的却是体内摄入蛋白质的情况。二、乏硫说未能将作用于人体的有机硫的存在形态与自然界存在的无机硫区别开来,而以地球化学范畴进行探讨,作了错误的判断。三、我们根据先驱者们的调查资料与实验结果,只能得出如下的推理:克山病是由于人体的蛋氨酸、色氨酸、赖氨酸、甘氨酸、精氨酸等摄入量不足,或食物中氨基酸不平衡,并缺乏胆碱、VPP、VC、VE、VB_(12)、VB_2等而引起的营养缺乏症。克山病的临床症状及病理改变皆原发于此等氨基酸的摄入不足,直接或间接地引起体内还原剂—还原型谷胱甘肽与半胱氨酸、NADH、NADPH 不足,以至无法还原 Fe~(3+),无法阻止膜上磷脂的不饱和脂肪酸的自动氧化所产生的及摄入酸败的脂肪所带来的过氧化质脂,使原本就因蛋氨酸,胆碱不足不能形成足够的磷脂酰胆碱的脆弱的膜崩解。结果造成溶酶体破裂,释出水解酶,水解酶水解并破坏了心肌组织,使其发生灶状坏死。同时并产生心脏抑制因子,致使循环衰竭、血压下降,最后患者死于循环衰竭。心律不齐、传导阻滞、心界扩大和心电异常与酪氨酸代谢的产物—儿茶酚胺、色氨酸产生的5—羟色胺和蛋氨酸产生的乙酰胆碱供应不足有关。 This article deduces the initial pathogenesis of Keshan disease by logical reasoning. Hope plans to reveal the root cause of Keshan disease. It is envisaged that the prevention and treatment of Keshan disease will be basically solved. We think that in the study of endemic diseases, logical reasoning methods are just as important as observation experiments. The relationship between them is mutually reinforcing and mutually reinforcing, and we deduce the initial etiology of Keshan disease. First, when we explored the initial etiology of Keshan disease, we found that there was “true value” in the lack of selenium, but it still had flaws contradicting and insurmountable or unexplainable with the facts. However, when we explored its “true value”, we investigated its flaws and found that its defects provided important clues for us to deduce the initial cause of Keshan disease. Selenium deficiency said that the lack of environmental selenium and lack of food and Keshan disease have a direct parallel relationship. But ignores the dependence of selenium on sulfur-containing amino acids and synchronization into the body, as well as the physiological role of selenium in humans and the synergy of sulfur-containing amino acids and their metabolites. Selenite acts only as a reductant in the body. Selenium can partially replace sulfur in the human body to form selenomethionine, selenomethionine, and selenomethionine to further make up proteins, including structural proteins and enzymes. The use of selenite as a reducing agent may destroy the reducing power of other reducing agents in the body. Selenium deficiency said by selenium enzyme - glutathione peroxidase content and activity is low, and deduced that the body’s lack of selenium is not careful, but it is precisely the impact of glutathione peroxidase protein intake is in vivo Case. Second, the lack of sulfur that can not be on the body of organic sulfur exists in the form of inorganic sulfur exist in nature, but to explore the area of ​​geochemistry, made a wrong judgment. Third, we based on the pioneer’s survey data and experimental results, can only come to the following reasoning: Keshan disease is due to the body’s methionine, tryptophan, lysine, glycine, arginine intake is insufficient, Or dietary amino acid imbalance, and the lack of choline, VPP, VC, VE, VB_ (12), VB_2 and other caused by nutritional deficiencies. Keshan disease clinical symptoms and pathological changes are primary in these amino acids intake, directly or indirectly caused by the body reductant - reduced glutathione and cysteine, NADH, NADPH inadequate, and can not be restored Fe 3+ can not stop the auto-oxidation of the unsaturated fatty acids in the phospholipids on the membrane and the intake of peroxydized lipids resulting from the rancid fat, which would otherwise not be sufficient due to methionine and choline deficiency Fragile membranes of phosphatidylcholine disintegrate. As a result lysosomal rupture, the release of hydrolase, hydrolase hydrolysis and destruction of myocardial tissue, so that the occurrence of focal necrosis. At the same time and produce cardiac inhibitory factor, resulting in circulatory failure, blood pressure drops, the last patient died of circulatory failure. Arrhythmia, conduction block, heart expansion and abnormal ECG and tyrosine metabolism products - catecholamines, tryptophan produced by serotonin and methionine produced insufficient supply of acetylcholine.