Richard F. Miller
{"title":"Chronic Fatigue Syndrome (CFS) and related illnesses: A case history supporting subacute mercury poisoning or \"micromercurialism\"","authors":"Richard F. Miller","doi":"10.1588/MEDVER.2005.02.00071","DOIUrl":null,"url":null,"abstract":"The immunological findings in CFS patients have now been explained, especially chronic T-cell activation as the result of TH2 cell production in difference to TH1 cell production. Significant depletion of the sulfhydrylcontaining(-SH) amino acid, L-cysteine and the sulfhydryl-containing(-SH) tripeptide, glutathione, concentrations are explained by the body’s attempt to excrete the mercury introduced by vaccination and/or diet, resulting in competing T-cell processes not able to downregulate each other. Once these sulfhydrylcontaining (-SH) amino acid/tripeptide concentrations are returned to normal, the TH1/TH2 ratio will normalize and said chronic TH2-cell activation would cease. Low selenium levels have also explained by the formation of potentially hydrophobic mercury selenides and this further explains the elevated mercury levels seen in organs like the brain, liver and testicles. The interruption of metabolic pathways, such as carbohydrate metabolism leading to Diabetes Mellitus II in select CFS patients, has also been elucidated and evidence presented which support the influence of heavy metals like mercury playing a significant role. © Copyright 2005 Pearblossom Private School, Inc.–Publishing Division. All rights reserved.","PeriodicalId":363866,"journal":{"name":"Medical Veritas: The Journal of Medical Truth","volume":"64 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2005-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Veritas: The Journal of Medical Truth","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1588/MEDVER.2005.02.00071","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
慢性疲劳综合征(CFS)及相关疾病:支持亚急性汞中毒或“微汞中毒”的病例史
现在已经解释了CFS患者的免疫学结果,特别是由于TH2细胞产生与TH1细胞产生不同而导致的慢性t细胞激活。含有巯基(-SH)的氨基酸、l-半胱氨酸和含有巯基(-SH)的三肽、谷胱甘肽浓度的显著减少,可以解释为人体试图排泄由疫苗接种和/或饮食引入的汞,导致竞争性t细胞过程无法相互下调。一旦这些含巯基(-SH)氨基酸/三肽浓度恢复正常,TH1/TH2比率将恢复正常,慢性TH2细胞激活将停止。低硒水平也可以解释为潜在疏水的硒化汞的形成,这进一步解释了大脑、肝脏和睾丸等器官中汞水平升高的原因。代谢途径的中断,如碳水化合物代谢导致慢性疲劳综合症患者II型糖尿病,也已被阐明,并提出证据支持重金属如汞的影响发挥重要作用。©版权所有2005梨花私立学校股份有限公司-出版部。版权所有。
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