Can glyphosate’s disruption of the gut microbiome and induction of sulfate deficiency explain the epidemic in gout and associated diseases in the industrialized world?
S. Seneff, N. Causton, G. Nigh, G. Koenig, D. Avalon
{"title":"Can glyphosate’s disruption of the gut microbiome and induction of sulfate deficiency explain the epidemic in gout and associated diseases in the industrialized world?","authors":"S. Seneff, N. Causton, G. Nigh, G. Koenig, D. Avalon","doi":"10.4024/04SE17A.JBPC.17.02","DOIUrl":null,"url":null,"abstract":"Gout is an ancient disease, which has been known at least since Babylonian times. The word “gout” is derived from the Latin word “gutta” (drop); it signifies the belief that a poison, seeping into the joint drop by drop, is the cause [1]. Much is understood about the aetiology of gout, although there are also still many mysteries yet to be resolved. Gout is an inflammatory joint disease that is typically episodic and localized to certain joints, especially the metatarsophalangeal (MTP)1 joint and other joints in feet and fingers. An acute episode of gout is usually triggered by urate crystals in the joint, which induce a cascade reaction beginning with the influx of immune cells, especially neutrophils, which release cytokines such as IL-1β and IL-6, causing an inflammatory response leading to oxidative damage and intense pain, and terminating when feedback responses finally dampen the signal. While gout is associated with high serum urate, the association is not as strong as would be expected. Many people with elevated serum urate never experience gout, and many gout sufferers have normal levels of serum urate [2]. Thus, it is generally agreed that something else","PeriodicalId":88911,"journal":{"name":"Journal of biological physics and chemistry : JBPC","volume":"17 1","pages":"53-76"},"PeriodicalIF":0.0000,"publicationDate":"2017-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biological physics and chemistry : JBPC","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4024/04SE17A.JBPC.17.02","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
Abstract
Gout is an ancient disease, which has been known at least since Babylonian times. The word “gout” is derived from the Latin word “gutta” (drop); it signifies the belief that a poison, seeping into the joint drop by drop, is the cause [1]. Much is understood about the aetiology of gout, although there are also still many mysteries yet to be resolved. Gout is an inflammatory joint disease that is typically episodic and localized to certain joints, especially the metatarsophalangeal (MTP)1 joint and other joints in feet and fingers. An acute episode of gout is usually triggered by urate crystals in the joint, which induce a cascade reaction beginning with the influx of immune cells, especially neutrophils, which release cytokines such as IL-1β and IL-6, causing an inflammatory response leading to oxidative damage and intense pain, and terminating when feedback responses finally dampen the signal. While gout is associated with high serum urate, the association is not as strong as would be expected. Many people with elevated serum urate never experience gout, and many gout sufferers have normal levels of serum urate [2]. Thus, it is generally agreed that something else