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
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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
草甘膦对肠道微生物群的破坏和硫酸盐缺乏的诱导能否解释工业化世界中痛风和相关疾病的流行?
痛风是一种古老的疾病,至少从巴比伦时代就已经为人所知。“痛风”一词源自拉丁语单词“gutta”(drop);这意味着人们相信,一滴一滴渗入关节的毒药是病因[1]。人们对痛风的病因有很多了解,尽管仍有许多谜团有待解决。痛风是一种炎症性关节疾病,通常是偶发性的,局限于某些关节,尤其是跖趾(MTP)1关节以及脚和手指的其他关节。痛风的急性发作通常由关节中的尿酸盐晶体引发,尿酸盐晶体诱导级联反应,从免疫细胞(尤其是中性粒细胞)的涌入开始,中性粒细胞会释放IL-1β和IL-6等细胞因子,引起炎症反应,导致氧化损伤和剧烈疼痛,并在反馈反应最终抑制信号时终止。虽然痛风与高血清尿酸盐有关,但这种联系并不像预期的那样强烈。许多血清尿酸盐升高的人从未经历过痛风,许多痛风患者的血清尿酸盐水平正常[2]。因此,人们普遍认为
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