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有证据表明,美国自闭症流行由对乙酰氨基酚(泰诺)引发,口服抗生素阿莫西林/克拉维酸(奥格门汀)使其加剧,而现在除草剂草甘膦(农达)使其呈指数级增长。

Evidence the U.S. autism epidemic initiated by acetaminophen (Tylenol) is aggravated by oral antibiotic amoxicillin/clavulanate (Augmentin) and now exponentially by herbicide glyphosate (Roundup).

作者信息

Good Peter

机构信息

Autism Studies, PO Box 1683, La Pine, OR 97739, USA.

出版信息

Clin Nutr ESPEN. 2018 Feb;23:171-183. doi: 10.1016/j.clnesp.2017.10.005. Epub 2017 Dec 1.

Abstract

Because certain hereditary diseases show autistic behavior, and autism often runs in families, researchers seek genes underlying the pathophysiology of autism, thus core behaviors. Other researchers argue environmental factors are decisive, citing compelling evidence of an autism epidemic in the United States beginning about 1980. Recognition that environmental factors influence gene expression led to synthesis of these views - an 'epigenetic epidemic' provoked by pervasive environmental agents altering expression of vulnerable genes, inducing characteristic autistic biochemistries in many mothers and infants. Two toxins most implicated in the U.S. autism epidemic are analgesic/antipyretic acetaminophen (Tylenol) and oral antibiotic amoxicillin/clavulanate (Augmentin). Recently herbicide glyphosate (Roundup) was exponentially implicated. What do these toxins have in common? Acetaminophen depletes sulfate and glutathione required to detoxify it. Oral antibiotics kill and glyphosate inhibits intestinal bacteria that synthesize methionine (precursor of sulfate and glutathione, and required to methylate DNA), bacteria that synthesize tryptophan (sole precursor of neuroinhibitor serotonin), and bacteria that restrain ammonia-generating anaerobes. Sulfate plus glutathione normally sulfate fetal adrenal androgen dehydroepiandrosterone to DHEAS - major precursor of placental/postnatal estrogens. Glyphosate (and heavy metals) also inhibit aromatase that turns androgens to estrogens. Placental/postnatal estrogens dehydrate/mature brain myelin sheaths, mature corpus callosum and left hemisphere preferentially, dilate brain blood vessels, and elevate brain serotonin and oxytocin. Stress-induced weak androgens and estrogen depletion coherently explain white matter asymmetry and dysconnection in autism, extreme male brain, low brain blood flow, hyperexcitability, social anxiety, and insufficient maternal oxytocin at birth to limit fetal brain chloride/water and mature GABA.

摘要

由于某些遗传性疾病会表现出自闭行为,且自闭症常常在家族中出现,研究人员在寻找自闭症病理生理学背后的基因,也就是核心行为背后的基因。其他研究人员则认为环境因素起决定性作用,他们引用了美国自1980年左右开始出现自闭症流行这一有力证据。认识到环境因素会影响基因表达后,这两种观点得以融合——一种由普遍存在的环境因素引发的“表观遗传流行”,这些环境因素改变了易感基因的表达,在许多母亲和婴儿中诱发了典型的自闭症生物化学变化。在美国自闭症流行中最受牵连的两种毒素是止痛/退烧药对乙酰氨基酚(泰诺林)和口服抗生素阿莫西林/克拉维酸(奥格门汀)。最近,除草剂草甘膦(农达)也被大量牵连进来。这些毒素有什么共同之处呢?对乙酰氨基酚会消耗将其解毒所需的硫酸盐和谷胱甘肽。口服抗生素会杀死肠道细菌,草甘膦会抑制肠道细菌,这些细菌能合成甲硫氨酸(硫酸盐和谷胱甘肽的前体,也是DNA甲基化所必需的)、合成色氨酸(神经抑制剂血清素的唯一前体)以及抑制产生氨的厌氧菌。硫酸盐加上谷胱甘肽通常会将胎儿肾上腺雄激素脱氢表雄酮硫酸化为硫酸脱氢表雄酮——胎盘/产后雌激素的主要前体。草甘膦(以及重金属)也会抑制将雄激素转化为雌激素的芳香化酶。胎盘/产后雌激素会使脑髓鞘脱水/成熟,优先使胼胝体和左半球成熟,扩张脑血管,并提高大脑中的血清素和催产素水平。压力诱导产生的弱雄激素和雌激素耗竭连贯地解释了自闭症中的白质不对称和连接障碍、极端男性大脑、低脑血流量、过度兴奋、社交焦虑以及出生时母体催产素不足,无法限制胎儿脑内氯化物/水含量并使γ-氨基丁酸成熟。

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