A naturally occurring trace metalloid element and known neurotoxin with atomic symbol Hg, atomic number 80, and atomic weight 200.59.- NCI Thesaurus, U.S. National Cancer Institute
Mercury has been an ingredient in vaccines in the form of Thimerosal, a ethylmercury-sulfidobenzoate that has been used as a preservative in vaccines; antivenins; and ointments. It was formerly used as a topical antiseptic. It degrades to ethylmercury and thiosalicylate. – NLM Medical Subject Headings, U.S. National Library of Medicine, 2021
Thimerosal An organomercurial compound and derivative of thiosalicyclic acid with antibacterial and antifungal properties. Although the mechanism of action has not been fully elucidated, thimerosal inhibits sulfhydryl-containing active site of various enzymes and binds to sulfhydryl compounds, such as glutathione, cysteine, and SH groups of proteins. In addition, thimerosal activates the InsP3 calcium channel on endoplasmic reticular membrane, thereby triggering the release of calcium from intracellular stores resulting in a calcium-induced calcium-influx of extracellular calcium. Consequently, thimerosal may induce or inhibit cellular functions dependent on calcium signaling. – NCI Thesaurus, U.S. National Cancer Institute, 2021
Mercury exposure can cause immune activation, cytokine release, altered urinary porphyrins, neuroinflammation, glial cell activation, apoptosis, dendritic cell abnormalities, mitochondrial dysfunction, glutathione depletion, reduced expression of methionine, impaired methylation, oxidative stress, and seizures.
“Some epidemiological studies investigating a possible relationship between high environmental exposure to methylmercury and impaired neurodevelopment have reported a positive dose-dependent effect.”
There is a “greater propensity of males to the long-term neurotoxic effects” of mercury. – doi.org/10.1007/s12035-017-0692-2
Males make up roughly three quarters of all Autism cases. – Mercury toxicity: Genetic susceptibility and synergistic effects
Highlights
• Thimerosal (TM) significantly affects mitochondrial bioenergetics in the brain.
• Mitochondrial integrity (membrane potential) was maintained after acute TM treatment.
• Ethylmercury released after the breakdown of TM compromised the cholinergic system.
• The brain is more sensitive to oxidative stress induced by TM compared to the liver.
Excerpt:
“The Cr, As and Al are found in high concentrations in the blood of an autistic child when compared to normal child reference values. The toxic metals, particularly aluminium, are primarily responsible for difficulties in socialization and language skills disabilities. Zinc and copper are important elements in regulating the gene expression of metallothioneins (MTs), and zinc deficiency may be a risk factor for ASD pathogenesis. Autistics frequently have zinc deficiency combined with copper excess; as part of the treatment protocol, it is critical to monitor zinc and copper levels in autistic people, particularly those with zinc deficiency. Zinc deficiency is linked to epileptic seizures, which are common in autistic patients. Higher serum manganese and copper significantly characterize people who have ASD. Autistic children have significantly decreased lead and cadmium in urine, whereas they have significantly higher urine Cr. A higher level of As and Hg was found in the ASD individual’s blood.”
Excerpt:
“The whole blood concentrations of Mo (p = 0.004), Cd (0.007), Sn (p = 0.003), and Pb (p = 0.037) were significantly higher in the ASD cases than in the controls. Moreover, Se (0.393), Hg (0.408), and Mn (- 0.373) concentrations were significantly correlated between whole blood and urine levels in ASD case subjects. There were significant correlations between whole blood Sb (0.406), Tl (0.365), Mo (- 0.4237), Mn (- 0.389), Zn (0.476), and Se (0.375) levels and core behaviors of ASD. Although the mechanism of trace element imbalance in ASD is unclear, these data demonstrate that core behaviors of ASD may be affected by certain trace elements. Further studies are recommended for exploring the mechanism of element imbalance and providing corresponding clinical treatment measures.”
Conclusions: Conflicts of interest (e.g., financial) that abound between health regulatory agencies and the pharmaceutical industry impact what is ultimately reckoned as medical consensus. Outcome reporting bias that is inherent to all researchers to some degree, obscures medical and scientific truth. Advancement of public health requires that researchers have integrity and an openness and willingness to collaborate to resolve contradictory findings. In fact, it is usually through meticulous, rigorous, scientific investigation of contradictory findings that medical science has advanced and contributed to improvements in public health – since medical consensus and orthodoxy can be incorrect.
Excerpt:
“Six case-control studies with 425 study subjects met our inclusion criteria. A total of four studies indicated higher levels of As, Pb, Hg, Cd, Al, Sn, Sb, Ba, TI, W, and Zr in whole blood, RBC, in whole blood, RBC, and hair samples of children with autism compared with control suggestive of a greater toxic metal exposure (immediate and long-term). Three studies identified significantly higher concentrations of Cd, Pb and Hg in urine and hair samples of autistic children compared to control suggesting decreased excretion and possible high body burden of these metals. The findings from this review demonstrate that high levels of toxic metals are associated with ASD, therefore, critical care is necessary to reduce body burden of these metals in children with ASD as a major therapeutic strategy.”
Excerpt:
“Accumulating evidence implies the gut-brain axis as a pathway for MeHg harmful neurotoxic effects and a potential factor for later neurodegenerative disorders. The MeHg may induce a hormesis-related neuronal toxicity. Hormesis is an important redox dependent aging-associated neurodegenerative/ neuroprotective issue (Calabrese et al., 2010). The use of antioxidants, such as plant polyphenols (Calabrese et al., 2010; Leri et al., 2020) and protective nutrients (Oria et al., 2020) may be beneficial in reducing the MeHg-driven neuroinflammatory state and associated cell death with the interplay of the intestinal microbiota.”
Excerpts:
“Aberrant migration of inhibitory interneurons can alter the formation of cortical circuitry and lead to severe neurologic disorders including epilepsy, autism, and schizophrenia.”
“These findings highlight key roles for JNK signaling in leading process branching, nucleokinesis, and the trafficking of centrosomes and cilia during interneuron migration, and further implicates JNK signaling as an important mediator of cortical development.”
Excerpt:
“Results: A significant and positive correlation was found between hair metal burden (lead, aluminum, arsenic and cadmium levels) and severity of ASD symptoms (social communication deficits and repetitive, restrictive behaviors). Hair zinc level were inversely related with age while there was a negative, significant association between hair zinc level and severity of autistic symptoms (defective functional play and creativity and increase of stereotyped behavior). Lead, molybdenum and manganese hair levels were inversely correlated with cognitive level (full intelligence quotient) in ASD individuals.
Conclusions: The present study suggests the importance to combine metallomics analysis with pertinent disease features in ASD to identify potential environmental risk factors on an individual level possibly in the early developmental period.”
Except:
“There is a growing body of work to support the role of inflammatory cytokines in ASD. An emerging focus of research into the etiology of ASD has suggested neuroinflammation as one of the major candidates underlying the biologica model [5]. Plasma levels of IL-1β, IL-6 and IL-8 were increased in children with ASD and correlated with regressive autism, as well as impaired communication and aberrant behavior [6-8]. Vargas [9] showed an active neuroinflammatory process in the cerebral cortex, white matter, and in the cerebellum of autistic patients. Immunocytochemichal studies showed marked activation of microglia [5].”
Excerpt:
“The literature strongly supports that autism is most accurately seen as an acquired cellular detoxification deficiency syndrome with heterogeneous genetic predisposition that manifests pathophysiologic consequences of accumulated, run-away cellular toxicity. At a more general level, it is a form of a toxicant-induced loss of tolerance of toxins, and of chronic and sustained ER overload (“ER hyperstress”), contributing to neuronal and glial apoptosis via the unfolded protein response (UPR). Inherited risk of impaired cellular detoxification and circulating metal re-toxification in neurons and glial cells accompanied by chronic UPR is key.”
