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Toxic metal in autism

Toxic metals in Autism: Autism is rapidly growing worldwide with a huge impact on families, the country, and therefore the economy. Genetic and environmental causes are thought to be the most groups of etiology of autism. Genetic mutations in multiple genes are identified, but they affect only but 1/3 of cases. Environmental causes, especially trace elements deficiency and excess, resulting in the event of Autism Spectrum Disorder (ASD) through several mechanisms is discussed during this editorial, with a mini literature survey. However, satisfactory evidence for clear mechanisms or etiology of autism remains lacking. Thus delays the event of an efficient treatment strategy for ASD. Autism Spectrum Disorder (ASD) is common and therefore the numbers are outgrowing. Current prevalence is about 1%. Changes in diagnostic criteria and improved awareness and reporting are amongst the explanations why the amount is growing so rapidly, over the last three decades. However, the numbers are growing so rapidly worldwide that it’s going to show a rise in incidents beyond these confounders. Diagnosis of ASD is difficult within the absence of a particular biomarker or anatomical site of the defect and frequent changes in its diagnostic criteria. Subsequently, the prevalence studies are also challenging The etiology of ASD is yet to get, but there are genetic, epigenetic, and environmental factors identified as possible causes. Numerous genetic variants are identified by genetic sequencing of ASD patients and lots of said involve glycosylation-related proteins and enzymes. The rapid increase in numbers during a previous couple of decades supports a serious role in environmental factors over genetic causes alone. The opposite possibility is that the environmental factors could also be taken to activate the genetic or epigenetic mechanisms of the event of autism. The deficiency of some trace elements like zinc (Zn), manganese (Mn), molybdenum (Mo), aluminum (Al), and selenium (Se) was found to be deficient in children with ASD. Iron (Fe) deficiency and vitamin (eg: B9-folate) deficiency has also shown associations with ASD. the surplus of some elements like copper (Cu), lead (Pb), mercury (Hg), and cadmium (Cd) has also shown significant associations. Maternal micronutrient deficiency and toxin exposure can cause defective fetal brain development. Prenatal exposure to pesticides, alcohol, cocaine, smoking, and heavy metal can cause toxicity those results in ASD. Fish consumption, living on the brink of gasoline stations and use of aluminum cooking pans are identified as associations to ASD by means of maternal toxin exposure. Pollution by industrial facilities has been linked to increased prevalence of ASD, by showing higher prevalence closure to such facilities. The association to deficiency or more than trace elements is usually questioned and did not show a transparent relationship thus giving challenges to look for a cause for ASD. There are some theories on the mechanism of development of ASD looking into different aspects of consumption, metabolism, and excretion of these trace elements. Inadequate maternal intake, malabsorption in mothers or in newborns and infants, harmful toxin exposures in mothers like employment-related hazards, smoking, alcohol, and illicit substance abuse are amongst them. Medicines can also be a source of toxicity and also can cause defects in metabolism. Some believe it could even be associated with the defective excretory function of toxic elements in children which will cause accumulations Vaccine for measles, mumps, and rubella (MMR), given at youth is additionally blamed for the association to the event of ASD Abnormalities within the intestinal functions as digestion and absorption discussed widely. Malabsorption syndromes like celiac disease and other gluten-sensitive diseases like no celiac gluten sensitivity (NCGS) are studied. However, there’s no satisfactory evidence of a transparent relationship. Some studies and theories have looked into the oxidative metabolism, homeostasis of thiamine, and deposition of heavy metals as mechanisms of pathogenesis of ASD. Defective barrier function at interfaces just like the barrier, intestinal mucosa, skin, and placenta is additionally a possible mechanism that will cause both deficiencies and accumulation of elements. An interaction between the maternal system and epigenetic regulation within the fetal brain is another theory of the genesis of ASD phenotype. Epigenetic modifications and methylation defects via environmental effects is additionally a suggested newer mechanism. Based on the possible associations, the treatment strategies are to exchange deficient elements and take away excess elements. Supplement of Zn to mothers prenatally has shown the reduction of ASD or Autism behaviors in some studies. Thiamine supplementation in an effort to correct defective thiamine homeostasis is additionally suggested

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