Comparison of Characteristics
of Mercury Poisoning & Autism Gastro-intestinal Disturbances | | Mercury Poisoning | Autism | | Gastroenteritis, diarrhea; abdominal pain, constipation, "colitis" | Diarrhea, constipation, gaseousness, abdominal discomfort, "colitis" | | Anorexia, weight loss, nausea, poor appetite | Anorexia; feeding problems/vomiting | | Lesions of ileum & colon; increased gut permeability | Leaky gut syndrome | | Inhibits dipeptidyl peptidase IV, which cleaves casomorphin | Inadequate endopeptidase enzymes needed for breakdown of casein & gluten | | Abnormal Biochemistry | | Mercury Poisoning | Autism | | Binds -SH groups; blocks sulfate transporter in intestines, kidneys | Low sulfate levels | | Has special affinity for purines & pyrimidines | Purine & pyrimidine metabolism errors lead to autistic features | | Reduces availability of glutathione, needed in neurons, cells & liver to detoxify heavy met als | Low levels of glutathione; decreased ability of liver to detoxify heavy met als | | Causes significant reduction in glutathione peroxidase and glutathione reductase | Abnormal glutathione peroxidase activities in erythrocytes | | Disrupts mitochondrial activities, especially in brain | Mitochondrial dysfunction, especially in brain | | Immune Dysfunction | | Mercury Poisoning | Autism | | Sensitivity due to allergic or autoimmune reactions; sensitive individuals more likely to have allergies, asthma, autoimmune-like symptoms, especially rheumatoid-like ones | More likely to have allergies and asthma; familial presence of autoimmune diseases, especially rheumatoid arthritis; IgA deficiencies | | Can produce an immune response in CNS | On-going immune response in CNS | | Causes brain/MBP autoantibodies | Brain/MBP autoantibodies present | | Causes overproduction of Th2 subset; kills/inhibits lymphocytes, T-cells, and monocytes; decreases NK T-cell activity; induces or suppresses IFNg & IL-2 | Skewed immune-cell subset in the Th2 direction; decreased responses to T-cell mitogens; reduced NK T-cell function; increased IFNg & IL-12 | | CNS Structural Pathology | | Mercury Poisoning | Autism | | Selectively targets brain areas unable to detoxify or reduce Hg-induced oxidative stress | Specific areas of brain pathology; many functions spared | | Damage to Purkinje and granular cells | Damage to Purkinje and granular cells | | Accummulates in amygdala and hippocampus | Pathology in amygdala and hippocampus | | Causes abnormal neuronal cytoarchitecture; disrupts neuronal migration & cell division; reduces NCAMs | Neuronal disorganization; increased neuronal cell replication, increased glial cells; depressed expression of NCAMs | | Progressive microcephaly | Progressive microcephaly and macrocephaly | | Brain stem defects in some cases | Brain stem defects in some cases | | Abnormalities in Neuro-chemistry | | Mercury Poisoning | Autism | | Prevents presynaptic serotonin release & inhibits serotonin transport; causes calcium disruptions | Decreased serotonin synthesis in children; abnormal calcium metabolism | | Alters dopamine systems; peroxidine deficiency in rats resembles mercurialism in humans | Possibly high or low dopamine levels; positive response to peroxidine (lowers dopamine levels) | | Elevates epinephrine & norepinephrine levels by blocking enzyme that degrades epinephrine | Elevated norepinephrine and epinephrine | | Elevates glutamate | Elevated glutamate and aspartate | | Leads to cortical acetylcholine deficiency; increases muscarinic receptor density in hippocampus & cerebellum | Cortical acetylcholine deficiency; reduced muscarinic receptor binding in hippocampus | | Causes demyelinating neuropathy | Demyelination in brain | | EEG Abnormalities / Epilepsy | | Mercury Poisoning | Autism | | Causes abnormal EEGs, epileptiform activity | Abnormal EEGs, epileptiform activity | | Causes seizures, convulsions | Seizures; epilepsy | | Causes subtle, low amplitude seizure activity | Subtle, low amplitude seizure activities | | Population Characteristics | | Mercury Poisoning | Autism | | Effects more males than females | Male:female ratio estimated at 4:1 | | At low doses, only affects those geneticially susceptible | High heritability - concordance for MZ twins is 90% | | First added to childhood vaccines in 1930s | First "discovered" among children born in 1930s | | Exposure levels steadily increased since 1930s with rate of vaccination, number of vaccines | Prevalence of autism has steadily increased from 1 in 2000 (pre1970) to 1 in 500 (early 1990s), higher in 2000. | | Exposure occurs at 0 - 15 months; clinical silent stage means symptom emergence delayed; symptoms emerge gradually, starting with movement & sensation | Symptoms emerge from 4 months to 2 years old; symptoms emerge gradually, starting with movement & sensation | Charts generously provided by Safe Minds http://www.safeminds.org
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