The mercury/casein/gluten factor effect on opioid peptides as a mechanism in causing autism, schizophrenia, ADHD, MS, and other neurological conditions


Mercury and toxic metals block enzymes required to digest milk casein and wheat gluten, resulting in dumping morphine like substances in the blood that are neurotoxic and psychotic, as a major factor in schizophrenia, autism, ADHD, and MS. 

     A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to these allergic/immune reactive conditions(15-23,36,47,51,90). For example, mercury has been found to strongly inhibit the activity of xanthineoxidase and dipeptyl peptidase (DPP IV) which are required in the digestion of the milk protein casein or wheat protein gluten (15,16,17,19,20,91,23-26,90,92), and the same protein that is cluster differentiation antigen 26 (CD26) which helps T lymphocyte activation. CD26 or DPPIV is a cell surface glycoprotein that is very susceptible to inactivation by mercury binding to its cysteinyl domain. Mercury and other toxic metals also inhibit binding of opioid receptor agonists to opioid receptors, while magnesium stimulates binding to opioid receptors (15). Studies involving large samples of patients with autism, schizophrenia, or mania found that over 90 % of those tested had high levels of the milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24,25,27), and similarly for the corresponding enzyme needed to digest wheat gluten(24,26). Like casein, gluten breaks down into molecules with opioid traits, called gluteomorphine or gliadin. As with caseomorphin, it too can retain biological activity if the enzymes needed to digest it are not functioning properly..

Proteins in bovine milk are a common source of bioactive peptides. The peptides are released by the digestion of caseins and whey proteins (92).  In vitro the bioactive peptide beta-casomorphin 7 (BCM-7) is yielded by the successive gastrointestinal proteolytic digestion of bovine beta-casein variants A1 and B, but this was not seen in variant A2 or in goats milk. In hydrolysed milk with variant A1 of beta-casein, BCM-7 level is 4-fold higher than in A2 milk.  Variants A1 and A2 of beta-casein are common among many dairy cattle breeds. A1 is the most frequent in Holstein-Friesian (0.310–0.660), Ayrshire (0.432–0.720) and Red (0.710) cattle. In contrast, a high frequency of A2 is observed in Guernsey (0.880–0.970) and Jersey (0.490–0.721) cattle (92). In children with autism, most of whom have been found to have been exposed to high levels of toxic metals through vaccines, mother’s dental amalgams, or other sources; higher levels of BCM-7 is found in the blood(24-26).  

BCM-7 appears to play a significant role in the aetiology of human diseases (92). Epidemiological evidence from New Zealand claims that consumption of beta-casein A1 is associated with higher national mortality rates from ischaemic heart disease. It appears that the populations that consume milk containing high levels of beta-casein A2 have a lower incidence of cardiovascular disease and type 1 diabetes. Beta-casomorphin-7 has opioid properties including immunosuppression, which account for the specificity of the relation between the consumption of some but not all beta-casein variants and diabetes incidence.  BCM-7 has also been suggested as a possible cause of sudden infant death syndrome (SIDS). In addition, neurological disorders, such as autism and schizophrenia, appear to be associated with milk consumption and a higher level of BCM-7 (92).


The studies found high levels of Ig A antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein.   Beta-casomorphine-7  is a morphine like compound that results in neural disfunction(24,25), as well as being a direct histamine releaser in humans and inducing skin reactions (14,21,25c).  Similarly many also had a corresponding form of gluten protein with similar effects(24,26).   Elimination of milk and wheat products and sulfur foods from the diet has been found to improve the condition (40,28, etc.). 

 A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in autistic symptomology among the 56% most responsive to opioid effects (28).  The behavioral improvements were accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio.   Studies have found mercury causes increased levels of the CD8 T-cytotoxic-suppressors (29).   As noted previously, such populations of patients have also been found to have high levels of mercury and to recover after mercury detoxification (23,11,30,40,91).  As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs (91,11,96).   

        A mechanism in multiple sclerosis (MS) occurs due to a reduction in immune system activity. Specifically, it is the reduction in the number of the suppressor T-cells within the immune system that allows CD4 helper T-cells to do damage (31,97). Thus, during an acute relapse the overall number of T-cells is reduced, the normal balance of helper and suppressor T-cells is disrupted, and helper T-cells tend to predominate.  This is most pronounced during an acute relapse, but a similar situation occurs although perhaps to a lesser extent, in chronic progressive MS. Low dose naltrexone (LDN) has been found to commonly be effective in reducing MS symptoms and exerbations, apparently due its opioid suppressive effects (31). [ Chronic toxic exposures to toxics such as mercury are one documented factor that can cause such immune effects.  Reducing chronic exposures and detoxification have been documented to commonly bring improvement in these conditions and in MS symptoms (97).]


     Studies have also found heavy metals to deplete glutathione and bind 

to protein-bound sulfhydryl SH groups, resulting in inhibiting SH-containing enzymes and production of reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl radical (39,43,45-47, 63-65,89,97,91).  In addition to forming strong bonds with SH and other groups like OH, NH2, and Cl in amino acids which interfere with basic enzymatic processes, toxic metals exert part of their toxic effects by replacing essential metals such as zinc at their sites in enzymes. An example of this is mercury’s disabling of the metallothionein protein, which is necessary for the transport and detoxification of metals.   Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions (66), thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function.  Another large study (51) found a high percentage of autistic and PDD children are especially susceptible to metals due to the improper functioning of their metallothionein detoxification process, and that with proper treatment most recover.    Mercury has also been found to play a part in neuronal problems through blockage of the P‑450 enzymatic process (67,89).   Another study found accelerated lipofuscin deposition--consistent with oxidative injury to autistic brain in cortical areas serving language and communication (97). Compared with controls, children with autism had significantly higher urinary levels of lipid peroxidation. Double-blind, placebo-controlled trials of potent antioxidants--vitamin C or carnosine--significantly improved autistic behavior.


An IRB approved study assessing urinary levels of porphyrins found an apparent dose-response effect between autism severity and increased urinary coproporphyrins (68). Mercury has been well documented to cause neurological, mood and behavioral problems for children and others(8,9, etc.) Mercury also has additive and synergistic effects with other toxic metals and toxins so lower exposure levels of each can produce significant damage (9). Susceptibility factors also reduce some people’s ability to detoxify mercury and other toxins, making some more affected by toxic exposures.The papers discussed here show some of the ways that mercury can cause or be a factor in autism and other neurological conditions.



(8) Mercury and autism: accelerating evidence? Mutter J, Naumann J, et al; Neuro Endocrinol Lett. 2005 Oct;26(5):439-46; & Increased Release of Mercury from Dental Amalgam Fillings due to Maternal Exposure to Electromagnetic Fields as a Possible Mechanism for the High Rates of Autism in the Offspring: Introducing a Hypothesis. Mortazavi G, Haghani M, et al; J Biomed Phys Eng. 2016 Mar 1;6(1):41-6.

(9) Mercury and autism, &; &; & Cognitive and Behavioral Effects of Toxic Metals,; & (b)  Prenatal and neonatal effects of mercury on infants,


(11) LYMPHOCYTE IMMUNO‑STIMULATION ASSAY ‑MELISA”, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden   V.D.M. Stejskal,  paper presented at International Autism Conference, San Diego,2002 &;

   & “Mercury-specific Lymphocytes: an indication of mercury allergy in man”, J. Of Clinical Immunology, 1996, Vol 16(1);31-40; see:        

(12)   Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Sterzl I, Prochazkova J, Stejaskal VDM et al,  Neuroendocrinology Letters 1999; 20:221-228; & “MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity”, Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine,  Nov. 1998, Baltimore, Maryland. V.Stejskal,

(13)  Recovery from asthma, allergies,ALS  after removal of dental amalgam fillings. Redhe O, Pleva J.   Int J of Risk & Safety in Medicine 1994; 4:229-236.

(14)  An opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man.  Int Arch Allergy immunol 1992; 97(2): 115-20. Kurek M, Przybilla B, Hermann K, Ring J

(15)   Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology 1990; 29(5): 445-52.Tejwani GA, Hanissian SH.

(16)  Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. Mondal MS, Mitra S, J Inorg Biochem 1996; 62(4): 271-9; & Lead and mercury mutagenesis: Role of H2O2, superoxide dismutase, and xanthine oxidase,  Maria E. Ariza, Gautam N. Bijur, Marshall V. Williams,  Environ. Mol. Mutagen. 31:352-361, 1998; & Naidu BV, Fraga C, Salzman AL, Szabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant 22:784-93; &  Liaudet L, Szabó G, Szabó C. 2003. Oxidative stress and regional ischemia-reperfusion injury: the peroxynitrite – PARP connection. Coronary Artery Dis. 14:115-122; & Naidu BV, Fraga C, SalzmanALSzabó C, Verrier ED, Mulligan MS. 2003. Critical role of reactive nitrogen species in lung ischemia-reperfusion injury. J Heart Lung Transplant. 22: 784-93; & Virág L, Szabó E, Gergely P, Szabó C. 2003. Peroxynitrite- induced cytotoxicity: mechanisms and opportunities for intervention.  Toxicology Letters 140:113-124; & Xanthine oxidase and neutrophil infiltration in intestinal ischemia.  Grisham MB, Hernandez LA, Granger DN.  Am J Physiol. 1986 Oct;251(4 Pt 1):G567-74 , Xanthine oxidase and neutrophil infiltration in intestinal ischemia,

 (17)   In vitro inhibition of digestive enzymes by heavy metals and their reversal by chelating agents: Part 1, mercuric chloride intoxication.  Bull Environ Contam Toxicol 1978; 20(6): 729-35 Sastry KV, Gupta PK.; & W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of mercury on enzyme activities”, Environ Res, 1992, 57(1):96-106; & Horvath K, Papadimitriou JC, Rabsztyn A, Drachenberg C, Tildon JT; Gastrointestinal abnormalities in children with autistic disorder.  J Pediatr 1999,  135:559-63.

(18) Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways.   Toxicology, 1996, 111(1-3):43-65, M c Fadden SA,; &    Markovich et al,  "Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1", Toxicol  Appl Pharmacol,     1999,154(2):181‑7;  & Matts RL, Schatz JR, Hurst R, Kagen R.   Toxic heavy metal ions inhibit reduction of disulfide bonds.  J Biol Chem 1991; 266(19): 12695-702; &  T.L. Perry et al, “Hallevorden-SpatzDisease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985, 18(4):482-489; &  Ceaurriz et al, Role of gamma‑  glutamyltraspeptidase(GGC) and extracellular glutathione in disposition of inorganic mercury",J Appl Toxicol,1994, 14(3): 201‑

(19)  Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties.  J Clin Lab Anal.1996;10(6):435-40; & Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993 Jul;44(1):13-8; & Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of dipeptidyl peptidase IV from human placenta', Eur J Biochem 1982 Aug;126(2):359-65; & Kar NC, Pearson CM.  Dipeptyl Peptidases in human muscle disease.  Clin Chim Acta 1978; 82(1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174,etc.,

(20) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure.  Cell Physiol Biochem           1998; 8(5): 278-84. 

(21) Crinnion WJ.   Environmental toxins and their common health effects.  Altern Med Rev 2000, 5(1):52-63.  

(22)  Immunological findings in autism. Int Rev Neurobiol2005;71:317-41, Cohly HH, Panja A; & (b) Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackie B3 myocarditis). Toxicol Lett. 1996 Dec;89(1):19-28, Ilbäck NG, WesslénLFohlman J, Friman G; & Trace element distribution in heart tissue sections studied by nuclear microscopy is changed in Coxsackie virus B3 myocarditis in methyl mercury-exposed mice. Biol Trace Elem Res. 2000 Winter;78(1-3):131-47, Ilbäck NG, Lindh U, Wesslén L, Fohlman J, Friman G; & (c) Assessment of mercury exposure and malaria in a Brazilian Amazon riverine community. Environ Res. 2002 Oct;90(2):69-75, Crompton P, Ventura AM, de Souza JM, Santos E, Strickland GT, Silbergeld E.

(23)Bernard S, Enayati A, Redwood L, Roger H, Binstock T.  Autism: a novel form of mercury poisoning.  Med Hypotheses 2001 Apr;56(4):462-71; &(b)Dr. A Holmes, Autism Treatment Center,Baton Rouge, La; , &(c)  Jaquelyn McCandless,  M.D., Autism Spectrum Treatment Center,  Woodland Hills, CA,&Jaquelyn McCandless, M.D, Children with Starving Brains, A Medical Treatment Guide for Autism Spectrum Disorder, 2003  www.autism‑;   & (d)L.Redwood, Mercury and Autism, Vitamin Research News, May 2001, 15(5):1-12; &(e) Andrew H. Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996 ,; &(f)Dr. R. Buttar, Autism, the Misdiagnosis of Our Future Generations, Congressional Testimony: Government Reform and Oversight Committee, U.S. House of Representatives, May 2004,

(24) J.R. Cade et al,  Autism and schizophrenia linked to malfunctioning enzyme for milk  protein digestion.  Autism, Mar 1999. ;& Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000.   & ; & "Beta-casomorphin induces Fos-like immunoreactivity in discrete brain regions relevant to schizophrenia and autism" Autism March 1999 vol 3(1) 67-83; Sun, ZJ, Cade JR, et al &   A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats, J.R. Cade, Z. Sun , Univ of Florida, USA , Autism, Vol. 3, No. 1, 85-95 (1999)  DOI: 10.1177/1362361399003001007  © 1999 The National Autistic Society, SAGE Publications  ; & Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone, Leboyer M, et al., Encephale 1993 Mar-Apr;19(2):95-102; & Food allergy and infantile autism. Lucarelli S, et al., Panminerva Med 1995 Sep;37(3):137-41;

 & Application of the Exorphin Hypothesis to Attention Deficit Hyperactivity Disorder:  A Theoretical Framework by  Ronald  Hoggan   A Thesis Submitted To The Faculty Of Graduate Studies In Partial Fulfilment Of The Requirements  For The Degree Of Master Of Arts,    Graduate Division Of Educational Research,Calgary, April, 1998  University of Calgary              

(25) Reichelt KL.  Biochemistry and psycholphisiology of autistic syndromes.  Tidsskr Nor Laegeforen 1994, 114(12):1432-4;       &   ReicheltKL et al, Biologically active peptide-containing fractions in schizophrenia and childhood autism.  Adv   Biochem Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and infantile autism.  Panminerva    Med 1995; 37(3):137-41; & Shel L, Autistic disorder and the endogenous opioid system.  Med Hypotheses 1997, 48(5):         413-4.

(26) Huebner FR, Lieberman KW, Rubino RP, Wall JS.  Demonstration of high opioid-like activity in isolated peptides from           wheat gluten hydrolysates.  Peptides 1984; 5(6):1139-47; & Wheat gluten as a pathogenic factor in schizophrenia. Singh MM, Kay SR, Science 1976 Jan 30;191(4225):401-2; & Demonstration of high opioid-like activity in isolated peptides from wheat gluten hydrolysates.  Huebner FR, Lieberman KW, Rubino RP, Wall JS.   Peptides. 1984 Nov-Dec;5(6):1139-47; & Naloxone antagonises effect of alpha-gliadin on leucocytemigration in patients with coeliac disease. Horváth K, Gráf L, Walcz E, Bodánszky H, Schuler D. Lancet. 1985 Jul 27;2(8448):184-5

(27) Willemsen-Swinkels SH, Buitelaar JK, Weijnen FG, Thisjssen JH, Van Engeland H.  Plasma beta-endorphin      concentrations in people with learning disability and self-injurious and/or autistic behavior.  Br J Psychiary 1996; 168(1):      105-9; & Leboyer M, Launay JM et al.   Difference between plasma N- and C-terminally directed beta-endorphin immunoreactivity in infantile autism.  Am J Psychiatry 1994; 151(12): 1797-1801.

(28) Scifo R, Marchetti B, et al.  Opioid-immune interactions in autism: behavioral and immunological assessment during a double-blind treatment with naltexone.  Ann Ist Super Sanita 1996; 32(3): 351-9.

(29) Eedy DJ, Burrows D, Dlifford T, Fay A.  Elevated T cell subpopulations in dental students.   J prosthet Dent 1990; 63(5):593-6;  & YonkL J et al, CD+4 helper T-cell depression in autism.  Immunol Lett, 1990, 25(4):341-5. 

(30) Edelson SB, Cantor DS.  Autism: xenobiotic influences.  Toxicol Ind Health 1998; 14(4): 553-63; & Liska, DJ.  The detoxification  enzyme systems.  Altern Med Rev 1998. 3(3):187-98; & ©  HRI-Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001;    www.hriptc.ort/Publish0900/index.html. 

(31) LDN for MS Trials/Experience

(39)  Pfieffer SI; Norton J; Nelson L; Shott S.  Efficacy of vitamin B6 and magnesium in the treatment of autism.  J Autism Dev Disord 1995 Oct;25(5):481‑93; &  Chuang D. Et al, National Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Lithium Protects Against Neuron Damage by Glutamate, Science News, 3-14-98,   p164;   & Moore al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276.  

(40) (Special Diets/Gluten-Casein Free), Parent Ratings of Behavioral Effects of Biomedical Interventions for large group of parents of children who had autism

(43) Rodier P.M.  Developing brain as a target of toxicity.  Environ Health Perspect 1995; 103(Supp 6): 73-76; &

Rice DC, Barone S, Critical Periods of Vulnerability for the Developing Nervous System: Evidence from human and animal models. Environ Health Persect 2000, 108(supp 3):511-533.

45) Grandjean P; Jurgensen PJ; Weihe P. Milk as a Source of Methylmercury Exposure in Infants.

Milk as a Source of Methylmercury Exposure in Infants.    Environ Health Perspect 1994 Jan;102(1):74‑7.

(46) (a)Science News, Methylmercury’s toxic toll. July 29, 2000, Vol  158, No.5, p77;  & National Research Council, Toxicological Effects of Methylmercury, National Acadamy Press, Wash, DC, 2000; &   U.S. CDC, 

Second National Report on Human Exposure to Environmental Chemicals,

     & U.S. Centers for Disease Control,   Mar 2001,  Blood and Hair Mercury Levels in Young Children  and Women of Childbearing Age ‑‑‑ United States,  1999;

& (b)Grandjean P, 2000,   Health effects of seafood contamination with methylmercury and PCBs in the Faroes. 

Atlantic Coast Contaminants Workshop, June 22-25, 2000, Bar Harbor Maine; & Environ Res, 1998; 77: 165-72 

(47)  Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V,   Plasma excitatory amino acids in autism.  Invest Clin 1996, 37(2):113-28;  & Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H.  Serotonin and amino acid content in platelets of autistic children.  Acta Psychiatr Scand 1993, 87(5): 312-6;  & Naruse H, Hayashi T, Takesada M, Yamazaki K.   Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new     related          treatment,  No To Hattatsu, 1989, 21(2):181-9; & Carlsson ML.  Is infantile autsim a hypoglutamatergic disorer?  J Neural Transm 1998, 105(4-5): 525-35.

(50) B. Windham, Cognitive and Behavioral Effects of Toxic Metals, (over 150 medical study references); & (b)  Prenatal and neonatal effects of mercury on infants,

(51) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning, 2000; & HRI‑Pfeiffer Center Autism Study; paper presented to Dan Conference, Jan 2001;;

 & Metal-Metabolism and Autism: Defective Functioning of Metallothionein Protein, Amy Holmes, MD;

(63)   P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; &  Stohs SJ, Bagchi D.  Oxidative mechanisms in the toxicity of metal ions.  Free Radic Biol   Med 1995; 18(2): 321-36.

(64) Spivey-Fox MR.  Nutritional influences on metal toxicity.  Environ Health Perspect 1979; 29: 95-104; & Pfeiffer SI et al, Efficacy of vitamin B6 and magnesium in the treatment of autism.  J Autism Dev Disord 1995, 25(5):481-93.

(65) Hernberg S; & Moore MR.   in Lead Toxicity, R.Singhal & J.Thomas(eds), Urban & Schwarzenberg, Inc. Baltimore, 1980;    & Govani S, Memo M.  “Chronic lead treatment differentially affects dopamine synthesis”, Toxicology 1979, 12:343-49;  &  Scheuhammer AM.  Cherian MG.  Effects of heavy metal cations and sulfhydyl reagents on striatal D2 dopamine receptors.  Biochem Pharmacol 1985, 34(19):3405-13.

(66) Lars Landner and Lennart Lindestrom.   Swedish Environmental Research Group(MFG), Copper in society      and the Environment, 2nd revised edition. 1999. 

(67)   J.C.Veltman et al, "Alterations of heme, cytochrome P‑450, and steroid metabolism by mercury in rat adrenal gland", Arch BiochemBiophys,1986, 248(2):467‑78; & A.G.Riedl et al, Neurodegenerative Disease Research

Center, King's College,UK, "P450 and hemeoxygenase enzymes in the basal ganglia and their role's in Parkinson's disease", Adv Neurol, 1999; 80:271‑86

(68) A prospective assessment of porphyrins in autistic disorders: a potential marker for heavy metal exposure.   Geier DA, Geier MR.  Neurotox Res. 2006 Aug;10(1):57-64: & Altered urinary porphyrins and mercury exposure as biomarkers for autism severity in Egyptian children with autism spectrum disorder. Khaled EM, Mequid NA, et al; Metab Brain Dis. 2016 Dec;31(6):1419-1426; 

(89)Makani A, Gollapudi S, Yel L, Chiplunkar S, Gupta S; Biochemical and molecular basis for thimerosal-induced apoptosi in T-cells; a major role of mitochondrial pathway; Genes and Immunity, 2002, 3:270-278; & (b) James S.J., Slikker W, Melnyk S, New E, Pogribna M, Jernigan S; Thimerosal neurotoxicity is associated with glutathione depletion: Protection with nutritional supplementation; Dept. of Pediatrics, College of Medicine, Univ. of Arkansas, and Arkansas Children’s Hospital Reserch Institute, Little Rock, Ark; NeurotoxicologyConference, Hawaii, February 2004


(90) Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism.  Vojdani A, Pangborn JB, et al,  Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):189-99.


(91)Annotated Bibliography: Adverse health effects related to mercury and amalgam fillings and clinically documented recoveries after amalgam replacement. Windham, B. (over 3000 peer-reviewed references);

(92) Polymorphism of bovine beta-casein and its potential effect on human health, J 

Appl Genet 48(3), 2007, pp. 189–198, Stanis³aw Kamiñski1, Anna Cieoeliñska1, El¿bieta Kostyra2; & Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption.  Diabetologia 1999 Aug;42(8):1032; Elliott RB, Harris DP, Hill JP, BibbyNJWasmuth HE.

(96) A clinical trial of combined anti-androgen and anti-heavy metal therapy in autistic disorders.  Geier DA, Geier MR. Neuro Endocrinol Lett. 2006 Dec;27(6):833-8; & A prospective assessment of androgen levels in patients with autistic spectrum disorders: biochemical underpinnings and suggested therapies. Geier DA, Geier MR.  Neuro Endocrinol Lett. 2007 Oct;28(5):565-73

(97) The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8; & Šterzl I, Procházková J, Hrdá P, Matucha P, Bártová J, Stejskal VDM: Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis. Neuro Endocrinol Lett, 2006, 27(Suppl.1): 25-30  ; & 

Mechanisms by which mercury and toxic metals are factors in Multiple Sclerosis and other neurological and autoimmune conditions, and by which mercury detoxification commonly brings improvement;  B Windham (Ed),