Vaccines, autism and thimerosol research

[TZ]

For those of you interested in the ACTUAL scientific data from non-political SCIENTISTS here are sources from WORLD experts in this field:
NIH..
http://www.niaid.nih.gov/factsheets/thimerosalqa.htm
Also since I'm sure somebody will screech about NIH being run by Big Pharma (not true)
Here is WHO (world health organization)
http://www.who.int/vaccine_safety/topics/mmr/mmr_autism/en/
So who should one believe? Someone who has never had a class in science but has the princely "Kennedy" name behind him? Or world class experts in the field who have NO FINANCIAL stakes in this? Gee hard to choose...:sarcasm:
Funny how I've NEVER met a biologist who believes this vaccines cause autism shit.

[Beregond2]

1. Exactly right.

Kennedy is going to be very embarrased one day by his association with this nonsense.

[lizerdbits]

2. But he was on teh teevee

and he has a famous name! Science is too complicated for me to understand so I'll just let a famous person tell me what to think and make posts on message board of 15 links that don't actually conclude what I say they do. :rofl:

[NoodleBoy]

3. kick,

[xchrom]

4. kick

[LeftishBrit]

5. kick

[Warpy]

6. Well, pointy headed scientists are all the same

and we all know they don't give a damn about sick kids, not even their own kids, when the profits of pudgy white men in three piece suits are at stake.

Besides, science is such a monolith. You need people outside it to come up with all the real cures, right?








Uh, :sarcasm:

[philb]

11. Pediatric vaccines also cause autism in monkeys in clinical trials

PEDIATRIC VACCINES INFLUENCE PRIMATE BEHAVIOR
"Pediatric Vaccines Influence Primate Behavior, and Amygdala Growth and Opioid Ligand Binding", L. Hewitson et al, University of Pittsburgh, 7th International Meeting For Autism Research in London, May 2008. http://www.ageofautism.com/2008/05/sick-monkeys-st.html
found autism-like signs and symptoms in infant monkeys vaccinated in a similar pattern to children in the 1990s.
"Microarray Analysis of GI Tissue in a Macaque Model of the Effects of Infant Vaccination," Steven Walker et al,
performed gene array analysis on the intestinal tissues of the vaccinated and unvaccinated animals
"vaccinated animals exhibited progressively severe chronic active inflammation whereas unexposed animals did not. We have found many significant differences in the GI tissue gene expression profiles between vaccinated and unvaccinated animals."
05/16/2008
SICK MONKEYS: RESEARCH LINKS VACCINE LOAD, AUTISM SIGNS
The first research project to examine effects of the total vaccine load received by children in the 1990s has found autism-like signs and symptoms in infant monkeys vaccinated the same way. The study's principal investigator, Laura Hewitson from the University of Pittsburgh, reports developmental delays, behavior problems and brain changes in macaque monkeys that mimic "certain neurological abnormalities of autism."
The findings are being reported Friday and Saturday at a major international autism conference in London.

Although couched in scientific language, Hewitson's findings are explosive. They suggest, for the first time, that our closest animal cousins develop characteristics of autism when subjected to the same immunizations – such as the MMR shot -- and vaccine formulations – such as the mercury preservative thimerosal -- that American children received when autism diagnoses exploded in the 1990s.
The first publicly reported results of this research project come in both oral and poster presentations on Friday and Saturday at the International Meeting For Autism Research in London. Poster presentations must go through a form of peer review before they are presented at the conference; the papers have not yet appeared in a scientific journal.
In addition to Hewitson's oral presentation today, on Saturday in one of two related poster presentations, the researchers also are reporting in their abstract that "vaccinated animals exhibited progressively severe chronic active inflammation whereas unexposed animals did not. We have found many significant differences in the GI tissue gene expression profiles between vaccinated and unvaccinated animals." Numerous scientific studies, as well as many parents, report severe GI ailments in children with regressive autism.
The results are sure to be controversial, in part because they lend credence to studies first published in 1998 by British pediatric gastroenterologist Andrew Wakefield, one of Hewitson's co-authors on these findings. He described an unusual inflammatory bowel condition in children who had regressed into autism after they received the measles-mumps-rubella (MMR) vaccination. Wakefield is currently fighting charges of medical misconduct in Britain over allegations of conflict-of-interest and improper procedures related to that paper. He denies the charges.
In the program for the conference, the 7th Annual International Meeting for Autism Research (IMFAR), there are three separate presentations listed that report results from the overall research program. The first, an oral presentation entitled "Pediatric Vaccines Influence Primate Behavior, and Amygdala Growth and Opioid Ligand Binding" (the "amygdala abstract") was led by Dr. Hewitson and lists 12 co-authors, including five of her colleagues from the University of Pittsburgh and Dr. Wakefield. Other authors are chemists, pathologists and psychologists from the universities of Kentucky, California-Irvine, and Washington.
Hewitson's introductory presentation will be followed by two poster presentations on Saturday; one of the two, "Pediatric Vaccines Influence Primate Behavior, and Brain Stem Volume and Opioid Ligand Binding", was led by Wakefield and includes six additional co-authors.
It focuses on the developmental effect of vaccine exposures on brain growth during infancy. The second, "Microarray Analysis of GI Tissue in a Macaque Model of the Effects of Infant Vaccination," was led by Steven Walker of Wake Forest University and performed gene array analysis on the intestinal tissues of the vaccinated and unvaccinated monkeys.
The studies address – albeit in animals, not children -- one of the major criticisms by parents and scientists concerned about a possible link between the greatly stepped-up immunization schedule in the 1990s, including higher exposure to the mercury preservative, and autism. While the Food and Drug Administration approves individual vaccines as safe and effective, and an advisory committee to the Centers for Disease Control and Prevention recommends the childhood immunization schedule adopted by the states, the overall health outcomes from the total vaccine load, versus no vaccinations at all, have never been compared, the authors said.
A bill requiring the government to conduct a study of autism rates in unvaccinated American children is pending in the U.S. House of Representatives, co-sponsored by Reps. Carolyn Maloney (D-N.Y.) and Tom Osborne (R.-Neb.). Just this week, former National Institutes of Health Director Bernadine Healy called for more research into a possible vaccine link to autism and said the question had not been settled, despite repeated assertions to that effect by the CDC, the Institute of Medicine and the American Academy of Pediatrics.
In the abstract for today's oral presentation, the authors noted that macaques, the type of monkey used in the study, "are commonly used in pre-clinical vaccine safety testing, but the combined childhood vaccine regimen, rather than individual vaccines, has not been studied. Childhood vaccines are a possible causal factor in autism, and abnormal behaviors and anomalous amygdala growth are potentially inter-related features of this condition."
The study found evidence of both behavioral and biological changes after the 13 macaque monkey infants were administered proportional doses, adjusted for age, of the vaccines recommended between 1994 and 1999. Three monkeys were not given any vaccines.
"Primate development, cognition and social behavior were assessed for both vaccinated and unvaccinated infants using standardized tests developed at the Washington National Primate Research Center." MRI and PET scans looked for brain changes after administration of the MMR.
"Compared with unexposed animals, significant neurodevelopmental deficits were evident for exposed animals in survival reflexes, tests of color discrimination and reversal, and learning sets," the authors reported. "Differences in behaviors were observed between exposed and unexposed animals and within the exposed group before and after MMR vaccination. Compared with unexposed animals, exposed animals showed attenuation of amygdala growth and differences in the amygdala binding of <11C>diprenorphine. Interaction models identified significant associations between specific aberrant social and non-social behaviors, isotope binding, and vaccine exposure."
One of the Saturday abstracts makes the further point that the research "revealed significant differences between exposed and unexposed animals" in the kinds of developmental behaviors a mother might be able to observe, "with delayed acquisition of root, suck, clasp hand, and clasp foot reflexes." They conclude by noting that "This animal model examines the neurological consequences of the childhood vaccine regimen, Functional and … brainstem anomalies were evident in vaccinated animals that may be relevant to some aspects of autism. The findings raise important safety issues while providing a potential animal model for examining aspects of causation and disease pathogenesis in acquired neurodevelopmental disorders."

[varkam]

22. BS Study

Here's why:

Finally, let's look at the microarray. Sending this particular abstract to me was a big mistake, as I've actually done gene expression profiling before using microarrays and am experienced with PCR and quantitative real time PCR. I can't say I'm an expert at cDNA microarrays, but I've picked up a few principles. Let's look at what the investigators say in the last abstract:

Whole genome microarray analysis was performed on RNA extracted from the GI tissue from 7 vaccinated and 2 unvaccinated animals at each of these 3 time points (27 samples total). Results: Histopathological examination revealed that vaccinated animals exhibited progressively severe chronic active inflammation, whereas unexposed animals did not. Gene expression comparisons between the groups (vaccinated versus unvaccinated) revealed only 120 genes differentially expressed (fc >1.5; log ratio p<0.001) at 10 weeks, whereas there were 450 genes differentially expressed at 14 weeks, and 324 differentially expressed genes between the 2 groups at necropsy.

One thing that leaps right out at me is the question of why on earth specimens from only slightly more than half of the vaccinated monkeys and only two out of the three unvaccinated monkeys were evaluated. What happened to the other specimens? No explanation is given for why specimens from all the monkeys weren't studied. This alone makes me highly suspicious of the all the results.

The second thing that leaps right out is the cutoff they were using. They appear to have used a cutoff for "differential expression" of a 1.5 times increase or decrease in the level of a given gene's transcript. In other words, a gene qualifies as being "differentially expressed" if its messenger RNA (mRNA) level in the vaccinated group is 1.5 times control or 1/1.5, or 0.67 times its level in the unvaccinated group. If I'm interpreting correctly how they did this, that's a very loose standard for deciding on whether a gene is differentially expressed in the vaccinated group or not, especially in a first pass experiment with low numbers like this one. (Let's put it this way: In one of the microarray experiments I did, all the genes of interest that I looked at had ratios of over 6, and one had a ratio of over 200, which, not surprisingly, really got our attention.) Although sometimes we will accept 1.5-fold differences, in general in doing a microarray experiment, on the first try we ignore any gene with less than a two-fold change, and we prefer to see three-fold or greater changes in expression levels of the messenger RNA. This is especially true when one uses a log ratio to calculate each gene expression level, given that the log ratio is prone to large changes due to error at low expression levels. This would be particularly true in a dataset that includes only two control samples, which is the absolute minimum number that statistics can be done on and totally inadequate for an experiment like this. The selection of this liberal cutoff strongly suggests to me that the investigators were trying to pad the number of differentially expressed genes. Even if they were referring to a true log ratio of 1.5 (i.e., a 21.5-fold change, or 2.8-fold change, which they may very well have been doing), this would still be fairly liberal for an experiment with only two samples in the control group. Remember, cDNA microarray expression profiling looks at thousands of genes at the same time; without truly rigorous statistics, there will be dozens, if not hundreds of false positives. That's one reason why In microarray experiments it is absolutely critical to verify any "positive" findings for genes that are up- or downregulated by doing:

* Reverse transcriptase quantitative real time PCR
* Western blot or immunoprecipitation to verify that the difference observed in the mRNA level is also seen at the protein level (assuming, of course, a suitable antibody is available)


Read more: http://scienceblogs.com/insolence/2008/05/some_monkey_business_in_autism_research.php

[semillama]

7. Well, the responses to this thread are about what you'd expect

and that's depressing.

[philb]

8. its been documented metals/vaccines blocking enzymes needed for digestion cause autism

in susceptable infants (mercury/aluminum/etc. with vaccines a major source of the exposure)

Autism and Schizophrenia subgroup related to blockage by toxic exposures of enzymes processing gluten and casein, B.Windham (Ed), 2008 www.flcv.com/autismgc.html

(affects at least 65% of autistic children (100) ) (overlaps with other mechanisms documented in (110) )

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 allergic/immune reactive conditions(15-23,28,36,47,51,98). For example mercury has been found to strongly inhibit the activity of xanthine oxidase(16) and dipeptyl peptidase (DPP IV) which are required in the digestion of the wheat protein gluten or the milk protein casein (15,17,19,20,22a,24,-26,98, 105) - 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 a large sample 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. 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 (105). 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(105). 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(105). 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 (105).

The studies also 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 of ASD children (100,28,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 was 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 (23,11,22a,30,40,96,100). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs(22a,11,96).

(11) V.D.M.Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE IMMUNO STIMULATION ASSAY MELISA”, paper presented at international autism conference & http://www.melisa.org/autism.php
& “Mercury-specific Lymphocytes: an indication of mercury allergy in man”, J. Of Clinical Immunology, 1996, Vol 16(1);31-40; see: www.melisa.org
(12) Sterzl I, Prochazkova J, Stejaskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & V.Stejskal, “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.
(13) Redhe O, Pleva J. Recovery from asthma, allergies,ALS after removal of dental amalgam fillings. Int J of Risk & Safety in Medicine 1994; 4:229-236.
(14) Kurek M, Przybilla B, Hermann K, Ring J. An opioid peptide from cows milk, beta-casomorphine-7, is a direct histamine releaser in man. Int Arch Allergy immunol 1992; 97(2): 115-20; & Nutritive Casein Formula Elicits Pseudoallergic Skin Reactions by Prick Testing, M. Kurek, T. Maczy´nska. Allergy and Immunology, Vol. 118, No. 2-4, 1999, & Developmental Disorders and Diary Products, Grains, Gluten and Other Proteins , Margaret Lahey and Shari Rosen, BAMFORD-LAHEY CHILDREN'S FOUNDATION
http://www.childrensdisabilities.info/allergies/developmentaldisordersprotein7.html

(15) Tejwani GA, Hanissian SH. Modulation of mu, delta, and kappa opioid receptors in rat brain by metal ions and histidine. Neuropharmology 1990; 29(5): 445-52.
(16) Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase activity by Hg2+ and other metal ions. 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, 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; & 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
http://www.inotekcorp.com/content/xo_inhibitors.asp

(17) Sastry KV, Gupta PK. 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; & 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) Mc Fadden SA, Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways. Toxicology, 1996, 111(1-3):43-65; & 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-Spatz Disease: 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., www.autismndi.com/
(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) Windham, B. Annotated Bibliography: Adverse health effects related to mercury and amalgam fillings and clinically documented recoveries after amalgam replacement. (over 3000 peer-reviewed references); www.flcv.com/amalg6.html
& (b) Prenatal and neonatal effects of mercury on infants, www.flcv.com/fetaln.html
(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 www.autism.com/ari/mercurylong.html; &(b)Dr. A Holmes, Autism Treatment Center,Baton Rouge, La; www.healing-arts.org/children/holmes.htm#wethink , &(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 rxguidebook.com/DesktopDefault.aspx?tabindex=11&tabid=15; & (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 , www.noamalgam.com/; &(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,
www.hyperbaricmedicalassociation.org/docs/0_BUTTAR1.PDF
(24) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999. http://news.ufl.edu/1999/03/15/autism/ ;& Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000. http://www.feingold.org/Research/cade.html & http://www.paleodiet.com/autism/ ; & "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 ; http://aut.sagepub.com/cgi/reprint/3/1/67 & 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 http://aut.sagepub.com/cgi/content/abstract/3/1/85 ; & 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; http://www.feingold.org/Research/autism.html ; & Peptides from Casomorphin & Gliadorphin, The Great Plains Laboratory, www.greatplainslaboratory.com/russian/glutencasein.html ; & Why Use the Gluten-Free and Casein-Free Diet in Autism and What the Results have Shown so Far, Peptides and Autism, Karl Reichelt, MD, PhD1 and A. M. Knivsberg PhD, Fall Defeat Autism Now!TM 2003 Conference *** Portland, Oregon *** October 3-5, 2003, http://www.autism.com/treatable/diet_reichelt.htm &
Milk Linked to Autism, Schizophrenia http://www.mercola.com/1999/archive/milk_linked_to_autism.htm
http://www.bzz1.com/coucowley/?page=page2
http://www.notmilk.com/zerodairy.html

(25) Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4; & Reichelt KL 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 leucocyte migration 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.
(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; http://www.autism.com/dan/index.htm

(98) 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.
(100) Results of treatment survey of 25,000 parents of autistic children, Autism Research Institute, www.autism.com/treatable/form34qr.htm
(105) 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, Bibby NJ, Wasmuth HE.


& rest in (110) www.flcv.com/kidshg.html

[philb]

9. Hypothyroidism caused by mercury/toxics another documented cause of autism/reduced IQs,etc.

Hypothyroidism during pregnancy as cause of developmental delays, reduced IQs, and autism- the mercury and toxic metal connection. B Windham, (Ed)

Studies have documented that mercury causes hypothyroidism (50,84,390,407), damage of thyroid RNA(458), autoimmune thyroiditis (369,382,91), and impairment of conversion of thyroid T4 hormone to the active T3 form(369,382,390,407,50d). These studies and clinical experience indicate that mercury and toxic metal exposures appear to be the most common cause of hypothyroidism and the majority treated by metals detoxification recover or significantly improve (503). Thousands of tests at medical labs and many studies have documented that dental amalgam is the largest source of mercury in most adults that have several amalgam fillings, with exposures much above government health guidelines (501). Studies have also documented that for most mothers who have several amalgam fillings, the mother’s dental fillings are the largest source of mercury in the fetus and a significant source in infants (502).
The estimated prevalence of hypothyroidism from a large federal health survey, NHANES III, was 4.6%, but the incidence was twice as high for women as for men and many with sub clinical hypothyroidism are not aware of their condition(3a). Another large study(3b) found that 11.7% tested had abnormal thyroid TSH levels with 9.5% being hypothyroid and 2.1% hyperthyroid. According to survey tests, 8 to 10 % of untreated women were found to have thyroid imbalances so the actual level of hypothyroidism is higher than commonly recognized(508). Even larger percentages of women had elevated levels of antithyroglobulin(anti-TG) or antithyroid peroxidase antibody(anti-TP). Tests have found approx. 30% of pregnant women to have low free T4 in the first trimester(509b).
Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain (10a). Hypothyroidism of the adults causes most frequently dementia and depression. Nearly all the hyperthyroid patients show minor psychiatric signs, and sometimes psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur(10a). These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission, and play an important role in regulating central noradrenergic and GABA function.
Studies indicate that slight thyroid deficiency/imbalance(sub clinical) during the perinatal period can result in delayed neuropsychological development in neonate and child or permanent neuropsychiatric damage in the developing fetus or autism or mental retardation (10,509,511). Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result in significantly reduced IQs (509a-e) and causes psychomotor deficits(509f). Women with the highest levels of thyroid-stimulating-hormone(TSH) and lowest free levels of thyroxin 17 weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age 8(509a). Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children. Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. "Collectively, reports show that 30-60% of women positive for TPO antibodies in pregnancy develop postpartum thyroiditis," the researchers point out (561,8), calling it "a strong association." Without treatment, many of the women with thyroiditis go on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About 7.5% of pregnant women develop thyroiditis after birth(8). Studies have also established a connection between maternal thyroid disease and babies born with heart defects(509h).
Infants of women with hypothyroxinemia at 12 weeks' gestation had significantly lower scores on the Neonatal Behavioral Assessment Scale orientation index compared with subjects(10b). Regression analysis showed that first-trimester maternal free thyroid hormone T4 was a significant predictor of orientation scores. This study confirmed that maternal hypothyroxinemia constitutes a serious risk factor for neurodevelopmental difficulties that can be identified in neonates as young as 3 weeks of age.

Mercury (especially mercury vapor from dental amalgam or organic mercury) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, thyroid gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces (14,19,85,99,273,274,407), and likewise rapidly crosses the placenta and accumulates in the fetus including the fetal brain and hormone glands at levels commonly higher than the level in the mother(20,22-27). Milk from mothers with 7 or more mercury amalgam dental fillings was found to have levels of mercury approximately 10 times that of amalgam free mothers(22b). The milk sampled ranged from 0.2 to 57 ug/L. In a population of German women, the concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L (26). A Japanese study found that the average mercury level in samples tested increased 60% between 1980 and 1990<25>. The study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway(25). The level of mercury in umbilical cord blood, meconium, and placenta is usually higher than that in mother's blood<23-25>.

The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic (392,394,etc.).
Alterations of cortical neuronal migration and cerebellar Purkinje cells have been observed in autism. Neuronal migration, via reelin regulation, requires triiodothyronine (T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases(407). Experimental animal models have shown that transient intrauterine deficits of thyroid hormones (as brief as 3 days) result in permanent alterations of cerebral cortical architecture reminiscent of those observed in brains of patients with autism. Early maternal hypothyroxinemia resulting in low T3 in the fetal brain during the period of neuronal cell migration (weeks 8-12 of pregnancy) may produce morphological brain changes leading to autism. Insufficient dietary iodine intake and a number of environmental antithyroid and goitrogenic agents such as mercury, soy, and peanuts can affect maternal thyroid function during pregnancy. The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic.

Mercury can have significant effects on thyroid function even though the main hormone levels remain in the normal range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely affects the activity of selenoenzymes, including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases(5-Di and 5'-DI) in the fetal brain, even though thyroxine(T4) levels are normal(390de). Another mechanism by which mercury exerts such effects is mercury’s effects on selenium levels which are required for conversion of T4 to T3(392,390d). Gpx activity is severely inhibited, while 5-DI levels are decreased and 5'-DI increased in the fetal brain, similar to hypothyroidism. Thus normal thyroid tests will not pick up this condition.

Mercury reduces the bloods ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc, selenium and Vit B12 (43,96,198,263,264,338, 339,392,427); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake, autoimmune thyroiditis, & hypothyroidism. (50,91,212,222,369,382,392,394,407,35). Minerals such as calcium, zinc, and manganese are also necessary for thyroid health and hormone production, and their absorption is blocked by mercury exposure. Because of the evidence of widespread effects on infants, the American Assoc. of Clinical Endocrinologists advises that all women considering becoming pregnant should get a serum thyrotropin test so that hypothyroidism can be diagnosed and treated early(558,7b). Since mercury and toxic metals are common causes of hypothyroidism, another test that should be considered is a hair element test for mercury or toxic metal exposures and essential mineral imbalances.

References
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[cosmik debris]

13. And this comes from the laughing stock of the Health Scare Forum

With your wall of text and your Dr. Google credentials.

I especially liked the amalgam parts.

After all, you ally 4moronicyears proved that amalgam was NOT a danger to children or any one else. Of course he didn't intend to do that, but just like you, he doesn't read or understand the studies he cites.

[philb]

10. Acute Lead poisoning in infants indistinguishable from autism.

Acute Lead poisoning in infants indistinguishable from autism.

We've heard a lot about the recalls for the toys made with lead paint. Lead poisoning can have severe impacts on a child and his or her family.
Problems for Noah Breakiron began at nine-months-old. He was often sick and out of control.
"We couldn't go to the grocery store, church, really anywhere due to the screaming," said Rob, Noah's dad.
Noah was diagnosed with autism, but then the underlying problem was discovered: lead poisoning. Noah had seven-times the upper limit of lead in his body.
"We were shocked," said Lisa Breakiron, Noah's mother. "We were absolutely shocked. Like, lead poisoning? That can't be right."
Lisa and Rob couldn't pinpoint how the lead got in Noah's body. But now, his parents believe it might have been from his toys.
"I can tell you when he was a toddler, he was always chewing on stuff," said Rob.
Chelation treatments have reduced Noah's lead levels and have made a huge impact.
"It was really powerful and amazing for us to watch. It was like literally watching a miracle right in front of your eyes," said Rob.
Pediatrician David Berger is Noah's doctor.
"We have a child here who is virtually indistinguishable from his peers and that's certainly not what he was a year or two years ago," said Dr. Berger.
Dr. Berger says a developing brain is much more sensitive to lead exposure. He says universal testing for lead in young kids should be done. It's a blood test doctors stopped doing routinely ten years ago, but one he says parents should ask for.
"This can cause significant long term problems and it's worthwhile checking for," said Dr. Berger.
"With Noah's level of lead poisoning, if that would have continued, he could have died," said Lisa.
Today, you can't tell that Noah's body is in a battle to remove the lead. He just seems like a typical four year old, and that's good news. Because the symptoms of autism and lead poisoning mimic each other.

http://www.wftv.com/health/15051675/detail.html?rss=orlc&psp=health

[cosmik debris]

12. Do you think we have forgotten that you posted a survey of pet

owners and presented it as a scientific study on autism?

That's the kind of thing that blows your credibility right out of the water.

[philb]

14. The author of the pet study was a guest on Calling All Pets, whose expert

is one of best known and respected researchers on pet issues.

The book that I quoted was also on best sellers list, and reviews were excellent;
plus I quoted other peer-reviewed studies that supported some of the statements of the author you are talking about whose article was included in my post with other cites.

you as usual are grasping for straws since you don't know as much about these issues as my sources, and can't counter their peer-reviewed studies and large volumes of clinical case data with any credible information to the contrary.

Some people have interest in pets and issues affecting pets are often relevant to people.

[philb]

15. Here's another example: Insecticides in pet shampoo may trigger autism

Insecticides in pet shampoo may trigger autism
15 May 2008 NewScientist.com news service Linda Geddes

Could insecticides in pet shampoos trigger autism spectrum disorders? That's the suggestion of one of the first large-scale population-based studies to look how environmental factors and their interactions with genes contribute to the condition.

Mothers of children with an autism spectrum disorder (ASD) were twice as likely to have reported using pet shampoos containing a class of insecticide called pyrethrins as those of healthy children, according to survey results presented Thursday at the International Meeting for Autism Research in London. The risk was greatest if the shampoo was used during the second trimester of pregnancy.

Meanwhile, another study suggests that exposure to organophosphate insecticides double the risk of developmental disorders, including autism. Organophosphates have previously been linked to Gulf War syndrome.

While many chemicals have previously been blamed for triggering autism, there have been very few rigorous studies designed to investigate the link.

Neuronal damage

To remedy this, Irva Hertz-Picciotto and her colleagues at the University of California in Davis, US, studied 333 children with ASD and 198 healthy children, and their families.

They collected blood and urine samples, as well as conducting in-depth questionnaires on medical history and any possible exposure to medications, household products or metals that could have occurred around the time of conception, during pregnancy, or after birth. They also collected information on lifestyle, and whether the children were breast-fed, for example.

Previous studies in insects and rodents have suggested that pyrethrins could damage the blood-brain barrier during early life, and cause neuronal damage. They may also interfere with the transmission of signals along nerve fibres.

"Autism is associated with an imbalance between excitatory and inhibitory neurotransmitters within the brain, and one could hypothesise that children with an imbalance in this system may be more sensitive to the effects of pyrethrins," says Isaac Pessah at UC Davis, who was also involved in the study.

'No single answer'

However, Hertz-Picciotto and other experts caution that pyrethrins were unlikely to be the only cause of autism, which is increasingly recognised as being caused by a complex interplay of both genetic and environmental factors.

"This is a candidate, but there is unlikely to be a single answer to what causes autism," says Tony Charman of University College London, UK, and chairman of IMFAR.

"The findings now need to be replicated and more studies need to be done to understand how this toxin affects development," he says.

Neither are pyrethrins likely to be the only chemicals that increase the risk of ASD.

Genetic susceptibility

For example, in a separate study, Brenda Eskenazi and her colleagues at the University of California in Berkeley, measured levels of metabolites from organophosphates in urine samples taken from 400 women during pregnancy, and their children. Such metabolites were associated with a two-fold risk of developmental disorders in the children.

As well as being used in agricultural products like sheep dip, organophosphates are used in head-lice treatments, pet shampoos and other household products.

Pessah says that chemicals like pyrethrins and organophosphates are likely to increase the risk of autism in children who already have an underlying genetic susceptibility.

"ASD is a spectrum of disorders, some of which are very mild, and chemical or environmental factors may shift that profile so that children who would otherwise not receive a diagnosis of ASD will receive one."

Geri Dawson, chief scientific officer at research charity Autism Speaks, agrees.

"Probably in the majority of cases autism is a complex disorder involving multiple genes and multiple environmental factors," she says. "However, at least if we can identify the environmental factors, there is something we can do about them."

[cosmik debris]

18. You'll believe anything won't you?

I've got a really nice bridge for sale--cheap!

[chicagomd]

24. Welcome back!

We missed you. Still spouting the same old bullshit, huh?

[cosmik debris]

16. I understand that you believe your own bullshit.

But just because you believe it doesn't mean that it is not bullshit

[philb]

17. Everything I've posted here is backed up by credible peer-reviewed studies & clinical cases

as anyone can see for themselves

You are playing silly games as usual, since you can't comment credibly with credible sources to back you up.

[cosmik debris]

19. No, it's not

You post bogus studies, fake lab reports, and you misrepresent the information to pretend that it supports your crusade.

In fact, you are a terrible source of information. You have been repeatedly discredited. And yet you keep coming back for more.

[varkam]

23. No, it isn't.

In fact, I would say that nothing that you have ever posted here is backed up by credible peer-reviewed studies and clinical cases.

[cosmik debris]

20. A survey of pet owners is NOT a scientific study of autism

And anyone crazy enough to believe that it is would probably by swamp land in Florida.

You do live in Florida, right? Do you mow your lawn with an air boat?

[trotsky]

21. ....

[Orrex]

25. Quick! Somebody shampoo that kitten!

But for god's sake, don't let a pregnant woman do it!