Newsgroup: it.salute
Titolo: Autismo dai Vaccini

La Merck ammette l'inoculazione del virus del cancro - La divisione vaccini
della farmaceutica Merck, ammette l'inoculazione del virus del cancro per
mezzo dei vaccini.
 La sconvolgente intervista censurata, condotta dallo studioso di storia
medica Edward Shorter per la televisione pubblica di Boston WGBH e la
Blackwell Science, � stata tagliata dal libro "The Health Century" a causa
dei sui contenuti - l'ammissione che la Merck ha tradizionalmente iniettato
il virus (SV40 ed altri) nella popolazione di tutto il mondo.
 Questo filmato contenuto nel documentario "In Lies We Trust: The CIA,
Hollywood & Bioterrorism", prodotto e creato liberamente dalle associazioni
di tutela dei consumatori e dall'esperto di salute pubblica, Dr. Leonard
Horowitz, caratterizza l'intervista al maggior esperto di vaccini del mondo,
il Dott. Maurice Hilleman, che spiega perch� la Merck ha diffuso l'AIDS, la
leucemia e altre orribili piaghe nel mondo :
http://www.youtube.com/watch?v=edikv0zbAlU
Nei vaccini venduti al terzo mondo si � scoperto che molti di questi
contenevano l'ormone B-hCG un anti fertile se immesso in un vaccino.
La corte Suprema delle Filippine ha scoperto che oltre 3 milioni di ragazze
e donne hanno assunto questi vaccini contaminati, cos� come in Nigeria,
Tailandia ecc...
Per chi non abbia ancora visto questi video-documenti scioccanti:
http://uk.youtube.com/watch?v=edikv0zbAlU
http://it.youtube.com/watch?v=wg-52mHIjhs&feature=related
Sembrerebbe che oltre al profitto a tutti i costi, ci sia dietro qualcosa
d'altro....impedire alle donne dei paesi del terzo mondo... di avere
figli....
I Vaccini creano Mutazioni Genetiche nei Mitocondri delle cellule, mutazioni
che sono trasmissibili alla prole, dalla via materna. Nelle cellule
infettate da virus si risvegliano i retrovirus piu' vecchi.
Dei ricercatori hanno osservato che quando il metabolismo della cellula
infettata da un virus (NdR: che puo' essere anche vaccinale) essa viene
ingannata al fine di riprodurre il virus che la infetta, pero' in essa
decade la funzionalit� di alcune reazioni biochimiche di contenimento e di
funzione cellulare: sintesi e specializzazione delle proteine,
specializzazione degli enzimi e duplicazione del DNA.
Quindi anche l'infezione da virus vaccinale e' in grado quindi di riattivare
genomi di precedenti virus, o di quelli iniettati con i vaccini ai genitori,
nonni, avi del vaccinato, virus, che erano divenuti parte del genoma delle
cellule dei genitori, nonni, avi, generando anticipatamente qualsiasi tipo
di patologia; il meccanismo si chiama slatentizzazione = liberare
anticipatamente patologie.
Di fatto i Vaccini sono un cocktail di Tossine altamente pericolose che
possono rimanere inerti per anni e riesplodere come bombe a tempo anche dopo
30-40 anni o piu', in uno stato febbrile. che alterano il Terreno in modo
importante, specie negli organismi non perfettamente sani, per problemi
ereditari e/o di alimentazione inadatta alla Perfetta Salute.
      Vaccinazioni per l'infanzia ed autismo: un caso accertato negli Stati
Uniti
      Mercoled� 9 Aprile 2008 - Gli studi clinici hanno fallito nel mostrare
un legame tra vaccinazione ed autismo, ma molti genitori di bambini
autistici hanno nutrito dubbi su queste conclusioni.
      Il Governo americano ha ora ammesso che la vaccinazione pu� avere
arrecato danni ad una bambina di 9 anni, ed ha annunciato che si far� carico
delle spese per la cura.
      Nel 2000 Hannah aveva 19 mesi ed uno sviluppo normale, quando
ricevette 5 iniezioni per la prevenzione di 9 malattie infettive.
      Nel 2001 alla bambina � stato diagnosticato il disturbo autistico.
      Per il fatto che il padre di Hannah era un neurologo al Johns Hopkins
Hospital, la bambina � stata sottoposta ad una serie di esami, che hanno
evidenziato un disordine a livello mitocondriale.
      Due teorie sono state ipotizzate: la prima che la bambina presentava
una sottostante malattia mitocondriale e che la vaccinazione ha
slatentizzato, la seconda � che la vaccinazione ha causato questo disordine.
      Il Governo ha optato per la prima ipotesi: la bambina aveva una
sottostante malattia mitocondriale che � stata aggravata dalla vaccinazione.
      Molti dei vaccini che Hannah ha ricevuto contenevano Tiomersale, un
preservativo a base di Mercurio.
      Negli Stati Uniti, il Tiomersale � stato rimosso dai vaccini
somministrati nell'infanzia a partire dal 2001.
      Rimane aperto il dibattito sulle vaccinazioni multiple nell'infanzia.
( Xagena Medicina )
      Fonte: The New York Times, 2008 - Medicina-Online.net  +  Autismo dai
VACCINI  +  Bibliografia su Autismo dai vaccini
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      E' in vendita il libro del dott. M. Montinari, Medico-Chirurgo della
Polizia di Stato di Firenze - Specialista in Chirurgia Pediatrica -
Specialista in Chirurgia d'Urgenza e P.S. - Iscritto Albo CTU Tribunale
Civile e Penale di Bari (n�582): 
monti...@libero.it
      Il dott. M. Montinari ha fino ad oggi in cura oltre 3.500 pazienti fra
cui oltre 1100 malati di autismo, da Vaccino.
      I titoli dei suoi libri sono: : "AUTISMO, nuove terapie per migliorare
e guarire"  +  Educazione alla Salute, parliamo di sostanze Stupefacenti ed
alcool, ediz. Marianna.
      Il primo libro contiene le sue ricerche  (su circa 800 pazienti)
indicano la responsabilita' delle Vaccinazioni come causa della malattia
(Autismo).... 230 pagine di documentazione medico Scientifica qualificata.
      Una traccia da seguire per medici, ricercatori e genitori che non
hanno perso la speranza di vedere guarire o stare molto meglio i loro figli
autistici...
      Tutti i dati scientifici, le diete, le alternative agli antibiotici e
le terapie di supporto, fisiologiche, linguistiche, psicologico e senso
motorio con l'indirizzario di terapeuti ed associazioni a cui rivolgersi. -
editore Macroedizioni
      vedi: Bibliografia Danni dei vaccini  +  Bibliografia danni 2  +
1.000 studi sui Danni dei Vaccini
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Relazione fra STRES OSSIDATIVO, MERCURIO (anche quello dei Vaccini) e
SOSTANZE TOSSICHE e AUTISMO
      J Neuroimmunol. 2009 Dec 23
      Oxidative stress in Egyptian children with autism: relation to
autoimmunity.
      By Mostafa GA, El-Hadidi ES, Hewedi DH, Abdou MM.
      Department of Pediatrics, Faculty of Medicine, Ain Shams University,
Cairo, Egypt.
      We are the first to study the relationship between oxidative stress
(by measuring plasma F2-isoprostane, as a marker of lipid peroxidation, and
glutathione peroxidase, as an antioxidant enzyme) and autoimmunity (as
indicated by serum antineuronal antibodies) in a group of 44 Egyptian
autistic children and 44 healthy matched-children.
      Our results showed that oxidative stress was found in 88.64% of
autistic children. Oxidative stress, resulting from elevated plasma
F2-isoprostane and/or reduced glutathione peroxidase, had significant risk
for antineuronal positivity, which was found in 54.5% of autistic children,
(odds ratio: 12.38 and 6.43, respectively, confidence interval: 1.37-112.10
and 1.21-34.19, respectively).
      Conclusions: the strong association between oxidative stress and
autoimmunity in autistic children may indicate the possible role of
oxidative stress, through induction of autoimmunity, in some autistic
patients. Therefore, studies considering the role of antioxidants and
immunotherapy in amelioration of autistic manifestations are recommended.
Copyright � 2009 Elsevier B.V. All rights reserved.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Behav Brain Funct. 2009 Oct
      Mercury exposure, nutritional deficiencies and metabolic disruptions
may affect learning in children.
      By Dufault R, Schnoll R, Lukiw WJ, Leblanc B, Cornett C, Patrick L,
Wallinga D, Gilbert SG, Crider R.
      United Tribes Technical College, Bismarck, ND, USA. 
rduf...@uttc.edu
.
      ABSTRACT: Among dietary factors, learning and behavior are influenced
not only by nutrients, but also by exposure to toxic food contaminants such
as mercury that can disrupt metabolic processes and alter neuronal
plasticity. Neurons lacking in plasticity are a factor in neurodevelopmental
disorders such as autism and mental retardation. Essential nutrients help
maintain normal neuronal plasticity.
      Nutritional deficiencies, including deficiencies in the long chain
polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid,
the amino acid methionine, and the trace minerals zinc and selenium, have
been shown to influence neuronal function and produce defects in neuronal
plasticity, as well as impact behavior in children with attention deficit
hyperactivity disorder. Nutritional deficiencies and mercury exposure have
been shown to alter neuronal function and increase oxidative stress among
children with autism. These dietary factors may be directly related to the
development of behavior disorders and learning disabilities.
      Mercury, either individually or in concert with other factors, may be
harmful if ingested in above average amounts or by sensitive individuals.
High fructose corn syrup has been shown to contain trace amounts of mercury
as a result of some manufacturing processes, and its consumption can also
lead to zinc loss.
      Consumption of certain artificial food color additives has also been
shown to lead to zinc deficiency. Dietary zinc is essential for maintaining
the metabolic processes required for mercury elimination. Since high
fructose corn syrup and artificial food color additives are common
ingredients in many foodstuffs, their consumption should be considered in
those individuals with nutritional deficits such as zinc deficiency or who
are allergic or sensitive to the effects of mercury or unable to effectively
metabolize and eliminate it from the body.
      NdR: see.the mercury inside the vaccines..
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Clin Biochem. 2009 Sep 23
      Measurement of selected ions related to oxidative stress and energy
metabolism in Saudi autistic children.
      By El-Ansary A, Al-Daihan S, Al-Dbass A, Al-Ayadhi L.
      Biochemistry Department, Science College, King Saud University, P.O
Box 22452, Zip code 11495, Riyadh, Saudi Arabia.
      OBJECTIVES:: Autism is a developmental disorder characterized by
social and emotional deficits, language impairments and stereotyped
behaviors that manifest in early postnatal life. This study aims to clarify
the role of selected ions related to energy metabolism as a consequence of
oxidative stress in the deterioration accompanied autism.
      MATERIALS AND METHODS:: Malonaldehyde as measure of lipid
peroxidation, Na(+)/K(+) ion pump (ATPase), together with the concentrations
of Na(+), K(+), Mg(2+), Ca(2+) and Pb(2+) were determined in plasma of 30
Saudi autistic patients and compared to 30 age-matching control samples.
      RESULTS:: The obtained data recorded that Saudi autistic patients have
a remarkable higher activities of Na(+)/K(+) ATPase and high levels of lipid
peroxidation compared to control. In addition, they have significantly
elevated levels of K(+) and Pb(2+) while Ca(2+) recorded a significantly
lower level compared to age-matching control subjects. On the other hand
both Mg(2+) and Na(+) were non-significantly changed in autistic patients.
      CONCLUSION:: Alteration of the selected measured ions confirms that
oxidative stress and defective mitochondrial energy production could
represent the primary causative factor in the pathogenesis of autism.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      J Cell Mol Med. 2009 Sep 14
      Chemical and molecular mechanisms of antioxidants: Experimental
approaches and model systems.
      By L� JM, Lin PH, Yao Q, Chen C.
      Molecular Surgeon Research Center, Division of Vascular Surgery and
Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor
College of Medicine, Houston, Texas, USA.
      ABSTRACT Free radicals derived from oxygen, nitrogen and sulfur
molecules in the biological system are highly active to react with other
molecules due to their unpaired electrons. These radicals are important part
of groups of molecules called reactive oxygen/nitrogen species (ROS/RNS),
which are produced during cellular metabolism and functional activities and
have important roles in cell signaling, apoptosis, gene expression and ion
transportation.
      However, excessive ROS attack bases in nucleic acids, amino acid side
chains in proteins and double bonds in unsaturated fatty acids, and cause
oxidative stress, which can damage DNA, RNA proteins and lipids resulting in
an increased risk for cardiovascular disease, cancer, autism, and other
diseases. Intracellular antioxidant enzymes and intake of dietary
antioxidants may help to maintain an adequate antioxidant status in the
body. In the past decades, new molecular techniques, cell cultures and
animal models have been established to study the effects and mechanisms of
antioxidants on ROS. The chemical and molecular approaches have been used to
study the mechanism and kinetics of antioxidants and to identify new potent
antioxidants.
      Antioxidants can decrease the oxidative damage directly via reacting
with free radicals or indirectly by inhibiting the activity or expression of
free radical generating enzymes or enhancing the activity or expression of
intracellular antioxidant enzymes.
      The new chemical and cell-free biological system has been applied in
dissecting the molecular action of antioxidants. This review focuses on the
research approaches that have been used to study oxidative stress and
antioxidants in the lipid peroxidation, DNA damage, protein modification as
well as enzyme activity, with emphasis on the chemical and cell-free
biological system.
      PMID: 19754673 [PubMed - as supplied by publisher]
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Expert Opin Pharmacother. 2009 Sep 10
      Autism: an emerging 'neuroimmune disorder' in search of therapy.
      By Theoharides TC, Kempuraj D, Redwood L.
      Molecular Immunopharmacology and Drug Discovery Laboratory, Tufts
University School of Medicine, Tufts Medical Center, Department of
Pharmacology, Boston, MA 02111, USA. 
theoharis....@tufts.edu
      BACKGROUND: Autism spectrum disorders (ASDs) are neurodevelopmental
disorders characterized by difficulties in communication and by repetitive
and stereotypic behaviors, as well as by social impairment, attention,
cognitive, and learning defects. ASDs present in early childhood and their
prevalence has increased significantly to 1/150 children. Despite a number
of theories, the actual reasons for this increase are still not clear. There
is no reliable screening test, and no definite pathogenesis or curative
therapy. Consequently, there is a major gap hampering development of
effective treatments.
      OBJECTIVE: To review recent publications on ASDs pathogenesis and
treatment with emphasis on neuroimmune processes and new therapeutic
approaches.
      METHODS: Mostly original papers (450) on epidemiology, possible
pathogenesis or treatment of ASDs in Medline from 1990 to May 2009 were
reviewed. All authors contributed to this review.
      RESULTS/CONCLUSION: Increased oxidative stress and immune
dysregulation are present in ASDs. Mast-cell activation may contribute to
gut-blood-brain barrier disruption and brain inflammation. No effective
treatments have emerged. Well-designed clinical trials with nonpsychotropic
drugs were few and ASD characteristics varied considerably, making
conclusions difficult. Psychotropic drugs are often used for stereotypic and
aggressive behaviors. Unique combinations with antioxidant and
anti-inflammatory flavonoids hold promise. New potential translational
research areas and possible treatments are suggested.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Publication Types, MeSH Terms, Grant Support
      Neurotox Res. 2009 Jul 16(1):87-95. Epub 2009 Apr 18.
      Sera from children with autism alter proliferation of human neuronal
progenitor cells exposed to oxidation.
      By Mazur-Kolecka B, Cohen IL, Jenkins EC, Flory M, Merz G, Ted Brown
W, Frackowiak J.
      Department of Developmental Neurobiology, NYS Institute for Basic
Research in Developmental Disabilities, Staten Island, New York, USA.
Bozena.Maz...@omr.state.ny.us
      Altered brain development during embryogenesis and early postnatal
life has been hypothesized to be responsible for the abnormal behaviors of
people with autism. The specific genetic background that alters
vulnerability to some environmental insults has been suggested in the
etiology of autism; however, the specific pathomechanisms have not been
identified. Recently, we showed that sera from children with autism alter
the maturation of human neuronal progenitor cells (NPCs) in culture. Results
suggest that pre-programmed neurogenesis, i.e., neuronal proliferation,
migration, differentiation, growth, and circuit organization, can be
affected differently by factors present in autistic sera. In this report, we
tested the effect of autistic sera on the vulnerability of NPCs to oxidative
stress-a recognized risk factor of autism.
      We found that mild oxidative stress reduced proliferation of
differentiating NPCs but not immature NPCs. This decrease of proliferation
was less prominent in cultures treated with sera from children with autism
than from age-matched controls. These results suggest that altered response
of NPCs to oxidative stress may play a role in the etiology of autism.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Bratisl Lek Listy. 2009;110 (4):247-50.
      Plasma concentrations of selected antioxidants in autistic children
and adolescents.
      By Krajcovicova-Kudlackova M, Valachovicova M, Mislanova C, Hudecova
Z, Sustrova M, Ostatnikova D.
      Slovak Medical University, Bratislava, Slovakia.
marica.k...@szu.sk
      Few studies have demonstrated an increased vulnerability to oxidative
stress in autism. The results of previous studies have shown that endogenous
antioxidant defence is insufficient, indicating that exogenous antioxidant
could play a crucial role for oxidative stress prevention in autism. Plasma
concentrations of vitamins C, E, A, carotenoids beta-carotene and lycopene
were measured in 51 subjects with autistic spectrum disorders aged 5-18
years (27 children aged 5-10 years, 24 subjects aged 11-18 years). Older
autistic group was compared with a group of healthy Slovak subjects aged
11-18 years.
      Older autistic subjects vs. healthy control showed significantly
higher vitamin C and beta-carotene plasma values with 92% and 71% vs 54% and
13% of optimal over-threshold values, respectively.
      This indicates a reduced risk of free radical disease. In younger vs.
older autistic group the similarly high plasma vitamin concentrations were
recorded. Favourable values of these vitamins suggested that consumption of
fruit and vegetables in autistic subjects is optimal. Autistic average
vitamin E and A plasma concentrations (non-significantly changed in
comparison to control group) were below-threshold with low percentage of
over-threshold values.
      Insufficient vitamin E and A plasma values indicate lower consumption
of food rich in vitamins A and E (e.g. whole-grain products, plant oils, oil
seeds, nuts, fat spreads and dairy products). Autistic average lycopene
concentration is lower in comparison to published non-Slovak data.
Conclusions of this pilot study suggest that plasma concentrations of
exogenous antioxidants, vitamins E and A, and lycopene in autistic subjects
are insufficient (Tab. 1, Ref. 30). Full Text (Free, PDF) 
www.bmj.sk
.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Free Radic Biol Med. 2009 Aug 15;47 (4):440-8. Epub 2009 May 21.
      Systemic oxidative stress in classic Rett syndrome.
      By De Felice C, Ciccoli L, Leoncini S, Signorini C, Rossi M,
Vannuccini L, Guazzi G, Latini G, Comporti M, Valacchi G, Hayek J.
      Neonatal Intensive Care Unit, University Hospital AOUS of Siena,
I-53100 Siena, Italy. - 
claudio...@hotmail.it
      Rett syndrome (RS), a progressive severe neurodevelopmental disorder
mainly caused by de novo mutations in the X-chromosomal MeCP2 gene encoding
the transcriptional regulator methyl-CpG-binding protein 2, is a leading
cause of mental retardation with autistic features in females. However, its
pathogenesis remains incompletely understood, and no effective therapy is
available to date. We hypothesized that a systemic oxidative stress may play
a key role in the pathogenesis of classic RS. Patients with classic RS
(n=59) and control subjects (n=43) were evaluated.
      Oxidative stress markers included intraerythrocyte non-protein-bound
iron (NPBI; i.e., free iron), plasma NPBI, F2-isoprostanes (F2-IsoPs, as
free, esterified, and total forms), and protein carbonyls. Lung
ventilation/perfusion (V/Q) ratio was assessed using a portable gas
analyzer, and RS clinical severity was evaluated using standard scales.
      Significantly increased intraerythrocyte NPBI (2.73-fold), plasma NPBI
(x 6.0), free F(2)-IsoP (x1.85), esterified F2-IsoP (x 1.69), total F2-IsoP
(x 1.66), and protein carbonyl (x 4.76) concentrations were evident in RS
subjects and associated with reduced (-10.53%) arterial oxygen levels
compared to controls.
      Biochemical evidence of oxidative stress was related to clinical
phenotype severity and lower peripheral and arterial oxygen levels.
Pulmonary V/Q mismatch was found in the majority of the RS population. These
data identify hypoxia-induced oxidative stress as a key factor in the
pathogenesis of classic RS and suggest new therapeutic approaches based on
oxidative stress modulation.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Altern Ther Health Med. 2009 Mar-Apr;15 (2):8; author reply 8.
      Autism: is it all in the head ?
      By Ghanizadeh A.
      Comment on: Altern Ther Health Med. 2008 Nov-Dec;14(6):12-5.
      Brain Dev. 2009 Feb 3.
      Genetic variant of glutathione peroxidase 1 in autism.
      By Ming X, Johnson WG, Stenroos ES, Mars A, Lambert GH, Buyske S.
      Department of Neurosciences and Neurology, UMDNJ-New Jersey Medical
School, 90 Bergen Street, DOC 8100, Newark, NJ 07103, USA.
      Genetic factors can contribute to autistic disorder (AD). Abnormal
genes of oxidative stress pathways and increased oxidative stress have been
reported in autism spectrum disorders. Polymorphisms of genes involved in
glutathione metabolism, e.g. GSTP1 and GSTM1 are reportedly associated with
autistic disorder. We investigated a GCG repeat polymorphism of a human
glutathione peroxidase (GPX1) polyalanine repeat (ALA5, ALA6 and ALA7) in
103 trios of AD (probands and parents) using the transmission disequilibrium
test. Significant transmission disequilibrium (p=0.044) was found in the
overall transmission of the three alleles. The ALA6 allele was under
transmitted (p=0.017).
      These results suggest that possessing this ALA6 allele may be
protective for AD. Future study of interaction of the GPX1 GCG repeat and
other gene polymorphisms such as the MnSOD ALA16 or the GPX1 Pro198Leu
polymorphism in this cohort of AD families may shed light in whether the
combination of the ALA6 allele with another polymorphism of antioxidant
allele contributes to the increased oxidative stress in autism.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Curr Neurol Neurosci Rep. 2009 Mar;9(2):129-36.
      Neurometabolic disorders and dysfunction in autism spectrum disorders.
      By Zecavati N, Spence SJ.
      Pediatrics and Developmental Neuropsychiatry Branch, National
Institute of Mental Health, 10 Center Drive, Bethesda, MD 20892, USA.
spen...@mail.nih.gov
      The cause of autism remains largely unknown because it is likely
multifactorial, arising from the interaction of biologic, genetic, and
environmental factors. The specific role of metabolic abnormalities also is
largely unknown, but current research may provide insight into the
pathophysiologic underpinnings of autism, at least in some patients. We
review a number of known neurometabolic disorders identified as having an
autistic phenotype.
      We also discuss the possible involvement of mitochondrial disorders
and dysfunction as well as a theory regarding an increased vulnerability to
oxidative stress, by which various environmental toxins produce metabolic
alterations that impair normal cellular function. Finally, we review various
strategies for metabolic work-up and treatment. Accurate diagnosis of
neurometabolic disorders and a broader understanding of underlying metabolic
disturbance even in the absence of known disease have important implications
both for individual patients and for research into the etiology of autism.
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      J Neurol Sci. 2009 May 15;280(1-2):101-8. Epub 2008 Sep 25.
      Biomarkers of environmental toxicity and susceptibility in autism.
      By Geier DA, Kern JK, Garver CR, Adams JB, Audhya T, Nataf R, Geier
MR.
      Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA.
      Comment in: J Neurol Sci. 2009 May 15;280(1-2):127-8; author reply
128-9; discussion 129-30.
      Autism spectrum disorders (ASDs) may result from a combination of
genetic/biochemical susceptibilities in the form of a reduced ability to
excrete mercury and/or increased environmental exposure at key developmental
times. Urinary porphyrins and transsulfuration metabolites in participants
diagnosed with an ASD were examined. A prospective, blinded study was
undertaken to evaluate a cohort of 28 participants with an ASD diagnosis for
Childhood Autism Rating Scale (CARS) scores, urinary porphyrins, and
transsulfuration metabolites. Testing was conducted using Vitamin
Diagnostics, Inc. (CLIA-approved) and Laboratoire Philippe Auguste
(ISO-approved).
      Participants with severe ASDs had significantly increased mercury
intoxication-associated urinary porphyrins (pentacarboxyporphyrin,
precoproporphyrin, and coproporphyrin) in comparison to participants with
mild ASDs, whereas other urinary porphyrins were similar in both groups.
Significantly decreased plasma levels of reduced glutathione (GSH),
cysteine, and sulfate were observed among study participants relative to
controls.
      In contrast, study participants had significantly increased plasma
oxidized glutathione (GSSG) relative to controls. Mercury
intoxication-associated urinary porphyrins were significantly correlated
with increasing CARS scores and GSSG levels, whereas other urinary
porphyrins did not show these relationships.
      The urinary porphyrin and CARS score correlations observed among study
participants suggest that mercury intoxication is significantly associated
with autistic symptoms. The transsulfuration abnormalities observed among
study participants indicate that mercury intoxication was associated with
increased oxidative stress and decreased detoxification capacity.
      PMID: 18817931 [PubMed - indexed for MEDLINE]
      Publication Types, MeSH Terms, Substances
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Trends Pharmacol Sci. 2008 Aug;29(8):375-82. Epub 2008 Jul 6.
      Novel therapeutic targets for autism.
      By Theoharides TC, Doyle R, Francis K, Conti P, Kalogeromitros D.
      Department of Pharmacology and Experimental Therapeutics, Tufts
University School of Medicine, Tufts Medical Center, Boston, MA 02111, USA.
theoharis....@tufts.edu
      Autism spectrum disorders (ASDs) are pervasive neurodevelopmental
disorders, diagnosed in early childhood when acquired skills are lost or the
acquisition of new skills becomes delayed. ASDs are associated with varying
degrees of dysfunctional communication and social skills, in addition to
repetitive and stereotypic behaviors. The diagnosis has increased
considerably to approximately one in 180 people, but it is not clear whether
this is because of a higher prevalence of the disorder, improved awareness
by clinicians or a combination of both. There are no defined mechanisms of
pathogenesis or curative therapy presently available. Oxidative stress,
overactivation of the hypothalamic-pituitary-adrenal axis and increased
gut-blood-brain-barrier permeability might be involved.
      The scope of this article is to integrate these findings and present
the opinion that non-allergic activation of gastrointestinal and brain mast
cells could contribute to many of the pathologic findings and provide unique
targets for ASD therapy. We make suggestions for new research directives and
possible novel therapies from readily available molecules.
      PMID: 18606459 [PubMed - indexed for MEDLINE]
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Related articles
      Publication Types, MeSH Terms, Grant Support
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      BMC Psychiatry. 2008 Apr 17;8 Suppl 1:S5.
      Fatty acids and oxidative stress in psychiatric disorders.
      By Tsaluchidu S, Cocchi M, Tonello L, Puri BK.
      Universit� di Bologna, Bologna, Italy. 
sofi...@alice.it
      BACKGROUND: The aim of this study was to determine whether there is
published evidence for increased oxidative stress in neuropsychiatric
disorders.
      METHODS: A PubMed search was carried out using the MeSH search term
'oxidative stress' in conjunction with each of the DSM-IV-TR diagnostic
categories of the American Psychiatric Association in order to identify
potential studies.
      RESULTS: There was published evidence of increased oxidative stress in
the following DSM-IV-TR diagnostic categories: mental retardation; autistic
disorder; Rett's disorder; attention-deficit hyperactivity disorder;
delirium; dementia; amnestic disorders; alcohol-related disorders;
amphetamine (or amphetamine-like)-related disorders; hallucinogen-related
disorders; nicotine-related disorders; opioid-related disorders;
schizophrenia and other psychotic disorders; mood disorders; anxiety
disorders; sexual dysfunctions; eating disorders; and sleep disorders.
      CONCLUSION: Most psychiatric disorders are associated with increased
oxidative stress. Patients suffering from that subgroup of these psychiatric
disorders in which there is increased lipid peroxidation might therefore
benefit from fatty acid supplementation (preferably with the inclusion of an
antioxidant-rich diet) while patients suffering from all these psychiatric
disorders might benefit from a change to a whole-food plant-based diet
devoid of refined carbohydrate products.
      PMID: 18433515 [PubMed - indexed for MEDLINE]
      PMCID: PMC2330073
      Related articlesFree article
      MeSH Terms, Substances
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Theor Biol Med Model. 2008 Apr 28;5:8.
      A mathematical model of glutathione metabolism.
      By Reed MC, Thomas RL, Pavisic J, James SJ, Ulrich CM, Nijhout HF.
      Department of Mathematics, Duke University, Durham, NC 27708, USA.
re...@math.duke.edu
      BACKGROUND: Glutathione (GSH) plays an important role in anti-oxidant
defense and detoxification reactions.
      It is primarily synthesized in the liver by the transsulfuration
pathway and exported to provide precursors for in situ GSH synthesis by
other tissues. Deficits in glutathione have been implicated in aging and a
host of diseases including Alzheimer's disease, Parkinson's disease,
cardiovascular disease, cancer, Down syndrome and autism.
      APPROACH: We explore the properties of glutathione metabolism in the
liver by experimenting with a mathematical model of one-carbon metabolism,
the transsulfuration pathway, and glutathione synthesis, transport, and
breakdown.
      The model is based on known properties of the enzymes and the
regulation of those enzymes by oxidative stress.
      We explore the half-life of glutathione, the regulation of glutathione
synthesis, and its sensitivity to fluctuations in amino acid input. We use
the model to simulate the metabolic profiles previously observed in Down
syndrome and autism and compare the model results to clinical data.
      CONCLUSION: We show that the glutathione pools in hepatic cells and in
the blood are quite insensitive to fluctuations in amino acid input and
offer an explanation based on model predictions. In contrast, we show that
hepatic glutathione pools are highly sensitive to the level of oxidative
stress. The model shows that overexpression of genes on chromosome 21 and an
increase in oxidative stress can explain the metabolic profile of Down
syndrome. The model also correctly simulates the metabolic profile of autism
when oxidative stress is substantially increased and the adenosine
concentration is raised. Finally, we discuss how individual variation arises
and its consequences for one-carbon and glutathione metabolism.
      PMID: 18442411 [PubMed - indexed for MEDLINE]
      PMCID: PMC2391141
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Related articlesFree article
      Publication Types, MeSH Terms, Substances, Grant Support
      >>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
      Int J Neuropsychopharmacol. 2008 Sep;11(6):851-76. Epub 2008 Jan 21.
      Oxidative stress in psychiatric disorders: evidence base and
therapeutic implications.
      By Ng F, Berk M, Dean O, Bush AI.
      Department of Clinical and Biomedical Sciences, Barwon Health,
University of Melbourne, Geelong, VIC, Australia.
feli...@barwonhealth.org.au
      Oxidative stress has been implicated in the pathogenesis of diverse
disease states, and may be a common pathogenic mechanism underlying many
major psychiatric disorders, as the brain has comparatively greater
vulnerability to oxidative damage. This review aims to examine the current
evidence for the role of oxidative stress in psychiatric disorders, and its
academic and clinical implications. A literature search was conducted using
the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Preview, and Cochrane
databases, with a time-frame extending to September 2007.
       The broadest data for oxidative stress mechanisms have been derived
from studies conducted in schizophrenia, where evidence is available from
different areas of oxidative research, including oxidative marker assays,
psychopharmacology studies, and clinical trials of antioxidants. For bipolar
disorder and depression, a solid foundation for oxidative stress hypotheses
has been provided by biochemical, genetic, pharmacological, preclinical
therapeutic studies and one clinical trial. Oxidative pathophysiology in
anxiety disorders is strongly supported by animal models, and also by human
biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine
in cocaine dependence, while early evidence is accumulating for oxidative
mechanisms in autism and attention deficit hyperactivity disorder.
      In conclusion, multi-dimensional data support the role of oxidative
stress in diverse psychiatric disorders. These data not only suggest that
oxidative mechanisms may form unifying common pathogenic pathways in
psychiatric disorders, but also introduce new targets for the development of
therapeutic interventions.
-- 
dr. G. Paolo Vanoli - Giornalista (Albo speciale) - Consulente in Scienza
della Nutrizione e Medicine Biologico Naturali - webmaster di:
www.mednat.org

dr. (diverso da dott.) G. Paolo Vanoli - Giornalista (Album Panini 
speciale) - Consulente (in pratica il nulla) in Scienza
della Nutrizione e Medicine Biologico Naturali (della serie le maiuscole 
fanno sempre effetto, anche quando si descrive il nulla) - webmaster di:
www.merdnat.org

 mezzo dei vaccini.
Cospirazione! E adesso chi mi salverï¿œ?
Ma si, SuperBicarbonato dai raggi fottonaturali!
Ivan.