|
AUTISMO
e VACCINI
la Prova
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):
montinari.m@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.
>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>
Giornalista scopre la verità sull’autismo - La
prova del
danno - 12 aprile 2010
Uno spettro sta perseguitando l'establishment
dei medici e dei giornalisti degli Stati Uniti: "Dove
sono le persone non vaccinate che soffrono di autismo
?"
Dan Olmsted
Fortunatamente vi sono alcune eccezioni
alla regola, ed una di queste ha il volto di un
giornalista serio - Dan Olmsted, che lavora come reporter
investigativo alla
United Press International (UPI), ed è autore della serie “Age
of Autism”.
Una delle cose più geniali che ha fatto è stato rispondere alla
domanda: “L’autismo si manifesta
anche fra popolazioni non vaccinate
?”
Sembra essere un compito semplice e questo avrebbe dovuto essere
oggetto di ricerca da parte del
CDC, ma non
lo hanno fatto perchè non ne avevano bisogno. Ancora una volta,
il CDC
sapeva bene che il mercurio
contenuto nei
vaccini stesse
causando un incremento nei disordini
neurocomportamentali.
Hanno deciso quindi che il loro dovere fosse quello di
insabbiare la cosa.
Ho impiegato i miei primi anni alla scuola di medicina a poche
miglia dal paese degli
Amish nel cuore della
Pennsylvania. Posso assicurarvi che gli Amish hanno le
nostre stesse sequenze genetiche, e vengono colpiti dalle
nostre stesse malattie. Non c’è ragione di credere che gli Amish
abbiano super-geni che li prevengono dal contrarre certe
malattie.
Olmsted ha analizzato la popolazione Amish
dove i genitori non hanno praticamente
mai vaccinato i propri figli nella sua serie “Age
of Autism: A glimpse of the Amish” Olmsted parla della
comunità Amish in Pennsylvania aiutato da un dottore di famiglia
di Lancaster che ha curato migliaia di pazienti Amish in oltre
un quarto di secolo. Questo dottore afferma di
non aver mai visto
un Amish affetto da autismo.
Olmsted ha anche intervistato Dick Warner, che ha un’azienda di
depurazione dell’acqua e di prodotti per la salute naturali, ed
è stato nelle famiglie Amish di tutto il paese. "Ho lavorato con
gli Amish sin dal 1980. Non ho
mai visto un bambino autistico Amish
– nemmeno uno," ha detto a Olmsted. "Lo avrei riconosciuto. Ho
ottime conoscenze in ambito medico. So come sono le persone
autistiche. Ho amici che hanno figli autistici," ha aggiunto.
Olmsted ha trovato una donna Amish a Lancaster con un figlio
autistico ma come evidenziato, il
bambino è stato adottato dalla Cina ed è stato
vaccinato. La
donna sa di altri due bambini autistici, ma ancora una volta sa
per certo che sono stati vaccinati.
Il 9 giugno del 2005, Olmsted ha parlato del tasso di autismo
nella comunità Amish presso Middlefield, Ohio, che era di 1 su
15.000, secondo il Dr. Heng Wang, il responsabile medico, alla
DDC Clinic for Special Needs Children.
"Finora," secondo Olmsted, "ci sono prove che meno di 10 Amish
abbiano l’autismo; ve ne dovrebbero essere varie centinaia se il
disordine avesse lo stesso tasso (150 a 1) del resto della
popolazione."
Il 7 dicembre 2005, in “Age of Autism” si evidenzia che migliaia
di bambini curati dalla Homefirst Health Services nella città di
Chicago abbiano almeno due cose in comune con i bambini Amish;
non erano mai stati
vaccinati e non hanno l’autismo.
Homefirst ha cinque uffici nell’area di Chicago e sei dottori in
totale. "Abbiamo avuto circa 30,000 o 35,000 bambini in cura, e
penso che non vi sia stato nemmeno un
caso di autismo fra i bambini non vaccinati," ha
detto il Dr Mayer Eisenstein, direttore medico nonché fondatore
nel 1973 della Homefirst.
Olmsted sottolinea come il tasso di autismo nelle scuole
pubbliche dell’Illinois sia di 38 su 10,000, secondo i dati
dell’Education Department. Nel trattare una popolazione di 30 /
35,000 bambini, ciò significa logicamente che Homefirst avrebbe
dovuto avere almeno 200 casi di bambini autistici ma negli anni
non se n’è visto nemmeno uno.
In un recente articolo, Olmsted fa notare come possa essere
individuato un luogo nel quale apparvero i primi casi di autismo
prima che il disordine esplodesse su scala nazionale ed afferma
che: Le periferie del Maryland sono state oggetto di ricerca
negli anni 30 e 40 esponendo le famiglie ad agenti chimici.”
Il centro di ricerca del Dipartimento dell’Agricoltura USA a
Beltsville, nella periferia del Maryland, appena fuori la
capitale della nazione, stava facendo delle sperimentazioni sui
funghi delle piante e sui modi per ucciderli usando come
fungicida l’etilmercurio - lo stesso tipo
Thimerosal utilizzato nei
vaccini.
L’etilmercurio era stato brevettato nel 1920 grazie al lavoro di
Morris S. Kharasch. Kharasch era un professore di chimica alla
University of
Maryland a College Park, vicino al centro di ricerca di
Beltsville.
Nel 1943, Leo Kanner, psichiatra infantile
alla Johns Hopkins University diagnosticò per primo l’autismo in
11 bambini nati attorno al 1930. Olmsted scoprì che
questi bambini avevano un genitore
che lavorava nelle ricerche sul mercurio o era per
qualche ragione stato esposto al etilmercurio per
trattare sementi, alberi e piante negli anni ’30.
Olmsted conclude: “Riassumendo: il primo caso di autismo sembra
propagarsi da un punto centrale ben definito – simile al big
bang. Ciò suggerisce una nuova e sconvolgente verità
sull’autismo: il nostro destino non è nei nostri geni.”
Olmsted deve essere ringraziato
per le sue ricerche ed indagini sulle cause dell’autismo. Ha
reso un enorme servizio al pianeta. Ha fatto ciò che la CDC
avrebbe dovuto fare, ma una volta ancora sappiamo che non ne
avevano bisogno dato che già conoscevano la verità.
Dalle maggiori Università o da "ciarlatani" ?
Una raccolta, eseguita da David Kirby, di studi molto recenti,
presentati dai migliori ricercatori universitari alle principali
conferenze sull'autismo o pubblicati sui più importanti e
rispettati giornali medici. Questo il commento di Kirby nel
presentarlo.
Ho messo insieme questo elenco di studi che trovo molto utile da
inviare a coloro che affermano che "non c'è evidenza". Molti
studi recenti, presentati dai migliori ricercatori delle più
importanti Università o pubblicati in giornali scientifici
ufficiali, hanno riportato le seguenti scoperte che supportano
un probabile link tra mercurio e autismo.
Alcuni di questi lavori sono stati definiti da CDC (Centro di
Controllo per le Malattie) "scienza spazzatura" condotta da
"ciarlatani":
-
Università di Washington /
National
Institutes Of Environmental Health Sciences - Pubblicato
In Environmental Health Perspective
Nei primati l'etilmercurio dei
vaccini (nella forma del
thimerosal), una volta entrato nel
cervello, si converte in
mercurio inorganico a un ritmo doppio o triplo del metilmercurio
(che si trova nei pesci) .
Il mercurio inorganico non ha un sistema naturale di trasporto
per poter uscire dal cervello, dove rimane a lungo, forse
per sempre. Uno studio precedente dello stesso gruppo di
ricercatori aveva trovato che il mercurio inorganico è la causa
di alterazioni nei tessuti cerebrali,
tra cui una grande dilatazione delle
cellule della
microglia (materia bianca), che è coerente coi ritrovamenti
di cervelli di maggiori dimensioni nei
bambini con autismo.
- Johns Hopkins
Bloomberg School Of Public Health - Published In
The Journal
Pediatrics
Il tasso di aumento dei casi di autismo
tra i bambini nati ogni anno negli Usa è rimasto relativamente
stabile fino al 1987, quando ha improvvisamente iniziato ad
aumentare,e da allora continua a
aumentare tra i bambini nati in ogni coorte
successiva. Un secondo aumento improvviso si è visto nel 1992, e
dopo pochi anni ha iniziato a livellarsi. (E' interessante
notare che tra l'87 e il '92, con l'introduzione dei nuovi
vaccini contenti
timerosal, l'esposizione totale al mercurio dalle vaccinazioni
infantili andava da 75 a 240 microgrammi). Nello stesso tempo,
l'incidenza del ritardo mentale e di altri disturbi infantili è
rimasta costante, per cui la spiegazione non può risiedere in
una "sostituzione diagnostica".
-
University
of Arkansas -
Arkansas
Children's Hospital - Published In
The Journal Biology
I bambini con autismo hanno livelli nulli o estremamente bassi
di tioli-sostanze biochimiche sulfur based--(un sinonimo di
tioli è mercaptani, o letteralmente "catturatori di
mercurio").Si pensa che la ragione sia genetica. Senza queste
sostanze ( i tioli), come ad es la proteina
glutatione, questi
bambini con variante genetica soffrono di
stress ossidativo,
e mostrano una ridotta capacità di eliminare i metalli pesanti
come il mercurio. Gli interventi biomedici con una varietà di
sostanze naturali hanno mostrato di poter riuscire ad aumentare
i livelli di tioli in questi bambini fino a livelli normali.
-
Columbia
University - Published in
Molecular Psychology
Topi con una predisposizione genetica all' autoimmunità hanno
mostrato reazioni orribili ai vaccini con timerosal, comparati
ai topi senza l'autoimmunità. I topi sensibili hanno mostrato
comportamenti ripetitivi e autolesionistici, tra i quali
grooming se stessi o i propri compagni incessantemente, a volte
fino alla morte. Avevano anche un aumento di volume cerebrale .
-
Northeastern University - Published in
Molecular Psychiatry
Il timerosal, quando esposto a cellule con certe mutazioni
genetiche, può interferire con critici processi metabolici, tra
i quali la metilazione. La metilazione è cruciale per una esatta
espressione dei geni e per la crescita del DNA e dell'RNA, e per
lo sviluppo dei neurotrasmettitori e degli acidi grassi
essenziali--inclusa la mielina--che proteggono i nervi e il
cervello. La metilazione è necessaria anche per lo sviluppo dei
tioli come il glutathione, e per altre funzioni di
detossificazione.
-
University
of Texas - Published in
The Journal Health And Place
Il mercurio rilasciato primariamente dalle centrali a carbone
può contribuire all'aumento dei casi di autismo. Lo studio ha
trovato che l'aumento dell'autismo nel Texas è andato di pari
passo con l'aumento delle emissioni di mercurio. Per ogni 1000
pound di mercurio rilasciato c'è stato un aumento del 61% di
percentuale di casi di autismo. Un autore dello studio ha detto
che si mostra una importante connessione tra l'esposizione
ambientale al mercurio e lo sviluppo dell'autismo.
La
prova del danno (Evidence of harm)
La prova evidente del grave danno, provocato dai vaccini, alla
salute dei bambini
Fonte: macrolibrarsi.it
Negli anni ’90 i casi di autismo registrati tra i bambini
americani hanno avuto un'impennata, passando da 1 ogni 10.000
nel 1987 alla scioccante incidenza, oggi, di 1 ogni 100. Questo
trend coincide con l'introduzione nel programma vaccinale
nazionale di numerosi nuovi
vaccini,
somministrati contemporaneamente e quasi subito dopo la nascita
o nei primi mesi di vita. In molte di queste dosi è presente un
eccipiente poco conosciuto chiamato thimerosal, che contiene una
certa quantità di mercurio e
di alluminio.
La Prova del danno studia e approfondisce questa preoccupante
situazione, che ha indotto molti genitori, medici, pubblici
ufficiali ed educatori a parlare di una vera e propria epidemia‚
e dei bambini che ne sono colpiti.
Seguendo le vicende di diverse famiglie, David Kirby racconta la
loro battaglia per capire come e perché i loro figli, nati sani,
sono scivolati nel silenzio e si sono perduti in disturbi di
comportamento che spesso provocano anche patologie fisiche.
Allarmate dalla quantità di mercurio presente nei vaccini,
queste famiglie hanno cercato risposte, senza trovarle, dai loro
medici, dalla scienza, dalle case farmaceutiche, rivolgendosi
infine ai Centri per il Controllo delle Malattie e la
Prevenzione (CDC)
e alla Food and Drug Administration (FDA).
Scavando in profondità, hanno trovato anche importanti alleati
all'interno del Congresso e in quel piccolo gruppo di medici e
ricercatori che crede che l'aumento dell'autismo e di altre
patologie sia correlato ai livelli tossici di mercurio che si
sono accumulati nell'organismo di alcuni bambini. A chi si
rivolge ? A tutti i genitori che vogliono essere consapevoli e
informati sui numerosi vaccini che spesso si considera normale
prassi inoculare nei bambini. A tutti quelli che desiderano
scegliere con coscienza e proteggere al meglio la salute dei
propri bambini.
Chi l'ha scritto, David Kirby, è stato
collaboratore del
New York
Times per otto anni, occupandosi, tra le altre cose, di
scienza e salute. Vive a Brooklin, New York.
Cosa ha di particolare "La prova del danno" pone interrogativi
importanti, rivela ostacoli e difficoltà impensabili che persone
disperate si sono trovate ad affrontare; persone che hanno
scelto di opporsi all'intreccio di potere tra governo federale,
enti sanitari e giganti farmaceutici.
Dagli incontri segreti tra
FDA, CDC e
ditte farmaceutiche alla misteriosa clausola
inserita nel 2002 nel testo della legge sulla sicurezza interna,
che vieta cause giudiziarie sulla questione del thimerosal, fino
alle audizioni pubbliche davanti al Congresso, questo libro
mostra un establishment medico deciso a negare la “prova del
danno” che potrebbe confermare il legame tra l'autismo e il
thimerosal nei vaccini.
Fonte: scienzamarcia.blogspot.com
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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. rdufault@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..
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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.
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J Cell Mol Med. 2009
Sep 14
Chemical and molecular mechanisms of antioxidants: Experimental
approaches and model systems.
By
Lü 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]
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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.theoharides@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.
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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.Mazur-Kolecka@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.kudlackova@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. -
claudiodefelix@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. spences2@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.theoharides@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.
Università di Bologna, Bologna, Italy. sofia.tsl@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.
reed@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
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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. felicitn@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.
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