Re: New study shows mechanism- even very low level of Mercury causes brain inflammation, autism

[Guest guest]

The file name for the study was too long, and it did not get saved. I'm

uploading it into the Files section now. (below is an excerpt)

the study is March 2010, brand new

liora

>

> brand new study in the Journal of Neuroinflammation. Please share widely.

>

> <http://www.jneuroinflammation.com/>

> <http://www.ncbi.nlm.nih.gov/pubmed/20222982>

>

>

> Mercury induces inflammatory mediator release from

> human mast cell " We, therefore, investigated whether HgCl2 could stimulate

human mast cells, an action that could

> be enhanced in subjects who already have an atopic background. "

>

> ... " We then investigated whether HgCl2 could stimulate release of

proinflammatory mediators from

> mast cells. "

>

> Discussion

> This is the first report to our knowledge showing that inorganic mercury in

concentrations as low

> as 0.1 μM can induce VEGF and IL-6 release from human cultured mast cells. We

also report

> for the first time that mercury has a significant synergistic effect with SP

(0.1 μM) on VEGF

> release; this amount of VEGF release is higher than what has previously been

reported for

> hCBMCs [19]. One paper has reported that HgCl2 can induce release of histamine

from primary

> lung and human leukemic mast cells (HMC-1 cells), but only at toxic levels of

0.33 mM [20].

> Here we show that HgCl2 induces β-hexosaminidase release, but only at a

concentration of 10

> μM. Mercury (10 μM) has previously been shown to induce release of

β-hexosaminidase, IL-4

> and TNF-α from a murine mast cell line and from mouse bone marrow-derived

cultured mast

> cells; the secretion of cytokines mediated by HgCl2 is additive to that which

follows

> FcepsilonRI-induced mast cell activation [11]. In contrast, HgCl2 does not

have an effect on its

> own on release of histamine and IL-4 from human basophil, but only enhances

allergic release at

> concentrations of 1 and 10 μM [12]. This is also true for IL-4 release from

rat mast cells [21].

> Clinical symptoms of mercury poisoning may be expected at blood levels of 1

μM [12].

> However, brain mast cells may react to lower mercury concentrations,

especially in vulnerable

> patient subpopulations.

>

> Mast cells, by virtue of their location in the skin, respiratory tract, and

gastrointestinal system are

> potential targets for environmental agents with immunotoxic effects [22]. Mast

cells are critical

> not only for allergic reactions, but also important in both innate and

acquired immunity [23], as

> well as in inflammation [24]. In view of the fact that a subgroup of ASD

patients have allergy

> symptoms that do not appear to be triggered by IgE, it is noteworthy that mast

cells can be

> stimulated by non-allergic triggers originating in the gut or the brain [24],

especially

> neuropeptides such as SP [25] and neurotensin (NT) [26]. Once activated, mast

cells secrete

> numerous vasoactive, neurosensitizing and proinflammatory molecules that are

relevant to ASD;

> these include histamine, proteases, VEGF, prostaglandin D2, as well as

cytokines such as IL-6

> [24]. In particular, mast cells can secrete VEGF [27, 28], an isoform of which

is vasodilatory

> [29] and is over expressed in delayed hypersensitivity reactions [30]. In

fact, mast cells can

> release VEGF [31], IL-6 [32] and other mediators “selectively†without

degranulation [33].

> Such mediators could disrupt the gut-blood and blood-brain barriers (BBB)

permitting brain

> inflammation [34]. It is important to note that mercury can cross the BBB

through a transport

> mechanism that can lead to significant brain concentrations, and that can

persist for prolonged

> periods of time [2, 35]. Activated brain mast cells can disrupt the BBB [36,

37] and further

> increase brain mercury levels.

>

> The mechanisms of heavy metal neurotoxicity are not fully understood. Mercury

increases

> cytosolic calcium levels in PC12 cells [38], and thimerosal does so in thymus

lymphocytes [39].

> Mercury may also increase cellular oxidative stress since neurons are highly

susceptible to

> reactive oxygen species (ROS) and neuronal mitochondria are especially

vulnerable to oxidative

> damage [40]. In fact, the primary dietary source of neurotoxic mercury

compounds is via the

> ingestion of methylmercury from fish, which has been previously linked to

neurological damage

> [41].

>

> Mercury’s activation of mast cell inflammatory mediator release may enhance

allergic reactions

> in atopic individuals and exacerbate IgE-dependent diseases [12]. Allergic

symptomatology is

> often present in ASD patients [34], and a survey of children with ASD in Italy

reported that the

> strongest association was with a history of allergies [42]. Moreover, a recent

study reported

> increased atopic diseases, as well as elevated serum IgE and eosinophils in

Asperger patients

> [43]. In a National Survey of Children’s Health, parents of autistic

children reported symptoms

> of allergies more often than other children, with food allergies showing the

greatest difference

> [44]. A case series study also reported higher rate of food allergies in ASD

children [45]. In one

> study, 30% of autistic children (n=30) had a history of atopy as compared to

2.5% of agematched

> “neurologic controls†(n=30), but there was no difference in serum IgE or

in skin prick

> tests to 12 common antigens [46], implicating triggers other than IgE. In

another study, ASD

> patients did not have increased incidence of allergic asthma or allergic

dermatitis [42], but this

> study included only ASD patients that were positive to RAST/skin testing.

Finally, a preliminary

> report indicated that the prevalence of ASD may be 10-fold higher [47] than

the general

> population (1/100 children) in mastocytosis patients [48], characterized by

increased number of

> hyperactive mast cells in many tissues, with symptoms that include allergies,

food intolerances

> and “brain fog†[49, 50].

>

> Some epidemiological studies have failed to find a significant relationship

between mercury

> exposure from vaccines and autism [3-7]. Nevertheless, 87% of children

included in the US

> Vaccine Adverse Event Reporting System (VAERS) have ASD [8]. Moreover, a paper

based on

> computerized medical records in the Vaccine Safety Datalink concluded there

was “significantly

> increased rate ratios for ASD with mercury exposure from Thimerosal-containing

vaccines†[9].

> Also, there are a series of epidemiological studies conducted in the USA that

have found

> significant associations between environmental sources of mercury exposure and

ASDs [51]. In

> addition, patients with severe ASD have evidence of significantly increased

urinary porphyrins

> consistent with mercury intoxication [52-55]. Mercury toxicity may also affect

critical

> methylation pathways in vulnerable cells [56].

>

> ASD are a group of pervasive developmental disorders that include autistic

disorder, Asperger’s

> disorder, and atypical autism - also known as pervasive developmental

disorder-not otherwise

> specified (PDD-NOS). These are neurodevelopmental disorders diagnosed in early

childhood

> [57]. They are characterized by various degrees of dysfunctional communication

and social

> skills, repetitive and stereotypic behaviors, as well as attention, cognitive,

learning and sensory

> defects [57, 58]. ASD cases have increased more than 10-fold during the last

decade to a

> prevalence of 1/100 children [44, 57, 59]. However, there is no known distinct

pathogenesis,

> there are no biomarkers, and there is no effective treatment [60].

>

> ASD may result from a combination of genetic/biochemical susceptibility and

epigenetic

> exposure to environmental factors, including reduced ability to excrete

mercury and/or exposure

> to mercury at critical developmental periods [2, 56]. A number of papers have

suggested that

> ASD may be associated with immune dysfunction [61], while a recent review made

the case that

> ASD may be a neuroimmune disorder involving mast cell activation [34].

>

>

> Conclusions

> The results of the present study support the biological plausibility of how

mercury could

> contribute to ASD pathogenesis by inducing VEGF and IL-6 release from mast

cells, and as a

> result disrupt the BBB and thus permit brain inflammation. Further studies

should investigate the

> effect of mercury and thimerosal alone or together with allergic and

non-immune triggers.

>

>

>

>

> Study Attached. 

>

>

> blessings,

> Liora Pearlman , ModeratorMom

> " Once our eyes are opened, we can't pretend we don't know what to do.

  G-d, who weighs our hearts and keeps our souls, knows that we know and

holds us responsible to act. "  Proverbs (Mishlei) 24:12 

> " Leave your drugs in the chemist's pot if you can heal the patient with food "

> HIPPOCRATES The Father of Medicine

>

>

>

>

>

>

>