What Herd Immunity Really Means

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I woke up one morning to a news piece on the measles outbreak at a Texas church whose preacher had the audacity to question vaccines.  Apparently there is a huge out break of this devastating disease which is making so many people sick.  Even a 4 month old baby got the disease!!!  Now the church has retracted its view and it is holding vaccine clinics in the church to urge members to get vaccinated.  Good for them. Right?

 

So now we must get ready for the great herd immunity debate to take place.  My facebook news feed is being inundated with accusations that the unvaxed children are putting the rest of the population at risk.  Normally, I can take these things in stride, as this is a debate of opinion and everyone is entitled to their own opinion.  That is part of what it means to have freedom of speech in this country.  Today, however, I do not feel so light-hearted and easy to accept the opinions of others.  Why you might ask?

 

Because I can see the storm churning in the distance.  I see the politics at play here.  This isn’t about opinion anymore.  This is about basic human rights.  Measles is being likened to small pox as if my unvaxed child is going to cause the downfall of the world.  This make me and him a menace to society.  It seems people listen to these news shows and they swallow all the emotional brainwashing hook line and sinker.  Reasonable people in most spheres of their lives are being convinced with the rhetoric of corporate greed.

 

I want to give fair warning here, because I am not sure I will be able to control myself if one of these people tried to speak to me in person about the importance of herd immunity.  In my current state I think I might just slap the first person who makes it their duty to educate me.  My child was mercury poisoned.  My child, in fact my entire family, has worked tirelessly to bring my child back from the cocoon created bt his inability to clear heavy metals and other toxins from his system.  Injecting toxins into my child means we will have to begin this process all over again and the past 6 years of hard work will be gone.  With an assault of this type on his system he may very well not ever recover.  Never be able to get a job, to have a family, to stand on his own two feet, or to take care of himself after I die.  Vaccinating my child is the same as murdering his future.  And I will let you in on a little secret:

 

To me, your child is not worth more than mine.  I refuse to willingly sacrifice my child so that your child doesn’t have to spend a couple weeks in discomfort.

 

Lets look at the numbers:

 

Number of deaths from measles prior to the vaccine: Out of the 3-4 million people per year who got measles only about 450 people died (all people, not just children).

 

Number of deaths from proper use of Rx medications:  100,000 people die each year from properly prescribed medications.

 

Number os deaths from car accidents: about 35,000 people die each year in car accidents

 

Number of children who will be diagnosed with autism this year:  With current rate of Autism in this country, approximately 45,000 children born EVERY YEAR will be diagnosed with Autism.  Approximately 662,500 children will be diagnosed with a learning delay EVERY YEAR.  These numbers do not take into account the rise in the rates of Autism each year, so these numbers are actually conservative.

 

Society has a lot of serious issue to worry about, but measles is not one if them.

 

I say true herd immunity is only gained by allowing our children to get childhood illnesses:

 

http://www.thehealthyhomeeconomist.com/the-herd-immunity-myth-and-how-it-pits-parent-against-parent/

 

http://www.vaccinationcouncil.org/2012/02/18/the-deadly-impossibility-of-herd-immunity-through-vaccination-by-dr-russell-blaylock/

 

So you still expect t me to vaccinate my child to save yours?  I say the vaccine doesn’t protect any child from the measles.

 

http://gaia-health.com/gaia-blog/2012-04-07/measles-outbreaks-centered-in-the-vaccinated-studies-show-vaccine-is-ineffective/

 

I say that if you vaccinate your child, you are putting the rest of society at risk for much worse diseases, and you are causing a strain on the economy because of the increased medical care your unhealthy child will require.

 

http://www.vaccinationcouncil.org/2013/01/18/the-ineffectiveness-of-measles-vaccines-and-other-unintended-consequences-by-dr-viera-scheibner-phd/

 

http://www.vaccinationcouncil.org/2013/01/29/measles-vaccines-part-ii-benefits-of-contracting-measles-by-dr-viera-scheibner-phd/

 

I am sure many people will be offended by my stance on the vaccine issue, and by the fact that I have the audacity to blame the parents of vaccinated children for destroying herd immunity, causing the spread of disease, and harming the US economy.

 

WELCOME TO THE CLUB!

 

Daily Kos: The Story of Julian (goodbye to autism)

The Story of Julian (goodbye to autism)

bylanellici

First, the Before picture

Here is my son Julian, at four years old: he couldn’t play with toys; he scowled most of the time; he had explosive, violent rages; had little or no recognition of danger; panicked easily; aggressive; little to no tolerance for changes of any sort; intolerant of light, loud noises, anyone touching him; constantly sick with asthma, ear infections, virus after virus after virus.

Julian would compulsively rub his head all over me and want to put his hands and head under my shirt. He made strange noises a lot of the time, something like the sound dolphins make. His outbursts of rage seemed most of the time to come out of nowhere.

How I found the way out, after the fold. It gets worse before it gets better.

He never played with his little sister, but rather could not tolerate her presence at all, and we couldn’t leave the two of them alone because Julian could unpredictably become aggressive. He never expressed empathy for people or animals. He was not developing any capacity to play by himself. At times he seemed not to be able to think clearly, although he was very intelligent. No pretend play whatsoever. At school he was self-contained; he didn’t explode, but made no friends and did not become actively involved in what was happening. He watched. He never waved hello — he didn’t seem to understand the point of greetings at all.

Our home life was, as you might guess, a disaster. My husband and I were deeply stressed out and my little daughter was routinely very frightened. We pretty much stayed home all the time because crowds made Julian so upset, but home was no place of calm no matter how much we worked at making it that way. On his third birthday I invited three kids and their moms over, people he had spent a lot of time with, and his reaction, when the first child arrived with a smile and a present, was to scream, “I HATE OTHER PEOPLE!” and run upstairs to his room and refuse to come back.

It’s also true that Julian could be extremely interesting to talk to. He invented his own terminologies, he asked questions such as “Who invented language?” while fighting the carseat buckle, he could draw pictures from perspectives that were absolutely his own, unique and strange and lovely.

At that point I was a nearly total believer in mainstream medicine. He got every vaccination on time, he went to every well-visit, I gave him fluoride drops because the pediatrician told me to, round after round of antibiotics because the pediatrician told me to. I followed directions. But I had a child who was a wreck, and sick nearly all the time. When I suggested that something might be wrong, she reassured me that he was fine (a story many many parents of autistic kids can tell). Julian was my first child, my mother died before he was one, my other relatives thought he behaved badly because I was a crummy parent — so I relied on the pediatrician’s observations.

But then Julian fell off a cliff. He spiraled into a meltdown that wouldn’t quit. Hours and hours of crying every day, violent, vicious hissing talk about how he wanted to chop me up into little pieces and put me in the trashcan, how he wanted to kill people, how he wanted to die. He was FOUR……..

via Daily Kos: The Story of Julian (goodbye to autism).

9 Questions That Stump Every Pro-Vaccine Advocate and Their Claims

Prescription placebos used in research and pra...

Prescription placebos used in research and practice (Photo credit: Wikipedia)

9 Questions That Stump Every

Pro-Vaccine Advocate and Their Claims

Lire en Français

Since the flu pandemic was declared, there have been several so-called “vaccine experts” coming out of the wood work attempting to justify the effectiveness of vaccines. All of them parrot the same ridiculous historical and pseudoscientific perspectives of vaccinations which are easily squelched with the following 9 questions.

Claim: The study of vaccines, their historical record of achievements, effectiveness, safety and mechanism in humans are well understood and proven in scientific and medical circles.

Fact: The claim is completely false.

1. What to ask: Could you please provide one double-blind, placebo-controlled study that can prove the safety and effectiveness of vaccines?

2. What to ask: Could you please provide scientific evidence on ANY study which can confirm the long-term safety and effectiveness of vaccines?

3. What to ask: Could you please provide scientific evidence which can prove that disease reduction in any part of the world, at any point in history was attributable to inoculation of populations?

4. What to ask: Could you please explain how the safety and mechanism of vaccines in the human body are scientifically proven if their pharmacokinetics (the study of bodily absorption, distribution, metabolism and excretion of ingredients) are never examined

or analyzed in any vaccine study?

Read more…..

via 9 Questions That Stump Every Pro-Vaccine Advocate and Their Claims.

Autism Study Reveals No Genetic Associations

Autism spectrum disorders (ASD) include everything from the relatively mild Asperger syndrome (characterized by more mild social and language impairments) to full-fledged autism (characterized by severe social and communicative handicaps, limited interests, and repetitive behaviors).  ASD is relatively common, and in the United States it is estimated that one out of every 54 boys is affected (the frequency in girls is considerably lower, averaging one affected girl out of every 252). Although genetics certainly plays a role in these conditions, exactly how is not fully understood, and this newest study, led by Richard Anney (Trinity College of Dublin) and Bernie Devlin (University of Pittsburgh School of Medicine), is the next a long line of scientific inquiries to this point.

Their study, known as the Autism Genome Project (AGP), was conducted in two stages. The first stage of consisted of a genome-wide association study using genetic data from 1400 families affected by autism; the second stage checked the associations discovered in the first stage using the genetic data from an additional 1301 ASD-affected families and included another new genome-wide association study which combined the study subjects from both stages.

When all the analyses were said and done, no SNPs (common genetic variations) were significantly associated with ASD. Furthermore, when some of the SNPs that had been identified in the first study as possibly associated with ASD were tested in the second-stage families, the associations failed to hold up.  This lack of common SNPs associated with ASD is both disappointing and enlightening.

Knowledge of what is not true, paradoxically, is knowledge of what is true.  For instance, if I tell you that my pet Tyger is not a dog, you are one step closer to knowing Tyger’s a cat.  Most of science progresses through “not trues” — the failed hypotheses that bring us closer to real understanding. A perfect example of this mode of scientific progress is this recent genetic study.  Their lack of findings was quite a finding.

The fact that no SNPs were associated with ASD in such a large study suggests that the effect of any one common SNP is quite small. Even when all the SNPs were used together to predict whether a study subject would have ASD, the model explained less than 1% of differences in risk for the condition.

The fact that these common SNPs have little power to predict ASD does not mean that genetics is unimportant.  Twin studies suggest that ASD is at least moderately heritable, suggesting that genetics does play a role.  This current study’s lack of findings supports the idea that common genetic variations may play a smaller role than rare mutations or copy number variation (the number of copies of a given gene) in ASD risk. Thus, the lack of ASD associations today has, hopefully, brought us closer to tomorrow’s discoveries.

via No Genetic Associations Found in Autism GWAS | The Spittoon.

Avoiding Autism: What to do when you’re pregnant.

We need to know how to help our autistic children.  Just as important is to avoid it in the first place.  Our future depends on our children and we cannot survive if we continue to allow our children to be so severely affected.

How can we avoid something if we don’t know what is causing it?  We ask the question, “What causes autism?”

It’s a loaded topic.  Filled with politics on all sides.

I hear the debate.  Over diagnosis, vaccines, environment, viruses, Lyme, strep, antibiotics, heavy metals or of course my favorite, evolution.  The theories are never-ending.

The more potential for profit, the more skewed the results of the research.

Our children are being lost in the debate.  The longer this discussion lasts, the more time we take to debate the issue, the more children fade.  Time is of the essence here and we as parents are the first defense our children have against this debilitating event.

We alone are the only wall to shield the next generation from imminent disaster.  We are alone to sort out the best thing to do. We are confused.  Frankly, nobody knows what causes autism.

The players?

  • Genetics: meaning there isn’t much we can do about it right?  Our kids are just born this way, or is something affecting the genes?  If so what?
  • Over diagnosis:  You won’t see many parents of autistic children accepting this one.  Politics might sell it to people who do not know Autism, but the rest of us aren’t buying what they are selling.
  • Vaccines:  Probably a contributor, but if it alone were the cause then we would not have unvaccinated Autistic biomed responders ( like my son).
  • Environment:  while our environment is terribly toxic there are certainly times in our history when the environment was easily as toxic (especially around the middle of the industrial age).

There are more, but I will skip to the point since I am not likely to name them all anyway.  I see desperate parents regularly asking how to avoid autism?

My Opinion:

Autism is iatrogenic.  Meaning: caused by doctors.  Not as individuals necessarily, but certainly as part of the larger system.  I am sure people are tired of hearing rantings over big pharma or discussions on the latest trend of diagnosing people with their symptoms (like my cousin, who took her dd to the doctor after she fainted for no clear reason, only to leave the office with a diagnosis of syncope…?).   I could likely write 20 blog entries complaining about our medical system, lol, but you all know me.  I am too much of a fixer to waste that much time on complaining (I reserve most of my ranting for my lovely family).

So what is the solution?

If your pregnant or thinking of getting pregnant I have a few tips I would recommend.

  1. Do not mess with detoxification unless you have about 18 months afterward.
  2. Get back to basics.  Eat good food not pesticide laden, GMO pseudofood.  Real food the way our grandmothers and our great-grandmothers used to cook.  Boil thee bones to make thy soup and other such nutrient dense real food techniques. Avoid artificial ick and additives, MSG, fake sugars, trans fats and hydrogenated oils, high fructose corn syrup, etc…
  3. Take a decent multi-vitamin to make up for what is lacking in our food.
  4. Fish oil is a must when pregnant: High quality fish oil higher in DHA than EPA (1500 mg DHA / 750 mg EPA is good)
  5. Control the toxic load as much as possible.  Don’t choose now to remodel your house.  Don’t use CFLs.  Stay clear of chlorine bleach, and other chemicals, fluoride, fabric softeners, aluminum and non stick cookware, etc…
  6. Above all stay away from Doctors unless it is absolutely necessary.  DO NOT Vaccinate!  DO NOT take Rx Meds!

Doctors treat disease they do not bestow health.  Do not use medication that is my motto. Doctors can run tests, check your health, and clue you in to a possible disease process. They are however, most beneficial when you are well-informed and do your homework.  and if you find a doctor who is annoyed by your desire to be part of the process, RUN!!!

We use vitamins and herbs at the first sign of illness and we seldom need to go to the doc.  I think the old adage, “An apple a day to keep the doctor away,” was right in one regard.

Keeping the doctor away is of utmost benefit to your health!

Looking for Autism: the saga continues

We are back in school this year as a first grader and I gave the teacher a couple of weeks to settle in before I went in to chat with her.  Since we aren’t homeschooling any more I really need this feedback from someone who deals with him all day long.  Not to mention she sees him with all his other peers where I would expect his deficits to stand out more.

So I asked her how she felt he was doing?  She just looked at me with a puzzled expression and said he is doing great.

ME:  “Ok, so what I mean is on a scale of 1-10 how do you think he is doing socially?”

TEACHER: “He is doing very well he plays with the other kids and enjoys recess and when he chooses to so an activity on his own like read a book he is fine if another student joins him and he returns to the group just like any other student would.”

(Obviously she is not understanding I want to know about his deficits, so I try again)

ME:  “That is great.  But if you had to assign a number to the kids.  and 1 is say this child doesn’t belong in a regular classroom and 10 is perfectly neuro-typical indistinguishable from his peers., and fits in the class exactly as he should  Where would my son fit?”

TEACHER:  “Well, I would say he is maybe a little more mature than the other children in the classroom.  We will know more after they finish the testing on Tuesday, but they might talk to about the possibility of moving him up a grade.”

(Now I am the one with the puzzled look on my face)

ME:  “Well, we did hold him back a year to give him the best chance at catching up socially.”

(but I am thick headed and I came here for a deficit darn it and I am determined to get one)

ME AGAIN:  “I know my son has a little bit of an odd word choice and some precocious language.  I am not really looking for something I need to change, but just something to watch to see how he is progressing.  Can you come up with any kind of behavior or thing that he does that kind of makes him stand out from the other kids a bit.  Something that perhaps could be watched and measured for progress?”

TEACHER:  “Well, I don’t know, I wouldn’t exactly call it a deficit.  In fact it is endearing, but when he gets very happy and excited he kind of jumps up in his chair and squeals with joy.  It is just a moment and it makes the rest of the class happy and laugh and it is contagious.  I really wouldn’t want to see it go away, but is that what you are looking for?”

We finished our conversation with some small talk and she said she would watch him a little closer and if she happened to notice anything she’d make a note of it for me.  I thanked her and assured her that she needn’t go out of her way, but I would be very appreciative of any feedback she had good or bad.

So the question remains.  Where oh where did this elusive Autism gene go?  I mean my son didn’t regress he was born Autistic.  For all intents and purposes he still should be.  Could he really have been cured of Autism.  I mean sure, we have always hoped.  We did biomed and chelated (still chelate) in the hopes that it would get rid of the Autism.  But did I ever really believe it?

No, I am still waiting for it to leap out and bite us in the butt.

I think I have a tiny glimpse into the world of PTSD.  I am still holding my breath and I am still watching and analyzing, and picking up on every possible deficit.  I do this silently to myself (I would not do it in front of my child) because I can’t really imagine that we may see a day without supplements and weekly rounds.

I been eating, drinking, sleeping , and dreaming Autism for so many years.  It is hard to imagine a life without it.  and I have been secretly afraid to actually think it would ever really be gone.

Maybe I can actually let myself hope?

 

The Science on Autism, Mitochondria, and Mercury

699 - Puzzle-Pastel - Pattern

 (Photo credit: Patrick Hoesly)

From  Safe Minds (http://www.safeminds.org/research/science-autism-mitochondria-mercury.html)

The U.S government has conceded a case in the Vaccine Injury Court. The case is a child diagnosed with autism who has a mitochondrial disorder. The child’s vaccinations triggered an adverse effect that led to her autism. David Kirby, author of Evidence of harm, has written an extensive article on the Huffington Post about the case and its implications.

Kirby mentions that mercury, including thimerosal, can trigger mitochondrial dysfunction. Mercury can also lead to oxidative stress (OS) and calcium (Ca2+) dysregulation, both of which are key features of mitochondrial dysfunction. Several studies have linked increased OS, Ca2+ imbalance, and mitochondrial dysfunction to autism.

Also, read David Kirby’s interview with Imus on WABC Radio.

To help readers understand the science relevant to this court case, SafeMinds has posted an assortment of research articles (in full or the abstracts) that pertain to mitochondria function, related physiology (that is, calcium homeostasis and oxidative stress), mercury (including thimerosal) and autism.

Dr. Jon Poling to Dr. Steven Novella on Age of Autism

By Dr. Jon Poling, father of Hannah Poling.

OPEN LETTER TO DR. STEVEN NOVELLA IN RESPONSE TO
“Has the Government Conceded Vaccines Cause Autism?”

Dr. Novella,
Thank you for generating interesting discussion regarding my little girl, Hannah Poling.  I would like to give you additional information in order to generate further productive discussions on this matter amongst the neurology community.  This information should assist you, Dr. DiMauro, and Dr. Trevethan, who have also commented publicly, to formulate better theories as to the significance of Hannah’s mitochondrial dysfunction in relation to her autism.
1. Mito Dysfunction or Mito Disease?  Chicken or Egg?

READ THE ENTIRE LETTER

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Uncoupling of ATP-Mediated Calcium Signaling and Dysregulated Interleukin-6 Secretion in Dendritic Cells by Nanomolar Thimerosal
Samuel R. Goth,1,2 Ruth A. Chu,2 Jeffrey P. Gregg,1,3,4 Gennady Cherednichenko,2 and Isaac N. Pessah1,2,4

1National Institute of Environmental Health Sciences Center for Children’s Environmental Health, 2Department of Veterinary Molecular Biosciences, and 3Department of Medical Pathology, University of California-Davis, Davis, California, USA; 4MIND (Medical Investigation of Neurodevelopmental Disorders) Institute, University of California-Davis, Sacramento, California, USA

Abstract
Dendritic cells (DCs) , a rare cell type widely distributed in the soma, are potent antigen-presenting cells that initiate primary immune responses. DCs rely on intracellular redox state and calcium (Ca2+) signals for proper development and function, but the relationship between these two signaling systems is unclear. Thimerosal (THI) is a mercurial used to preserve vaccines and consumer products, and is used experimentally to induce Ca2+ release from microsomal stores. We tested adenosine triphosphate (ATP) -mediated Ca2+ responses of DCs transiently exposed to nanomolar THI. Transcriptional and immunocytochemical analyses show that murine myeloid immature DCs (IDCs) and mature DCs (MDCs) express inositol 1,4,5-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) Ca2+ channels, known targets of THI. IDCs express the RyR1 isoform in a punctate distribution that is densest near plasma membranes and within dendritic processes, whereas IP3Rs are more generally distributed. RyR1 positively and negatively regulates purinergic signaling because ryanodine (Ry) blockade a) recruited 80% more ATP responders, b) shortened ATP-mediated Ca2+ transients > 2-fold, and c) produced a delayed and persistent rise (≥ 2-fold) in baseline Ca2+. THI (100 nM, 5 min) recruited more ATP responders, shortened the ATP-mediated Ca2+ transient (≥ 1.4-fold) , and produced a delayed rise (≥ 3-fold) in the Ca2+ baseline, mimicking Ry. THI and Ry, in combination, produced additive effects leading to uncoupling of IP3R and RyR1 signals. THI altered ATP-mediated interleukin-6 secretion, initially enhancing the rate of cytokine secretion but suppressing cytokine secretion overall in DCs.DCs are exquisitely sensitive to THI, with one mechanism involving the uncoupling of positive and negative regulation of Ca2+ signals contributed by RyR1. Key words: calcium, calcium channel, dendritic cell, ethyl mercury, immunotoxicity, interleukin-6, organic mercury, redox, thimerosal. Environ Health Perspect 114:1083-1091 (2006) . doi:10.1289/ehp.8881 available via http://dx.doi.org/ [Online 21 March 2006]

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Pharmacol Res. 2005 Oct;52(4):328-33.
Thimerosal-induced cytosolic Ca2+ elevation and subsequent cell death in human osteosarcoma cells.
Chang HTLiu CSChou CTHsieh CHChang CHChen WCLiu SIHsu SSChen JS, Jiann BPJan CR.
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan.

The effect of the oxidizing agent thimerosal on cytosolic free Ca(2+) concentration ([Ca(2+)]i) and proliferation has not been explored in human osteoblast-like cells. This study examined whether thimerosal alters Ca(2+) levels and causes cell death in MG63 human osteosarcoma cells. [Ca(2+)]i and cell death were measured using the fluorescent dyes fura-2 and WST-1, respectively. Thimerosal at concentrations above 5 microM increased [Ca(2+)]i in a concentration-dependent manner. The Ca(2+) signal was reduced by 80% by removing extracellular Ca(2+). The thimerosal-induced Ca(2+) influx was sensitive to blockade of La(3+), and dithiothreitol (50 microM) but was insensitive to nickel and several L-type Ca(2+) channel blockers. After pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor), thimerosal failed to induce [Ca(2+)]i rises. Inhibition of phospholipase C with 2 microM U73122 did not change thimerosal-induced [Ca(2+)]i rises. At concentrations of 5, 10 and 20 microM thimerosal killed 33, 55 and 100% cells, respectively. The cytotoxic effect of 5 microM thimerosal was reversed by 54% by prechelating cytosolic Ca(2+) with BAPTA. Collectively, in MG63 cells, thimerosal induced a [Ca(2+)]i rise by causing Ca(2+) release from endoplasmic reticulum stores and Ca(2+) influx from extracellular space. Furthermore, thimerosal can cause Ca(2+)-related cytotoxicity in a concentration-dependent manner.

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Toxicology. 2004 Jan 15;195(1):77-84.
Effect of thimerosal, a preservative in vaccines, on intracellular Ca2+ concentration of rat cerebellar neurons.
Ueha-Ishibashi TOyama YNakao HUmebayashi CNishizaki YTatsuishi TIwase KMurao KSeo H.
Laboratory of Cellular Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Tokushima 770-8502, Japan.

The effect of thimerosal, an organomercurial preservative in vaccines, on cerebellar neurons dissociated from 2-week-old rats was compared with those of methylmercury using a flow cytometer with appropriate fluorescent dyes. Thimerosal and methylmercury at concentrations ranging from 0.3 to 10 microM increased the intracellular concentration of Ca2+ ([Ca2+]i) in a concentration-dependent manner. The potency of 10 microM thimerosal to increase the [Ca2+]i was less than that of 10 microM methylmercury. Their effects on the [Ca2+]i were greatly attenuated, but not completely suppressed, under external Ca(2+)-free condition, suggesting a possibility that both agents increase membrane Ca2+ permeability and release Ca2+ from intracellular calcium stores. The effect of 10 microM thimerosal was not affected by simultaneous application of 30 microM L-cysteine whereas that of 10 microM methylmercury was significantly suppressed. The potency of thimerosal was similar to that of methylmercury in the presence of L-cysteine. Both agents at 1 microM or more similarly decreased the cellular content of glutathione in a concentration-dependent manner, suggesting an increase in oxidative stress. Results indicate that thimerosal exerts some cytotoxic actions on cerebellar granule neurons dissociated from 2-week-old rats and its potency is almost similar to that of methylmercury.

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Curr Opin Neurobiol. 2007 Feb;17(1):112-9. Epub 2007 Feb 1.
Molecular mechanisms of autism: a possible role for Ca2+ signaling.
Krey JFDolmetsch RE.
Autism spectrum disorders (ASDs) are a group of developmental disorders characterized by social and emotional deficits, language impairments and stereotyped behaviors that manifest in early postnatal life. The molecular mechanisms that underlie ASDs are not known, but several recent developments suggest that some forms of autism are caused by failures in activity-dependent regulation of neural development. Mutations of several voltage-gated and ligand-gated ion channels that regulate neuronal excitability and Ca2+ signaling have been associated with ASDs. In addition, Ca2+-regulated signaling proteins involved in synapse formation and dendritic growth have been implicated in ASDs. These recent advances suggest a set of signaling pathways that might have a role in generating these increasingly prevalent disorders.

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Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
Volume 423, Issues 1-2, 25 January 1999, Pages 65-72

Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line

Leticia Bucio, Cecilia García, Verónica Souza, Elizabeth Hernández, Cristina González, Miguel Betancourt and Ma. Concepción Gutiérrez-Ruiz

Abstract
A human hepatic cell line (WRL-68 cells) was employed to investigate the uptake of the toxic heavy metal mercury. Hg accumulation in WRL-68 cells is a time and concentration dependent process. A rapid initial phase of uptake was followed by a second slower phase. The transport does not require energy and at low HgCl2 concentrations (<50 μM) Hg transport occurs by temperature-insensitive processes. Subcellular distribution of Hg was: 48% in mitochondria, 38% in nucleus and only 8% in cytosolic fraction and 7% in microsomes. Little is known at the molecular level concerning the genotoxic effects following the acute exposure of eucaryotic cells to low concentrations of Hg. Our results showed that Hg induced DNA single-strand breaks or alkali labile sites using the single-cell gel electrophoresis assay (Comet assay). The percentage of damaged nucleus and the average length of DNA migration increased as metal concentration and time exposure increased. Lipid peroxidation, determined as malondialdehyde production in the presence of thiobarbituric acid, followed the same tendency, increased as HgCl2 concentration and time of exposure increased. DNA damage recovery took 8 h after partial metal removed with PBS–EGTA.

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Naviaux RK.  The spectrum of mitochondrial disease, in Mitochondrial and Metabolic Disorders-a primary care physician’s guide. Psy-Ed Corp., Oradell, NJ, pp. 3-10, 1997.

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Mutagenesis, Vol. 15, No. 6, 525-530, November 2000
Mutagenicity of mercury chloride and mechanisms of cellular defence: the role of metal-binding proteins

Franziska Schurz1, Monica Sabater-Vilar2 and Johanna Fink-Gremmels2*

Department of Analytical and Molecular Pharmacology, TNO Pharma Zeist and 2 Department of Veterinary Pharmacy, Pharmacology and Toxicology, University of Utrecht, The Netherlands

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Oxidative Stress in Autism, Chauhan (PDF)

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Oxidative Stress in Autism, Review (PDF)

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Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism, James et al (PDF)

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Developmental Regression and Mitochondrial Dysfunction in a Child With Autism(PDF)

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Mitochondrial Energy-Deficient Endophenotype in Autism (PDF)

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Oxidative Stress in Autism: Elevated Cerebellar 3-nitrotyrosine Levels (PDF)

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Bridging from Cells to Cognition in Autism Pathophysiology: Biological
Pathways to Defective Brain Function and Plasticity
 (PDF)

1Matthew P. Anderson, 2Brian S. Hooker and 3Martha R. Herbert

American Journal of Biochemistry and Biotechnology 4 (2): 167-176, 2008

We review evidence to support a model where the disease process underlying autism may begin when an in utero or early postnatal environmental, infectious, seizure, or autoimmune insult triggers an immune response that increases reactive oxygen species (ROS) production in the brain that leads to DNA damage (nuclear and mitochondrial) and metabolic enzyme blockade and that these inflammatory and oxidative stressors persist beyond early development (with potential further exacerbations), producing ongoing functional consequences.

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Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment(PDF)

Daniel A. Rossignol, J. Jeffrey Bradstreet

Abstract: Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernable mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions. Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.

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Mitochondrial delivery is essential for synaptic potentiation.  

Biol Bull. 2007 Apr;212(2):169-75.  Tong JJ

Biophysics and Physiology, University of California, Irvine, CA 92697, USA. tongja@uci.edu

Mitochondria, as portable generators that power synaptic function, regulate the ATP supply and calcium homeostasis in the neuron. As molecular interactions within the synapses before and after the potentiation are beginning to be elucidated, the deciding moment during the tetanic stimulation that gives rise to the strengthening of the synapse remains a mystery. Here, I recorded electrically from an intact Drosophila nervous system, while simultaneously using time-lapse confocal microscopy to visualize mitochondria labeled with green fluorescent protein. I show that tetanic stimulation triggers a fast delivery of mitochondria to the synapse, which facilitates synaptic potentiation. Rotenone, an inhibitor of mitochondrial electron transport chain complex I, suppresses mitochondrial transport and abolishes the potentiation of the synapse. Expression of neurofibromin, which improves mitochondrial ATP synthesis in the neuron, enhances the movements of mitochondria to the synapse and promotes post-tetanic potentiation. These findings provide unprecedented evidence that the mitochondrial delivery to the synapse is critical for cellular learning.

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Mitochondria at the synapse.

Neuroscientist. 2006 Aug;12(4):291-9.

Ly CVVerstreken P

Department of Neuroscience and Molecular and Human Genetics, Howard Hughes Medical Institute Baylor College of Medicine, Houston, TX 77030, USA. cindy.ly@bcm.tmc.edu

Synapses are packed with mitochondria, complex organelles with roles in energy metabolism, cell signaling, and calcium homeostasis. However, the precise mechanisms by which mitochondria influence neurotrans mission remain undefined. In this review, the authors discuss pharmacological and genetic analyses of synaptic mitochondrial function, focusing on their role in Ca2+ buffering and ATP production. Additionally, they will summarize recent data that implicate synaptic mitochondria in the regulation of neurotransmitter release during intense neuronal activity and link these findings to the pathogenesis of neurodegenerative diseases that feature disrupted synaptic mitochondria, including amyotrophic lateral sclerosis and hereditary spastic paraplegia.

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J Child Neurol. 2002 Jun;17(6):435-9.

Mitochondrial dysfunction in patients with hypotonia, epilepsy, autism, and developmental delay: HEADD syndrome

Fillano JJ, Goldenthal MJ, Rhodes CH, Marín-García J.
Department of Pediatrics, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.

A group of 12 children clinically presenting with hypotonia, intractable epilepsy, autism, and developmental delay, who did not fall into previously described categories of mitochondrial encephalomyopathy, were evaluated for mitochondrial respiratory enzyme activity levels, mitochondrial DNA, and mitochondrial structural abnormalities. Reduced levels in specific respiratory activities were found solely in enzymes with subunits encoded by mitochondrial DNA in seven of eight biopsied skeletal muscle specimens evaluated. Five cases exhibited increased levels of large-scale mitochondrial DNA deletions, whereas pathogenic point mutations previously described in association with mitochondrial encephalomyopathies were not found. Mitochondrial structural abnormalities were present in three of four patients examined. Our findings suggest that mitochondrial dysfunction, including extensive abnormalities in specific enzyme activities, mitochondrial structure, and mitochondrial DNA integrity, may be present in children with a clinical constellation including hypotonia, epileptic seizures, autism, and developmental delay. The acronym HEADD is presented here to facilitate pursuit of mitochondrial defects in patients with this clinical constellation after other causes have been excluded.

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Histol Histopathol. 2005 Jul;20(3):957-67.

Role of oxidative damage in the pathogenesis of viral infections of the nervous system.

Valyi-Nagy T, Dermody TS.
Department of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.

Oxidative stress, primarily due to increased generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS), is a feature of many viral infections. ROS and RNS modulate the permissiveness of cells to viral replication, regulate host inflammatory and immune responses, and cause oxidative damage to both host tissue and progeny virus. The lipid-rich nervous system is particularly susceptible to lipid peroxidation, an autocatalytic process that damages lipid-containing structures and yields reactive by-products, which can covalently modify and damage cellular macromolecules. Oxidative injury is a component of acute encephalitis caused by herpes simplex virus type 1 and reovirus, neurodegenerative disease caused by human immunodeficiency virus and murine leukemia virus, and subacute sclerosing panencephalitis caused by measles virus. The extent to which oxidative damage plays a beneficial role for the host by limiting viral replication is largely unknown. An enhanced understanding of the role of oxidative damage in viral infections of the nervous system may lead to therapeutic strategies to reduce tissue damage during viral infection without impeding the host antiviral response.

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Mitochondria and neuronal activity (PDF)

Oliver Kann and Richard Kovács

Am J Physiol Cell Physiol 292:641-657, 2007. First published Nov 8, 2006; doi:10.1152/ajpcell.00222.2006

Mitochondria are central for various cellular processes that include ATP production, intracellular Ca2 signaling, and generation of reactive oxygen species. Neurons critically depend on mitochondrial function to establish membrane excitability and to execute the complex processes of neurotransmission and plasticity. While much information about mitochondrial properties is available from studies on isolated mitochondria and dissociated cell cultures, less is known about mitochondrial function in intact neurons in brain tissue. However, a detailed description of the interactions between mitochondrial function, energy metabolism, and neuronal activity is crucial for the understanding of the complex physiological behavior of neurons, as well as the pathophysiology of various neurological diseases. The combination of new fluorescence imaging techniques, electrophysiology, and brain slice preparations provides a powerful tool to study mitochondrial function during neuronal activity, with high spatiotemporal resolution. This review summarizes recent findings on mitochondrial Ca2 transport, mitochondrial membrane potential (m), and energy metabolism during neuronal activity. We will first discuss interactions of these parameters for experimental stimulation conditions that can be related to the physiological range. We will then describe how mitochondrial and metabolic dysfunction develops during pathological neuronal activity, focusing on temporal lobe epilepsy and its experimental models. The aim is to illustrate that 1) the structure of the mitochondrial compartment is highly dynamic in neurons, 2) there is a fine-tuned coupling between neuronal activity and mitochondrial function, and 3) mitochondria are of central importance for the complex behavior of neurons.

Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis

Logo for mitochondrial DNA

Introduction 

Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by impaired social interaction and communication, as well as isolated interests and repetitive or stereotyped behaviors [1]. ASDs pose a significant burden to affected individuals, their families and society. This burden comes both from the debilitating and lifelong nature of ASDs and from their prevalence. It is now estimated that about one out of every 166 children is affected with ASD [2]. Most cases are idiopathic, although there are many uncommon or rare genetic and metabolic causes of autism that are increasingly recognized [3]–[5].

In 1998, Lombard postulated mitochondrial dysfunction as a cause of autism [6]. Prior and subsequent case reports provided biochemical data indicating perturbation of mitochondrial energy metabolism in some individuals with ASD [7]–[12], including mtDNA mutations in several [10], [13], [14]. Recently, Oliveira and colleagues published a population-based survey of school-age children with ASD. They found that 7% of those who were fully tested met criteria for definite mitochondrial respiratory chain disorders and were also clinically indistinguishable from other children with ASD [15]. This work is notable because it suggests that mitochondrial disorders of energy production may be present in a substantial percentage of children with ASD. To better describe the clinical spectrum of children with ‘mitochondrial autism’, we undertook a chart review of the biochemical, genetic, and histopathological findings in 25 patients with ASD who had unequivocal evidence of a disorder of oxidative phosphorylation.

via PLoS ONE: Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis.

Reduced levels of mercury in first baby haircuts of autistic children

Reported rates of autism have increased sharply in the United States and the United Kingdom. One possible factor underlying these increases is increased exposure to mercury through thimerosal-containing vaccines, but vaccine exposures need to be evaluated in the context of cumulative exposures during gestation and early infancy.

Differential rates of postnatal mercury elimination may explain why similar gestational and infant exposures produce variable neurological effects. First baby haircut samples were obtained from 94 children diagnosed with autism using Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) criteria and 45 age- and gender-matched controls. Information on diet, dental amalgam fillings, vaccine history, Rho D immunoglobulin administration, and autism symptom severity was collected through a maternal survey questionnaire and clinical observation.

Hair mercury levels in the autistic group were 0.47 ppm versus 3.63 ppm in controls, a significant difference. The mothers in the autistic group had significantly higher levels of mercury exposure through Rho D immunoglobulin injections and amalgam fillings than control mothers. Within the autistic group, hair mercury levels varied significantly across mildly, moderately, and severely autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm, respectively.

Hair mercury levels among controls were significantly correlated with the number of the mothers’ amalgam fillings and their fish consumption as well as exposure to mercury through childhood vaccines, correlations that were absent in the autistic group.

Hair excretion patterns among autistic infants were significantly reduced relative to control.

These data cast doubt on the efficacy of traditional hair analysis as a measure of total mercury exposure in a subset of the population.In light of the biological plausibility of mercury’s role in neurodevelopmental disorders, the present study provides further insight into one possible mechanism by which early mercury exposures could increase the risk of autism.

via Reduced levels of mercury in first bab… [Int J Toxicol. 2003 Jul-Aug] – PubMed – NCBI.

Ancestry of pink disease (caused by mercury) identified as a risk factor for autism spectrum disorders.

Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children.

The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD.

Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates.

The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 22) to be significantly higher than the comparable general population prevalence rate (1 in 160).

The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.

via Ancestry of pink disease (infanti… [J Toxicol Environ Health A. 2011] – PubMed – NCBI.

Did Acetaminophen Provoke the Autism Epidemic?

tylenol bottle closeup

http://www.altmedrev.com/publications/14/4/364.pdf

I was invited to view a webinar on a possible connection between Autism and Acetaminophen some months ago.  When I was first told about the next great claim of a definitive cause for Autism, I was skeptical.  I had listened to so many debates on causation and autism.  Honestly, after awhile, the obvious politics involved becomes very tiresome.

I voiced my skepticism, but as this mother proceeded to describe some of the accusations against Acetaminophen (Tylenol), I started to listen more closely.  That is when it hit me.  Unlike all the other causation theories, this could actually explain my child’s Autism and his remarkable improvement through chelation.

You see, my son did not match the typical case histories of othAcetaminophen and Autismer Autistic children.  In fact, I almost failed to pursue biomedical treatments because he did not have a typical story.

My child did not regress.  He never developed normally.  After his diagnosis it became apparent that he was born with Autism.

My child did not have any health problems or frequent ear infections.  In fact the only ear infection and subsequent round of antibiotics he had ever had was at 2.2 years of age, well after his Autism was apparent.

My child was never vaccinated.  I did not receive any vaccines or Rhogam while pregnant.

This was my 5th child.  If his Autism was solely due to my toxic body burden one would expect my previous children to be more affected.

We did not move.  My 3rd child and 4th child were both born and raised in the exact same apartment building as my 5th child.  The environment hadn’t changed.

I really was at a loss and none of the typical biomed explanations quite fit our experience.  Still biomed advocates were proposing using natural safe approaches, like diet modification along with vitamins and other supplements.  These weren’t things that could damage my child, so I really had no reason not to at least give it a go.

We did the GFCF diet and saw improvement.  We did yeast treatments and gut supports, and saw improvement.  He improved on zinc.  He improved on B6.  He improved with almost every intervention we tried.

Then we found AC chelation and he improved to point that most would consider him recovered.  He is in a typical school with typical peers with no supports.  He has friends and has been invited to parties.  In fact, at the end of this year they tested him for the gifted program and determined that he was academically gifted and will start going to an enrichment school one day a week because his typical classroom isn’t quite academically challenging enough.  He is flourishing.  (He does still have some precocious speech and slightly odd gestures but no sign  of Autism.  He was diagnosed with low functioning Autism at age 2.5).

With that kind of drastic improvement with chelation protocol, it was apparent he was metal toxic.  But how?  By now the how didn’t matter much to me.  We left the how question alone to dangle in the wind as we had found the solution, so it didn’t seem important to figure out exactly how the problem started or what the cause could have been.

Never the less the question always dangled, it never totally disappeared from our minds.

Insert the Acetaminophen theory.

You know what was different about my 5th child’s med history?  I was over due and very uncomfortable during my last trimester.  It was so bad that I could not even get two full hours of sleep per night.  I was miserable and exhausted.  My midwife was concerned about whether I would have the energy to mount a proper labor and delivery.  I asked her if there was anything safe I could take while pregnant to help me sleep.  ( I just knew her answer would be no).  She said yes and came back with an Rx for Tylenol 3 with codeine.

I told her I thought it was over kill, “I am uncomfortable but I am not in pain.  I just need some sleep.”

She said that it didn’t cross the placental wall and that although I didn’t need the pain relief, it was the only thing they could give me that was safe for my baby.

I took Tylenol 3 almost every night for 2 weeks.

Quote from article:

Acetaminophen taken during pregnancy may provoke autism present at birth…

Finally, a possible explanation for what we had experienced.  The Tylenol I took may have interfered with his ability to detox environmental toxins as well as impaired his brain function and immune system.  The toxins his body built up could be responsible for the rest.  Is this truth or theory?

At this point it is only theory.  But it is the first theory that had a chance of explaining what we saw, and the research is convincing.  It is solid enough that I would never give Tylenol to another child.  I would recommend all children and pregnant mothers avoid Tylenol and other acetaminophen containing products.  Until more research is done it only makes sense to be cautious.

I have to fix this, me and only me (cont.)

continued from post https://throughthepuzzle.com/2012/05/06/i-have-to-fix-this-me-and-only-me/

(Religious Post Follows)

As I said in my earlier post.  I was teetering on the brink….. of what?  Who knows, but it was not going to be pretty.

Some people have tons of friends.  I on the other hand could never be described as Ms popularity.  I can always find people to chat with, but I do not make many real friendships.  You know…. the ones with substance.  Over the years I have been blessed with a few wonderful people in my life though.

My very good friends (the ones I truly value) are the people who can tell me when I am not thinking straight.  When I am making mistakes.  They are the ones who care enough to give me a dose of reality when I seriously need it.  (Even if I don’t want it).  Here’s hoping you all have friends like that.

Well, I was talking to one of my best friend during this time and I will never forget the impact of her words.  I think she saved my life.

In a nutshell she said, “Who do you think you are anyway?”

“What makes you think you have the power to fix anything?”

“Don’t you think that’s just a little arrogant?”

She was so right.  I had lost sight of the truth.  I can not control the future. I can not fix my child. I do not hold the key to life or health or anything else in the palm of my hand.  I can not cure.  And my child’s future was written long before any of us even existed.  That thought was so comforting.  The extreme pressure that I was feeling was instantly gone. This is God’s plan.  It is divine decree.  We give the supplements, but God cures.

But perhaps you hate a thing and it is good for you; and perhaps you love a thingand it is bad for you. And Allah Knows, while you know not” [Qur’an 2:216]

Indeed Autism has been one of the best things that could have happened to our family.  I say that knowing full well how much I hate it.  But God has granted us healing and we have found the way out.  Every member in my family has benefited, all six of my children, even my husband (who is also chelating).  And in this process, I have been blessed with the ability to help families all over the globe.  I pass on this information, just as it was passed on to me, and there is hope for the future of our children, by the will of God.  Al Hamdulillah!

“Where is our son?”… “He’s over there.”…”Where?”… “Over there waiting his turn.”

Root Beer

We went home for the Katy railroad Memorial Day celebration this weekend.  The kids have the greatest time.  There are lots of rides, carnival food, a petting zoo, and tons of railroad themed events.  Best of all there is homemade root beer.  The girls look forward to the root beer all year long and I listen to all the plans for how many refills they are going to get for at least three days prior to the big event.

While this is great fun for the whole family, for me it generally either meant keeping my ASD son home or chasing him all over the park only to escort a screaming meltdown back to the car an hour later.

The kids are older this year and our boy is doing so well my husband felt ambitious and decided to take them all while I would meet them there a little later.

I was a bit apprehensive but figured hey what the heck, go for it.

When my mom and I got there we walked around searching for the family.  We saw crowds of people, brightly colored tents, noise and activity bustled all around us.  Children were lined up waiting for face paintings, clowns making balloon animals, and bounce house activities of all kinds.

Finally we spotted my husband among the other happy parents celebrating the holiday.  Standing there… alone?  Ok, he let the other kids go off to peruse the goodies of their choice, but what about our ASD kiddo?

Me:  “Hun, where’s our son?”  (with a puzzled look on my face)

DH:  “He’s over there.”

ME:   “Where?”  (I say frantically scanning the area)

DH:  “Over there waiting his turn.”

That is when my eyes landed on a little mop headed boy waiting in line with all the other children for his turn on the……. on the….. heck I don’t remember what he was waiting in line for.  It really didn’t matter.  He was patiently waiting, standing, hot, sweaty, red-faced from all the previous activities he had already enjoyed and ginning from ear to ear.

This year we all had fun! 

(Especially this mother’s heart. Thank you AC

chelation.)

Mercury Toxicity: What to do about it.

In the book Amalgam Illness by Andrew Hall Cutler the author has an excellent explanation on why ALA chelation is the only safe, effective means to remove mercury from the Brain and CNS.

In short: metalic mercury, organic mercury, methylmercury and ethylmercury are all processes by the body and can then be transformed into inorganic mercury.

When this happens in the brain and CNS the inorganic mercury is trapped.  The body has no mechanism for getting it out past the Blood Brain Barrier.

Alpha Lipoic Acid is the only safe and effective chelator that we currently have available to us which can cross the blood brain barrier and remove inorganic mercury from the brain.

Mercury has the potential to cause many of the same behavioral symptoms seen in children with Autsim.  If mercury is the root cause for the behavior and physical symptoms the person is suffering from, then appropriate, safe chelation has the potential to recover the person from the ailments they are experiencing.

In my opinion since ALA is a wonderful Antioxident when not in the presance of heavy metals and has the potential to offer relief if the symptoms are caused by metals it only makes sense to give it a whirl.  See Safe Chelation for details.

ATSDR – Public Health Statement: Mercury.

At the above link you will find information on the following:

1.1 What is mercury?

1.2 What happens to mercury when it enters the environment?

1.3 How might I be exposed to mercury?

1.4 How can mercury enter and leave my body?

1.5 How can mercury affect my health?

1.6 How can mercury affect children?

1.7 How can families reduce the risk of exposure to mercury?

1.8 Is there a medical test to determine whether I have been exposed to mercury?

1.9 What recommendations has the federal government made to protect human health?

References

Where can I get more information?

Lead Toxicity: Where Is Lead Found?

Summary: Where Is Lead Found?

Lead Source Contaminated Media

Lead solder/pipes

Drinking water

Packages or storage containers

Food, beverages

Paint (pre-1978)

Household dust and soil

Production sources

Imported foods, remedies, cosmetics, jewelry

Mining and smelting

Outdoor air and dust

Workplaces involving lead

Outdoor and indoor air and dust

Gasoline (pre-1988)

Soil

via Lead (Pb) Toxicity: Where Is Lead Found? | ATSDR – Environmental Medicine & Environmental Health Education – CSEM.

Follow the link above for the full article as well as a very good printable resource on sources of lead toxicity.

Tip:  Since calcium apposes leads absorption and storage (especially bone stores) getting adequate calcium is especially important for growing children.  Raw milk, cheese, and yogurt as well as quality calcium supplements and bone broths are excellent sources of calcium.