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?

 

War of the Worlds: The Flu Saga

The World of Flu as Manipulated by the CDC

by David Burd

http://www.ageofautism.com/2012/08/the-world-of-flu-as-manipulated-by-the-cdc.html

War of the Worlds

Until three years ago and the Swine/H1N1 Summer Panic in 2009,  for over ten years U.S. Government Health officials had designated the first week of December as National Flu Shot Week. The data for Summer 2009 shows blood tests for flu were performed by the millions as compared to “normal” years when such tests were not performed at all until late Fall. Never mind that an edict dictated virtually all blood results to be arbitrarily declared to be H1N1 and all the other flu variants shoved into the H1N1 category.  Never mind that all flu variants have always been omnipresent all year long, just not tested for until late Fall.

Never mind countries such as Canada, where parents are more skeptical about the shots, pediatric flu- associated mortality is but a small fraction per-capita that of the U.S.  Never mind CDC officials declared there was no risk whatsoever from the multiple batch shot lots preserved with mercury and urged on an unwitting American public.

Never mind in 2009 that  TV doctor personality Nancy Snyderman declared on national TV for all Americans to “just get your damn flu shot.”

Never mind that every year since 2003 when flu shots were sometimes put on fast-track promotion as early as  September that U.S. pediatric flu-associated deaths those years also spiked.  Never mind (see my post in Age of Autism, June 2, 2010) that U.S.  protocols for treating kids hospitalized for flu to be dosed with the chemotherapy antiviral drug Ribavirin, a drug that ALWAYS destroys red blood cells thus causing hemolytic anemia – never mind no other country in the world is insane enough to employ this protocol.

Never mind the great Flu Shot Shortage in the Winter of 2004-2005, when British factories supplying U.S. flu shots were shut down, and this coincided with the lowest pediatric flu-associated deaths on record, until this last 2011-2012 season when data shows U.S. parents largely avoided flu shots for their children after realizing how dangerous the shots were, and are, especially when they realized CDC says TWO flu shots be given to infants at 6 and 7 months respectively, each one loaded with mercury unless a non-mercury shot be explicitly demanded.

Never mind that all the other vaccine ingredients, called excipients, are all toxic to humans, magnified as least 10-fold in vulnerable undeveloped infants who are but one-twentieth the weight of adults but get shots of 25 milliliters compared to an adult dose of 50 milliliters and who have mature, hardened systems compared to newborn 6-month olds.

Never mind that vaccine batches may have unknown contaminants, or may be improperly stored, or that Australia two years ago in Spring, 2010, a national emergency abruptly stopped all flu shots for kids when massive numbers of convulsing children were rushed to hospitals after getting their flu shots.  Never mind the bought-off U.S. mainstream media suppressed the Australian episode, keeping ignorant the American public, never mind this was kept mum by  “just get your damn flu shot” Dr. Nancy Snyderman.

Never mind that well nourished mothers breast feeding their babies supply all the necessary protection against such as flu, never mind that the vast majority of American babies taken to hospitals with flu had serious chronic health pre-conditions and/or were significantly premature.  Never mind that any serious health condition in U.S. babies is declared by CDC as always a mere coincidence having nothing to do with massive amounts of recently injected toxic vaccine ingredients as from the flu vaccine.

Which brings me back to the present: Here in late July, 2012, my local Rite Aid drugstore in Alexandria, Virginia has plastered its interior  aisles with countless flu-shot promotion posters to go along with gigantic outdoor posters.  Whatever happened to the December National Flu Shot promotion week?

David M. Burd        Alexandria, Virginia      August 12, 2012

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

________________

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]

________________

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.

________________

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.

________________

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.

________________

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.

________________

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.

________________

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

________________

Oxidative Stress in Autism, Chauhan (PDF)

________________

Oxidative Stress in Autism, Review (PDF)

________________

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

________________

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

________________

Mitochondrial Energy-Deficient Endophenotype in Autism (PDF)

________________

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

________________

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.

________________

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.

________________

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.

________________

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.

________________

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.

________________

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.

________________

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.

Sulfur Exclusion Diet

Cysteine is an essential amino acid and helpful for many body processes including (along with glycine and glutamic acid, the formation of glutathione (essential for detox).  Sulfur foods are rich in the amino acids methionine and cysteine.  Some children need to be fed more sulfur rich foods while others have to much free cysteine and need to restrict dietary sources.

Sulfur is a monothiol meaning that, when in excess, it can attach to heavy metals and “bounce them around” without actually causing them to exit the body in any significant amount.  This creates some behavior issues and lots of yeast issues.

Unfortunately there is no longer any lab testing available to evaluate plasma cysteine status .  This has nothing to do with cysteine status, plasma sulfate status, or liver sulfation status.  These can be independently high low or normal.  The only effective way of determining whether your child would benefit from high or low dietary sulfur intake is through a sulfur exclusion diet trial.

Indications:
Difficulty controlling yeast even with large amounts of anti-fungals and probiotics.  Yeast seems to acclimate to any anti-fungal used within a short period of time (this does not apply to Rx anti-fungals).  A lot of hyperness, poor behavior, meltdowns, self limiting to sulfur foods, etc…

The sulfur exclusion trial is done as follows:

All high sulfur/thiol foods and supplements containing thiol groups (see list below) are strictly avoided for a 5-7 day period to allow the effect of the last ingestion to wear off. The negative effects of sulfur occur over a 4-7 day period after the last sulfur ingestion, which means you need to exclude all sulfur foods AND sulfur supplements for at least a week before you know what is going on.

Then, after 5-7 days the high sulfur/thiol foods are added sharply back to your diet and you eat a lot of them for a week, noticing what happens to your health over this time. If you feel worse soon after introducing sulfur foods, you do not need to do this for a week as it indicates you are better off eliminating sulfur foods.  (http://livingnetwork.co.za/chelationnetwork/food/high-sulfur-sulphur-food-list/)

If your health improves while off the sulfur foods and regresses after adding them back, you have an intolerance to them and should avoid them.

(To make the most of your diet trial and test for a dairy intolerance too.  First reintroduce general sulfur foods, but not eggs, dairy, or soy.  Next bring back eggs. After a few days bring back dairy, and finally soy).  If your child reacts negatively to the general foods there is no need to continue.  If you child does fine on the general foods but reacts negatively to eggs, remove them for a few days then reintroduce dairy separately.  By this you should be able to determine if your child has a sulfur sensitivity or a casein intolerance.

This list is copyright Andrew Hall Cutler Phd, reproduced with permission.

For more information get the book:

Amalgam Illness Diagnosis and Treatment

http://www.noamalgam.com/

Foods/supplements high in sulfur/thiols:

artichokes, Jerusalem but not French
asparagus
bakery products containing whey, cysteine, eggs or enzymes
bean curd/tofu milk
bean sprouts
beans of all sort
bok choy
broccoli
brussels sprouts
cabbage
carob
cauliflower
cheese of all sorts
chives
chocolate
coffee
collard greens
dairy products
eggs
garlic
green beans
greens
lentils of all sorts
milk from any animal
miso soup
onions
papaya (slightly)
peas
peanuts
pineapple (slightly)
rutabaga
spinach
tofu
turmeric (though not high in thiols, it  is really good at raising thiol levels)
yeast extract
NAC- N-acetyl cysteine
bromelain and papain
cysteine
MSM
methionine (converts down into cysteine)

Foods low in sulfur/thiols:

acorn squash
almond milk
artichokes (french)
avocado
nuts – almonds, cashews, walnuts, etc.. (not peanuts or soy they are legumes)
beef
beets
brown sugar
grains – wheat, rice, corn, bulgar, buckwheat, barley, oats
butter
carrots
celery
Poultry dark meat/ liver
cinnamon
coconut dried/fresh
cod liver oil
corn (sweet)
cottonseed oil
eggplant
ginger root fresh
herbs fresh – basil thyme, rosemary
lettuce – but not other greens
mushrooms
parsley
parsnips
pears
potatoes
seeds – sunflower, linseeds, pumpkinseeds, flax (not sesame)
sesame oil , but not  seeds
spaghetti squash
squashes – acorn, butternut, spaghetti, summer, winter, yellow crooked neck, zucchini
sweet potato
vinegar (white)
whole-wheat flower
winter squash
yams

Related articles

Gluten Free/ Casein Free

Gluten-Free, Casein-Free Diet 

Gluten (in wheat, rye, barley, and possibly oats) and casein (in all dairy products) can cause problems:

1. They are common food allergens, especially in children and adults with autism.
2. Certain peptides from gluten and casein can bind to opioid-receptors in the brain, and can have a potent effect on behavior (like heroin or morphine), causing problems including sleepiness, inattention/”zoning out”, and aggressive and self-abusive behavior. Like opioids, they can be highly addictive, and a lack of them can cause severe behaviors.

These problems appear to be due to:

1) A failure of the digestive tract to fully digest the gluten and casein peptides into single amino acids
2) Inflammation of the gut, allowing the gluten and casein peptides to enter the bloodstream and reach opioid receptors in the brain.
3) Gluten can increase symptoms of Auto-immune disorders

• Total, 100% avoidance of all gluten products and all dairy products. Even small amounts, like a bite of a cookie, can cause allergic and/or opioid problems. Many foods have trace contamination with gluten, such as dusting French fries and raisins with wheat powder to keep them from sticking, so it can be very difficult to avoid all foods and contaminated foods. (Tip: if your child begins to self limit or obsess over any food question it.)
• Digestive enzymes can also be helpful, especially if there is an accidental exposure, but they are probably not as helpful as a total avoidance of casein and gluten.
• Many children with autism also benefit by removing corn and/or soy products.

Benefits:
Children who most crave dairy and/or wheat, and who eat a lot of it, are most likely to benefit. Casein-free diets usually produce benefits within a month, and sometimes within a week. Gluten free diets usually take 1-3 months to produce benefits. In some children there is a worsening of symptoms for a few days (similar to a drug withdrawal) followed by improvement.

Dairy/Casien Free

Since sulfur issues are very common in our children, before embarking on a long commitment to be Casein Free, it is recommended to rule out sulfur issues.  The most direct and logical approach is to begin a low sulfur diet trial.  At the end of the exclusion week first introduce any foods on the high sulfur list other than eggs or dairy.  After a few days if your child has no reaction, you can introduce eggs.  Eat quite a few eggs over the next few days, if you still see no reaction introduce dairy.  If you then see a reaction to the dairy you can be sure your child has a true casein intolerance.

How to Read a Label for a Milk-Free Diet
All FDA-regulated manufactured food products that contain milk as an ingredient are required by U.S. law to list the word “milk” on the product label.

Avoid foods that contain milk or any of these ingredients:
Butter, butter fat, butter oil, butter acid
butter ester(s)
Buttermilk
Casein
Casein Hydrolysate
Caseinates (in all forms)
Cheese
Cottage Cheese
Curds
Custard
Diacetyl
Ghee
Half-and-half
Lactalbum, Lactalbumin phosphate   Lactoferrin
Lactose
Lactulose
Milk (in all forms)
Milk protein hydrolysate
Pudding
Recaldent (R)
Rennet Casein
Sour cream, sour cream solids
Tagatose
Whey (in all forms)
whey protein hydrolysate
Yogurt

Milk is sometimes found in the following:
Artificial butter flavor
Baked Goods
Caramel Candies
Chocolate
Lactic acid starter culture and other bacterial cultures
Luncheon meat, Hot dogs, Sausages   Margarine
Nisin
Nondairy products
Nougat
Calcium Additives

How To Find a Thyroid Doctor

Sometimes it can be difficult to find a doctor knowledgeable in treating children with sub-clinical thyroid disorder.

I generally skip most endocrinologist as they stick pretty closely to text book synthroid.

Naturapathic Doctors and Chiropractors can Rx natural thyroid in some states, However in most they cannot get you the med you need.

After spending money on way to many intake appointments I got smart.  I called the local compounding pharmacies and asked if they ever fill scripts for Armour.  Then asked for referrals.  It can sometimes be necessary to travel a ways to find a doctor (I know parents who have driven 2 hours one way to obtain their thyroid medication).

I have successfully found thyroid doctor for several parents I have consulted with from all over the country.  Remember that often you only need to visit these doctors once per year to maintain your script.

When calling I ask the following questions:

1.  Does the doctor ever prescribe natural thyroid?
2.  Does the doctor consider both test results and symptoms when determining whether or not to treat the thyroid?
3.  Does the doctor feel comfortable treating cases of sub-clinical thyroid in children?

Often the person on the other end will either know right away that the doctor can do this, or they will take your number and call you back.

Once you find a doctor be sure to bring with you a list of your child’s thyroid symptoms and basal temps to your first appointment.

Trying to find the Autism: Theory of Mind

We have had our son tested every few years to see how he is doing/progressing.

I did let the testers know that he had a diagnosis of Autism, but I did not give them the actual tests to look at as I wanted their unbiased assessment on how he was doing at the time of the test.

The past summer (2011) we had him tested by the school district.  They ran all the typical Autism tests, they tested his sensory issues, they even tested his cognitive abilities this time as he was able to read and could get more thorough testing than in previous years.  They then decided to test his speech as well.  We had a total of 5 appointments to complete the variety of tests.

About a week or so after the last test we had the results appointment.  They found that his mispronunciation of the letter “L” was not age appropriate and he qualified for 1 hour per week of speech to address this.

Huh?

Ok and………?   Nothing.  No autism.  No Pdd.  No Aspergers.  Not on the spectrum.  No part time in the Special needs classroom.  No aid or shadow.  Nothing.

There are a lot of parents who claim their child is recovered and I do not make that claim as I can still see a few things that make him look slightly different from his peers (some slight oddness in the way his arms move when he runs, some precocious language, and a sporadically his tone is, well, odd).  So recovered? No, but is there any Autism?

Well another parents mentioned the Sally and Ann test for theory of mind, so I did this with him, fully expecting him to fail.  He passed.  He passed both what is she thinking and what does he think she is thinking.  Wow!

I decided to go a bit further this past week and really see if I could find the Autism.

I searched online and found a variety of links for theory of mind sample tests and questions.  I read him all the questions I could find. In all he took 5 tests and he passed he missed all of 2 questions.  He got questions correct that were labeled as memory (of course this is to be expected as it has always been his strong suit), TOM1, TOM2, and TOM4.

Now these were just internet sample test given by his Mom, but I tend to be hard.  I did not give him any clues or repeat options when he got one wrong.  I was really looking for some measure to go by to watch these last skills come online.  See we started by using the ATEC (his first score was132), when he scored 0 on that we went to the child brain pdd test.  he started in the 70’s on that test.  When that went to 0 I had nothing else to use, this is what prompted me to look for these TOM questions.  Now I am just at a loss.

I can see the Autism in his slight oddness of posture and word/phrase selection, but I can’t seem to get a handle on anything else.

Could that really be all we have left to address………………………?  I suppose only time will tell.

http://www.staff.ncl.ac.uk/daniel.nettle/liddlenettle.pdf

http://www.iidc.indiana.edu/?pageId=424

http://www.psychologytoday.com/blog/aspergers-diary/200805/empathy-mindblindness-and-theory-mind

http://psych.wisc.edu/lang/pdf/Gernsbacher_autistic_modules.pdf

http://www.staff.ncl.ac.uk/daniel.nettle/liddlenettle.pdf

Just say NO to EDTA

 

There are many Docs out there who still use EDTA to chelate autistic children.  If you find yourself with a doctor who is recommending this type of chelation you should certainly run in the other direction.

There are many different methods of chelation being promoted today and we must be vigilant in choosing what is safe for our children.

There is a lot of hype in the media about the dangers of chelation therapy.  They regularly accuse chelation as dangerous, saying it has killed one child already.  They are correct.  IV EDTA has in fact killed a child.  A young boy died tragically and unnecessarily by improper use of a form of EDTA.

EDTA binds to other needed minerals as well as to heavy metals depleting the body of necessary nutrients.  What happened to this boy was a tragedy as the wrong medicine was administered.  CaEDTA is EDTA bound with calcium so that when it is administered it doesn’t deplete the bodies calcium levels. This boy was mistakenly given sodium EDTA instead of CaEDTA.  It was given in a high dose through and IV and the rapid excretion of Calcium caused him to suffer a cardiac arrest and die.  We feel very sad for this family just as we feel sad for the many children who have been injured by iatrogenic (doctor caused) means.

Unfortunately the negatives of EDTA do not stop by simply using the correct med (caEDTA) as those chelation docs would suggest.  There is a second insult which this medicine causes in our children.  Research by Boyd Haley has demonstrated that when used in the presence of mercury toxicity the EDTA binds with the mercury forming HgEDTA.  This substance has been shown to interact with brain tubulin (a neuroprotein) and increases the damage caused by mercury.

While EDTA is an effective treatment for cardiovascular plaques and is effective at removing lead, it should not be used in Autistic children (DMSA is an alternative chelator of lead and can be safely used orally).  For cardiovascluar patients who wish to pursue EDTA treatment it should only be used when preceded by safe mercury detox (using ALA) to clear mercury from fatty tissues including the brain.

 

haley_study_edta_and_mercury

 

 

 

Open Sesame……. or rather beware of Sesame Sticks?

Dry sesame seeds

Well, I was just typing up a draft of a post I was going to call Finding the Autism or Searching for Autism or some such thing, all about our search for some measurable way to continue to watch him improve.

I may still post it at some point because it is about theory of mind tests and may contain some points of interest for some of you, but…….

 

Our search for the elusive autism came to a standstill today.

My powers of observation seem to be getting a little soft.  Sunday afternoon he was simply not himself.  Very over emotional, and whiny.  He was over reacting to almost everything.  I can’t call them meltdowns precisely as they wasn’t that severe, but I just kept thinking… What in the world was going on.  It has been many months since we’ve seen anything like this.

Adrenal?  No he got all his adrenals

Thyroid?  no he’s been getting that.  In fact I have considered retesting to see if he is ready for a decrease.

Yeast?  maybe…. it might be back… we are on round.  Hmmm,  but he isn’t hyper exactly…. hmmm

OMG its the sesame.

We picked up some lovely sesame sticks from the health foods store.  I thought these would be better than chips and personally I think they taste great.

My son thought they tasted great too, and he “enjoyed” quite a few of them.

Remember my Diet and Autism post about the low sulfur diet and how we don’t need it anymore?  Well…. we may not need to be low sulfur but perhaps a cup of sesame seeds was a little over kill.

Of course I didn’t come to this realization until almost bedtime.  I used to be a little faster on the draw.  Perhaps not having to be on the edge of my seat to figure out what supp I needed to toss at him has made me a little too comfortable.

Having finally put two and two together, I gave some OoO.  He was still a bit off yesterday (Monday), but he is back to his normal self today.  I imagine I will need to watch him for an increase in his “desire” for sulfur foods again now that he has been reminded how much he loves them, lol.  Or maybe he’ll just want sesame sticks.

Once upon a time his self-limiting was so bad that he only ate about 5 or so foods.  Those were dark

times.  But it just goes to show, while we are doing wonderfully over all, it isn’t time to relax completely just yet.

Whew… glad Sunday is only a memory.

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.

Mercury concentration in ambient air and the risk of autism

Appollo Beach power plant 01432

Ecologic studies of the spatial relationship between disease and sources of environmental contamination can help to ascertain the degree of risk to populations from contamination and to inform legislation to ameliorate the risk.

Population risks associated with persistent low-level mercury exposure have recently begun to be of concern and current reports implicate environmental mercury as a potential contributor in the etiology of various developmental and neurodegenerative diseases including autism and Alzheimer’s disease.

In this demonstration of preliminary findings, we demonstrate for Bexar County Texas and Santa Clara County California, the hypothesis that the spatial structure of the occurrence of autism has a positive co-variation with the spatial structure of the distribution of mercury in ambient air.

The relative risk of autism is greater in the geographic areas of higher levels of ambient mercury.

We find that the higher levels of ambient mercury are geographically associated with point sources of mercury emission, such as coal-fired power plants and cement plants with coal-fired kilns. Although this does not indicate a cause, these results should not be dismissed, but rather seen as a preliminary step for generating a hypothesis for further investigation.

via The value of ecologic studies: mercury co… [Rev Environ Health. 2011] – 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.