FOR IMMEDIATE RELEASE
Orthomolecular Medicine News Service, October 8, 2007
Vitamin Supplements Help Protect Children from Heavy Metals, Reduce Behavioral Disorders
(OMNS October 8, 2007) The ability of vitamin C to protect animals from heavy metal poisoning is well established. Recent controlled trials with yeast, fish, mice, rats, chickens, clams, guinea pigs, and turkeys all came to the same conclusion: Vitamin C protects growing animals from heavy metals poisoning. [1-7]
Benefits with an animal model do not always translate to equal benefits for humans. In this case, however, the benefit has been proven for a wide range of animals. The odds that vitamin C will protect human children are high.
There is a virtual epidemic of behavior problems, learning disabilities, ADHD and autism, and the number of children receiving special education services continues to rise steeply. Although not all causes are yet identified, growing evidence suggests that heavy metal pollution is a significant factor, and vitamin C is part of the solution.
Dr. Erik Paterson, of British Columbia, reports:
"When I was a consulting physician for a center for the mentally challenged, a patient showing behavioral changes was found to have blood lead some ten times higher than the acceptable levels. I administered vitamin C at a dose of 4,000 mg/day. I anticipated a slow response. The following year I rechecked his blood lead level. It had gone up, much to my initial dismay. But then I thought that perhaps what was happening was that the vitamin C was mobilizing the lead from his tissues. So we persisted. The next year, on rechecking, the lead levels had markedly dropped to well below the initial result. As the years went by, the levels became almost undetectable, and his behavior was markedly improved."
World-wide, coal and high sulfur fuel oil combustion release close to 300,000 tons per year of heavy metals, 100,000 tons of which are considered hazardous air pollutants by the US Environmental Protection Agency. [8] This includes arsenic, beryllium, cadmium, cobalt, chromium, mercury, manganese, nickel, lead, antimony, selenium, uranium, and thorium. These metals are also released to the air by the industrial processes that mine and refine metal-containing ores.
Heavy metals dispersed in the air as invisible particles are blown by the winds and therefore become widely dispersed. Few mothers or children can avoid both contaminated air and food, helping to explain why behavior problems are striking rich and poor alike.
University of Victoria professor Harold Foster, PhD, says, "Pregnant women need special protection because their fetus may be poisoned in the womb, so interfering with its development. In addition to vitamin C, nutrient minerals are also protective against heavy metal toxins. For example, selenium is antagonistic to (and so protective against) arsenic, mercury and cadmium."
Metals have always been a part of the environment, and our bodies have evolved methods to protect against them. This process involves vitamin-dependent metabolic pathways. [9] Additional vitamin intake, through the use of nutrient supplementation, can help speed up the removal process. Daily consumption of additional vitamin C and selenium is likely to protect children by helping to eliminate heavy metals from their bodies. One easy and inexpensive way to increase intake of these nutrients is by taking a vitamin C supplement with each meal, along with a multivitamin containing selenium. Vitamin supplements are remarkably safe for children. [10]
References:
[1] Borane VR, Zambare SP. Role of ascorbic acid in lead and cadmium induced changes on the blood glucose level of the freshwater fish, Channa orientalis. Journal of Aquatic Biology, 2006. 21(2), 244-248.
[2] Gajawat, Sunita; Sancheti, Garima; Goyal, P. K. Vitamin C against concomitant exposure to heavy metal and radiation: a study on variations in hepatic cellular counts. Asian Journal of Experimental Sciences, 2005. 19(2), 53-58.
[3] Shousha, Wafaa Gh. The curative and protective effects of L-ascorbic acid & zinc sulphate on thyroid dysfunction and lipid peroxidation in cadmium-intoxicated rats. Egyptian Journal of Biochemistry & Molecular Biology, 2004. 22(1), 1-16.
[4] Vasiljeva, Svetlana; Berzina, Nadezda; Remeza, Inesa. Changes in chicken immunity induced by cadmium, and the protective effect of ascorbic acid. Proceedings of the Latvian Academy of Sciences, Section B: Natural, Exact and Applied Sciences, 2003. 57(6), 232-237.
[5] Mahajan, A. Y.; Zambare, S. P. Ascorbate effect on copper sulphate and mercuric chloride induced alterations of protein levels in freshwater bivalve Corbicula striatella. Asian Journal of Microbiology, Biotechnology & Environmental Sciences, 2001. 3(1-2), 95-100.
[6] Norwood, Joel, Jr.; Ledbetter, Alan D.; Doerfler, Donald L.; Hatch, Gary E. Residual oil fly ash inhalation in guinea pigs: influence of ascorbate and glutathione depletion. Toxicological Sciences, 2001. 61(1), 144-153.
[7] Guillot, I.; Bernard, P.; Rambeck, W. A. Influence of vitamin C on the retention of cadmium in turkeys. Tiergesundheitsdienst Bayern, Germany. Editors: Schubert, Flachowsky, Bitsch. Vitamine und Zusatzstoffe in der Ernaehrung von Mensch und Tier, Symposium, 5th, Jena, Sept. 28-29, 1995, 233-237.
[8] EPA Study on Nickel Releases from Burning Coal (The study shows about 10% of nickel in coal is released to the air. The press release estimates 10% of the other metals in coal with similar properties to nickel are also released to the air.) http://www.orthomolecular.org/12all/lt/t_go.php?i=61&e=MjQzMTM=&l=http://www.epa.gov/ttn/chief/le/nickel.pdf
[9] Lewinska, Anna; Bartosz, Grzegorz. Protection of yeast lacking the Ure2 protein against the toxicity of heavy metals and hydroperoxides by antioxidants. Free Radical Research, 2007. 41(5), 580-590.
[10] Saul AW. Vitamins and food supplements: safe and effective. Testimony before the Government of Canada, 38th Parliament, 1st Session, Standing Committee on Health. Ottawa, May 12, 2005. http://www.orthomolecular.org/12all/lt/t_go.php?i=61&e=MjQzMTM=&l=http://www.doctoryourself.com/testimony.htm
Vitamins are safe.
There is not even one death per year from vitamin supplementation. http://www.orthomolecular.org/12all/lt/t_go.php?i=61&e=MjQzMTM=&l=http://orthomolecular.org/resources/omns/v03n04.shtml
Nutritional Medicine is Orthomolecular Medicine
Linus Pauling defined orthomolecular medicine as "the treatment of disease by the provision of the optimum molecular environment, especially the optimum concentrations of substances normally present in the human body." Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org/12all/lt/t_go.php?i=61&e=MjQzMTM=&l=http://www.orthomolecular.org/
The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.
Editorial Review Board:
Abram Hoffer, M.D., Ph.D.Harold D. Foster, Ph.D.Bradford Weeks, M.D.Carolyn Dean, M.D., N.D.Erik Paterson, M.D.Thomas Levy, M.D., J.D.Steve Hickey, Ph.D.
Andrew W. Saul, Editor and contact person. email: drsaul@doctoryourself.com .
Tuesday, 9 October 2007
Monday, 1 October 2007
Friday, 28 September 2007
Journal Watch on limitations of Thimerosal Study in New England Journal
Thimerosal and Neurotoxicity
The effect of mercury exposure in children once again proves difficult to determine.
Considerable controversy surrounds the question of whether mercury preservatives in vaccines, such as thimerosal, are associated with impaired behaviors or cognition in children (see Journal Watch Psychiatry Aug 4 2004). These researchers examined 42 measures of neuropsychological and behavioral functioning in children aged 7 to 10 years from four HMOs. Using histories of vaccination, immunoglobulin experience, and other records, the researchers retrospectively calculated mercury exposure at three time points: neonatal (i.e., maternal), the first 28 days of life, and the first 7 months.
Children with low birth weight, meningitis, encephalitis, or other serious neurological diagnoses were excluded. The 1047 tested children represented only 30% of those eligible. Children of parents with the highest socioeconomic indicators had the highest exposure. Small yet significant negative and positive associations, some sex-specific, were identified between some individual neuropsychological tests and thimerosal exposure.
Comment: The authors, who expertly analyzed these data statistically, conclude that thimerosal does not produce meaningful clinical problems. However, the validity of this conclusion needs to be questioned because of possible confounding in the study sample. First, only 30% of cases were studied; how these cases may have differed from those who did not participate was not discussed. Second, the data were collected retrospectively. Third, the cases that were excluded — e.g., low-birth-weight babies — might be the ones most vulnerable to the effect of a neuroactive substance, but this issue was not addressed. Finally, the threshold dose for neurological impairment is unknown; therefore, to dismiss the vaccines given between ages 12 months and 7 years may be premature. Parents who ask about this issue still need to be informed of the complexities of studying this problem.
— Barbara Geller, MD
Published in Journal Watch Psychiatry September 26, 2007
Citation(s):
Thompson WW et al. Early thimerosal exposure and neuropsychological outcomes at 7 to 10 years. N Engl J Med 2007 Sep 27; 357:1281.
Original article (Subscription may be required)
Medline abstract (Free)
The effect of mercury exposure in children once again proves difficult to determine.
Considerable controversy surrounds the question of whether mercury preservatives in vaccines, such as thimerosal, are associated with impaired behaviors or cognition in children (see Journal Watch Psychiatry Aug 4 2004). These researchers examined 42 measures of neuropsychological and behavioral functioning in children aged 7 to 10 years from four HMOs. Using histories of vaccination, immunoglobulin experience, and other records, the researchers retrospectively calculated mercury exposure at three time points: neonatal (i.e., maternal), the first 28 days of life, and the first 7 months.
Children with low birth weight, meningitis, encephalitis, or other serious neurological diagnoses were excluded. The 1047 tested children represented only 30% of those eligible. Children of parents with the highest socioeconomic indicators had the highest exposure. Small yet significant negative and positive associations, some sex-specific, were identified between some individual neuropsychological tests and thimerosal exposure.
Comment: The authors, who expertly analyzed these data statistically, conclude that thimerosal does not produce meaningful clinical problems. However, the validity of this conclusion needs to be questioned because of possible confounding in the study sample. First, only 30% of cases were studied; how these cases may have differed from those who did not participate was not discussed. Second, the data were collected retrospectively. Third, the cases that were excluded — e.g., low-birth-weight babies — might be the ones most vulnerable to the effect of a neuroactive substance, but this issue was not addressed. Finally, the threshold dose for neurological impairment is unknown; therefore, to dismiss the vaccines given between ages 12 months and 7 years may be premature. Parents who ask about this issue still need to be informed of the complexities of studying this problem.
— Barbara Geller, MD
Published in Journal Watch Psychiatry September 26, 2007
Citation(s):
Thompson WW et al. Early thimerosal exposure and neuropsychological outcomes at 7 to 10 years. N Engl J Med 2007 Sep 27; 357:1281.
Original article (Subscription may be required)
Medline abstract (Free)
Thursday, 27 September 2007
Conflicts of interest in new CDC Thimerosal study
Dr. Thompson reports being a former employee of Merck; Dr. Marcy, receiving consulting fees from Merck, Sanofi Pasteur, GlaxoSmithKline, and MedImmune; Dr. Jackson, receiving grant support from Wyeth, Sanofi Pasteur, GlaxoSmithKline, and Novartis, lecture fees from Sanofi Pasteur, and consulting fees from Wyeth and Abbott and serving as a consultant to the FDA Vaccines and Related Biological Products Advisory Committee; Dr. Lieu, serving as a consultant to the CDC Advisory Committee on Immunization Practices; Dr. Black, receiving consulting fees from MedImmune, GlaxoSmithKline, Novartis, and Merck and grant support from MedImmune, GlaxoSmithKline, Aventis, Merck, and Novartis; and Dr. Davis receiving consulting fees from Merck and grant support from Merck and GlaxoSmithKline. No other potential conflict of interest relevant to this article was reported.
Toxic metal exposure and breast cancer
As a breast cancer sufferer in 1997 facing the horror that black diagnosis brings to your own life and your family, any research which can throw a light onto its causes and treatment is welcomed by me.
I was diagnosed with what the oncologist called a fast growing Grade 3 breast cancer in January 1997 and went on to have surgery in February, started a daily radiotherapy routine shortly after, then had months of chemotherapy and Tamoxifen.
Knowing the history now of heavy metals in vaccines, particularly Thimerosal with its 49.6% Mercury since 1930, and my own reaction to that vaccine as a baby, I am not surprised I ended up with jaundice as a teenager and breast cancer in my forties.
New ways of looking at the epidemic of these conditions and others including disorders such as ADHD, Autism, Tics, speech and language impairments, allergies etc are urgently needed.
In an advanced world with the Pharmaceutical Industry earning billions we should not have epidemics of such problems. Something seems to be going very wrong.
Perhaps we could start by looking at conflicts of interest with Big Pharma crossing boundaries in Government departments and funding the big studies whilst ignoring the clinical facts of individual cases.
Meanwhile its down to every individual to do their homework and make their own decisions about what they want to do with their own bodies.
http://www.townsendletter.com/AugSept2007/toxicmetalbreastcancer0807.htm
I was diagnosed with what the oncologist called a fast growing Grade 3 breast cancer in January 1997 and went on to have surgery in February, started a daily radiotherapy routine shortly after, then had months of chemotherapy and Tamoxifen.
Knowing the history now of heavy metals in vaccines, particularly Thimerosal with its 49.6% Mercury since 1930, and my own reaction to that vaccine as a baby, I am not surprised I ended up with jaundice as a teenager and breast cancer in my forties.
New ways of looking at the epidemic of these conditions and others including disorders such as ADHD, Autism, Tics, speech and language impairments, allergies etc are urgently needed.
In an advanced world with the Pharmaceutical Industry earning billions we should not have epidemics of such problems. Something seems to be going very wrong.
Perhaps we could start by looking at conflicts of interest with Big Pharma crossing boundaries in Government departments and funding the big studies whilst ignoring the clinical facts of individual cases.
Meanwhile its down to every individual to do their homework and make their own decisions about what they want to do with their own bodies.
http://www.townsendletter.com/AugSept2007/toxicmetalbreastcancer0807.htm
Wednesday, 26 September 2007
US CDC Thimerosal study report by David Kirby - "possible adverse association between neonatal exposure to mercury and language development."
Read David Kirby - Evidence of Harm - on this study and his conference call to the CDC today.
Despite the various flaws of the epidemiological study, which we are now becoming so used to in this extraordinary field, they are at least honest enough to admit to the adverse reactions.
http://www.huffingtonpost.com/david-kirby/cdc-mercury-in-vaccines-_b_66007.html
Despite the various flaws of the epidemiological study, which we are now becoming so used to in this extraordinary field, they are at least honest enough to admit to the adverse reactions.
http://www.huffingtonpost.com/david-kirby/cdc-mercury-in-vaccines-_b_66007.html
USA TODAY Generation Rescue AD - Less autism ADHD and Asthma in Unvaccinated kids
It has taken the parents of children in America to run the survey and then place an ADVERT in USA Today to get this crucailly important message out.
Why was the survey/study not done by the CDC? Why is it not done by the Department of Health in the UK? By WHO?
Why, when the survey was done, and the expected results found, would the media not pick up on it?
How bad does the epidemic of neurodevelopmental conditions and allergies have to get before the obvious issue is raised?
Not doing the obvious survey and media failure to not even publish the result when it is done,
does rather speak volumes.
Congratulations Generation Rescue. You are living up to your name.
http://www.generationrescue.org/pdf/070626.pdf
Why was the survey/study not done by the CDC? Why is it not done by the Department of Health in the UK? By WHO?
Why, when the survey was done, and the expected results found, would the media not pick up on it?
How bad does the epidemic of neurodevelopmental conditions and allergies have to get before the obvious issue is raised?
Not doing the obvious survey and media failure to not even publish the result when it is done,
does rather speak volumes.
Congratulations Generation Rescue. You are living up to your name.
http://www.generationrescue.org/pdf/070626.pdf
Anne Dachel and Dr Boyd Haley on Channel 13 - on how Thimerosal in vaccines can lead to autism
Channel 13 write up:
"When Ann Dachel of Eau Claire brought her son John in for a routine vaccination, she never expected his behavior was about to change."He didn't pick up on things around the time that he was 18 months to two-years-old, he wasn't speaking, he stopped babbling, I never would have connected that to vaccinations," Dachel said.But, after some research on her own, she soon did, discovering what she calls a clear connection between the increasing autism rate and rising exposure to vaccines with toxic substances like aluminum, MSG, formaldehyde and mercury."Our kids in the 1990's were getting just enormous load of mercury in their vaccines and that's when autism really exploded," she said.Ann's theory has some backing in the academic research world.
Dr. Boyd Haley, a leading University of Kentucky Researcher on the topic says thimerosal, a vaccine preservative with nearly 50 percent mercury has contributed to epidemic levels of autism in the US."Thimerosal is one of the most neuro-toxic compounds that's available or that we could even reasonably be exposed to, so common sense says you would look at that first and you would look at that very, very hard," Haley said.But, he says CDC research has been limited to population studies in Europe, areas he says don't have the high rate of vaccination we have here.He also says the CDC mandated the vaccine program in 1988 without any safety testing. However, according to a statement by the CDC scientific evidence does not support the idea that vaccine causes autism."The amount of mercury they are injecting into these babies on the day of birth would be safe by EPA standards eating fish, if the baby weighed 275 pounds," Haley said.
Dr. Haley says infants can't excrete mercury and though mercury isn't always found in the urine, hair or blood of children with autism, Arizona State Researchers have found considerably more mercury in their baby teeth than those without.Eau Claire Health Department Director Richard Thoune believes the benefits of vaccines, outweigh the risks.However, Dr. Haley says because of it's toxicity, the FDA took thimerosal off the market as a topical application in 1978, but it is still found in flu vaccine."
"When Ann Dachel of Eau Claire brought her son John in for a routine vaccination, she never expected his behavior was about to change."He didn't pick up on things around the time that he was 18 months to two-years-old, he wasn't speaking, he stopped babbling, I never would have connected that to vaccinations," Dachel said.But, after some research on her own, she soon did, discovering what she calls a clear connection between the increasing autism rate and rising exposure to vaccines with toxic substances like aluminum, MSG, formaldehyde and mercury."Our kids in the 1990's were getting just enormous load of mercury in their vaccines and that's when autism really exploded," she said.Ann's theory has some backing in the academic research world.
Dr. Boyd Haley, a leading University of Kentucky Researcher on the topic says thimerosal, a vaccine preservative with nearly 50 percent mercury has contributed to epidemic levels of autism in the US."Thimerosal is one of the most neuro-toxic compounds that's available or that we could even reasonably be exposed to, so common sense says you would look at that first and you would look at that very, very hard," Haley said.But, he says CDC research has been limited to population studies in Europe, areas he says don't have the high rate of vaccination we have here.He also says the CDC mandated the vaccine program in 1988 without any safety testing. However, according to a statement by the CDC scientific evidence does not support the idea that vaccine causes autism."The amount of mercury they are injecting into these babies on the day of birth would be safe by EPA standards eating fish, if the baby weighed 275 pounds," Haley said.
Dr. Haley says infants can't excrete mercury and though mercury isn't always found in the urine, hair or blood of children with autism, Arizona State Researchers have found considerably more mercury in their baby teeth than those without.Eau Claire Health Department Director Richard Thoune believes the benefits of vaccines, outweigh the risks.However, Dr. Haley says because of it's toxicity, the FDA took thimerosal off the market as a topical application in 1978, but it is still found in flu vaccine."
Thursday, 20 September 2007
Bolen Report - A new public health crisis - an epidemic of autism
Another new report - remember, you can't have a genetic epidemic, this has to be environmental.
http://www.bolenreport.net/feature_articles/feature_article061.htm
http://www.bolenreport.net/feature_articles/feature_article061.htm
The Autism Epidemic - finally the media starts to get it
Despite every effort by Governments to limit diagnoses of autism and dictate to Government professionals to 'not label' , like the efforts of the boy with his finger in the dyke, none of this has worked and we are now drowning in the tidal wave.
The number of children with autism has sky rocketed and even if Governments don't care about the suffering of the children and their families, they usually do care about money.
This tidal wave will bankrupt us all.
Finally it looks as if this message at least is getting out and as there are some responsible Media out there, the story is leaking out, at last.
http://www.mercurynews.com/politics/ci_6935084
The number of children with autism has sky rocketed and even if Governments don't care about the suffering of the children and their families, they usually do care about money.
This tidal wave will bankrupt us all.
Finally it looks as if this message at least is getting out and as there are some responsible Media out there, the story is leaking out, at last.
http://www.mercurynews.com/politics/ci_6935084
Tuesday, 14 August 2007
Cot Deaths and Vaccines - Child Protection turned on its head
Recently a new paper was published by Hey and Bacon on the sensitive subject of how many mothers might have murdered their babies who died of 'cot death'. Yet a known and well researched link (under a heavy cloak of commercial secrecy) is that of an adverse reaction to some vaccinations but this is never mentioned. Over the years there have been many forms of spin and shifting sands of blame and counter blame but none so deeply distressing as the accusation that a mother has killed her child.
What stands out when mothers are accused is that adverse reactions to vaccine are routinely NEVER included in the differential diagnosis. This is deeply worrying, as it is a well known form of iatrogenic abuse. However rare, it happens, but if we do not acknowledge that it happens, and could have happened to the child in question, then as all other possibilities fall away, the mother stands accused.
Over the last decade we have seen dramatic developments within legal circles when it was established that Professor Sir Roy Meadow gave a wrong statistic in the case of Sally Clark, the mother whose children died after vaccines were given. His 73 million to 1 statistic was applied to the possibility that the children could have died from natural causes. It shouted out the message that these were impossible odds, so the mother must have killed them. A possible link to vaccines was never even brought into the Court. Professor Meadow was struck off and then re-instated as Expert opinions are just opinions, after all.
Sally Clark has now died as well as two of her children and we now have another published paper by Hey and Bacon which has raised the issue again and appears to want to take us back to the old position that more mothers do kill their children, supporting Meadow's thinking, even though the statistic he used to back it up and the way in which he used it has been thoroughly discredited.
The recent Hey and Bacon BMJ (British Medical Journal) article was written about by various people and Nigel Hawkes at Times took up the story.
Times Online allows for comments and my own comment was published along with a medic who writes in support of Professor Sir Roy Meadow and the idea that murder is more common than recent legal cases and the media interpretations would have us believe.
A cynic might suggest that this was a clean up operation. A non cynic might say this was new research backing up Meadow's thinking about mothers and murder.
However, this was not new research and I was to discover that Hey and Bacon did not even have access to the records of the cases in the research by Carpenter et al.
I discovered this through information provided to me by a mother who also lost two sons to cot death following vaccines and whose children were in the research on which these various studies have been based. She was disturbed by this 'new' research and wrote to all of the authors of the original Carpenter paper and the more recent Bacon and Hey paper. Only Dr Bacon had the decency to reply. She also wrote to the Times Online.
Her lengthy, detailed and highly important contribution was not published.
She sent her letter to me and I am re-producing it below as it raises issues of enormous concern, not least the fact that ranks close in and parents are refused information about their children even though careers have been built on the data .
Dear Sir,
I write in response to Nigel Hawkes article in Times online
Cot Death Suspicions are revived
I am a mother who had 2 SIDS deaths many years ago and am shocked at this paper by Hey and Bacon as it leaves out far too much information to reach the position it reaches in its rather clumsy attempt to (yet again) blame mothers and exonerate medics. Perhaps I can help with some of the information that has been omitted. Perhaps the public might then start asking questions about this research.
I became aware many years after my children’s deaths that data in relation to them had been used in published research. I was taken aback by this as I had not been informed of their inclusion nor had the authors of these ‘papers’ sought permission from myself for their inclusion.
‘Data’ in relation to my children was apparently used in the original Emery paper.
This paper was revisited by Carpenter et al in 2005 – and discussed by Gornall.
Hey and Bacon’s recent paper is again a revisiting of Carpenter et al and the original paper.
I set about trying to discover exactly what apparent data in relation to my children had been used in these papers.
Initially I tried ‘locally’ to obtain records in relation to my children; I then discovered that records in relation to my children ‘could not be found’.
These included GP, Health Visitor, Clinic, Midwifery and Birth, Vaccination, Hospital admission, Outpatient and Ambulance records.
With regard to Post Mortem records, all that was available was a brief 2 page Official Coroners Record for each child, which gave scant details and a cause of death as SIDS for both children. I knew that there had to be a Post Mortem File in relation to each child which obviously contained specific details of my children’s Post Mortems i.e. tests carried out, date and time of PM, samples taken etc.
It later was confirmed that my children’s Post Mortem Files ‘could also not be found’.
There were 40+ SIDS deaths in my city area (including my own children) these 40+ deaths occurred within a total of 2 years. For a population of approx 250.000 this appeared to be a high incidence. In fact this is documented by a GP as being ‘a significant blip’.
I discovered that all 40+ SIDS victims Post Mortem Files apparently also ‘could not be found’. It was clear that Post Mortem samples and organs were retained from many of these SIDS victims (including my own). Though why this happened, what was being tested for and the results of these tests apparently ‘were not available’ or ‘could not be found’.
Given the ‘research’ being carried out in my area by SIDS researchers I find it impossible to believe records in relation to 40+ children apparently have simply ‘disappeared’.
My second child was enrolled pre birth in Care Of the Next Infant Programme.
I reasoned that as my children had apparently been included in Emery’s original paper and others, it was reasonable to assume that CONI and or the authors of these papers had access to the missing records in relation to my children.
To have apparently included my children in these papers without this data would be professional suicide and would mean the criticisms levied against these papers had great merit and warranted investigation.
This would also mean that Hey and Bacon’s recent paper could be open to the same criticism.
CONI researchers released to me the daily ‘tick’ charts (filled out by myself and my children’s father), they also released to me daily weight charts (again filled out by myself and my child’s father) and weekly Health Visitor Contact sheets along with a few other telephone and contact records.
I knew that to have apparently included my children in ‘research and these published papers’ the authors of these papers needed to have had more detailed information in relation to my children that that which was released.
However I was told in no uncertain terms that these were the only records held. I am astounded.
There was a clear protocol for a ‘death on CONI scheme’, (As outlined by Emery and others)
The original paper states:
We studied all deaths in 6373 infants who had completed the CONI programme by December, 1999. After a CONI death, we made detailed enquiries into the previous death and the CONI death, including a family interview, a review of autopsies, and case discussion.
My children died pre 1999 and so by default would have been included in this paper.
However those that released the few papers detailed above deny any involvement after my son’s death, they and the authors of these papers refuse to answer specific questions in relation to my children’s inclusion in these papers.
Those that released these scant records to me deny that any information in relation to my children’s deaths was obtained.
I find this hard to believe especially has I have already said that Emery had stated in ‘other papers’ that my children died from probable inborn metabolic disorder and or familial cause. How could he reach these conclusions WITHOUT these records?
Though the people that released these scant records deny obtaining any post mortem records or information in relation to my children, in the papers released to me by them there was one page of the Official Coroners record, this could only have been obtained either from the Pathologist or the Coroner, which tells me that CONI did indeed request/obtain records in relation to my children.
We were visited at home by one of the authors of these papers pre my son’s birth and post his death. (As per the protocol for birth and death on scheme.) Recruitment of my child’s GP, Health Visitor and Paediatricians was secured by this person in relation to co operation and participation in their research. (As per their own protocol).
If no records were obtained re my children’s deaths, then why the visit to us as per their own protocol, why the recruitment of the GP, Health Visitor and Paediatricians? Any data gathered would be useless as research, WITHOUT complete records in relation to my children’s lives and deaths. So far the person who visited has declined to answer.
John Emery, sadly now deceased, contacted the Pathologist on the day of my son’s Post Mortem. (Though researchers at CONI deny this contact took place, I have the evidence to show this contact did indeed take place)
If it is true that CONI/Emery did not contact the pathologist and that records were NOT collected in relation to my children, then my children’s apparent inclusion in these papers means that these papers are worthless as research, they are based on incomplete data, their own ‘protocols’ for a death on scheme were not followed and it also means that they could not possibly have reached the conclusions they did based on ‘evidence’.
I say it would also mean the revisiting of these papers by Carpenter et al and Bacon and Hey is based upon flawed data.
One has to ask how many other children’s data used in these papers is incomplete.
If they did indeed have this data in relation to my children, then this means that the authors of these papers are withholding this data from the parents of the children they have ‘researched’. Data that parents have a right to have, worse still, it maybe that this data may aid some parents in legal proceedings and that gross miscarriages of justice may have occurred. Data they are withholding.
As a parent this data is apparently not available locally in relation to my own children. Therefore it is reasonable to assume that there may be parents involved in legal proceedings whose records in relation to their children have also ‘gone missing’. These parents, like my self previously, may not be aware that this data is apparently held or at least accessible by the authors of these papers. I certainly would not have been aware of my children’s apparent inclusion in published papers if I had not set about this path in recent years. The authors of these papers certainly do not volunteer this information to parents.
As I have said if the authors of these papers did not have this data in relation to my children and included them in research papers without this data, then these papers are worthless as research and deserve the criticisms levied against them. If Bacon and Hey also used incomplete data then they too will deserve such criticisms.
They CANNOT have it both ways.
I have contacted the authors of these papers in recent months and put it to them that to have apparently included my children in these papers, the authors must have been in possession of the entire records in relation to my children. I put it to them that to have apparently included my children in these papers based on the scant records released by CONI would have been professional suicide.
I have asked the authors of these papers to confirm or deny that my children were included in any of these papers, to date they have not even acknowledged my request. I have been stone walled by these ‘authors’.
I also put it them that in relation to my own children ‘they made detailed enquiries into the previous death and the CONI death, including a family interview, a review of autopsies, and case discussions took place’. I put it too them that I could not believe that their own protocols were not followed in relation to my own child’s death. A family interview did indeed take place pre and post my child’s death. Was I really expected to believe that a review of autopsy, detailed enquiries and case discussions did not take place? I think not.
I asked the authors of these papers what form the detailed enquries into my children’s lives and deaths took, were records and samples obtained? I asked if a review of my own children’s autopsies had taken place and what this entailed, I asked if a case discussion had taken place in relation to my own children and what data was used in these ‘discussions’. I asked the authors of these papers to release to me any and all data that they had used in preparation of these papers in accordance with their own protocols, relating to my own children…….. 2 months later I am still awaiting a response.
Certain quarters have actually told me that they now refuse to acknowledge or answer my questions, concerns or requests.
The point is that the authors of these papers CANNOT have it both ways. They either have these records or they don’t.
They either based these papers on complete data or they didn’t.
They included my children or they didn’t.
I say that these papers are not open to scrutiny by the very parents of the children they include.
With regards to Professor Meadow being right or wrong, I have evidence to show that in my area the SIDS rate was relatively high, especially amongst the Royal Naval Community. In at least 3 military married quarter estates there were a higher percentage of SIDS deaths then amongst the civilian population. In one area alone there were over 6 SIDS deaths in just over 18 months.
I am in possession of a letter from a Pathologist which states:
These multiple SIDS cases are very worrying. We have had several down here of three’s and fours and despite every care it seems impossible to do anything about it. All of the investigations seem to turn out negative and we even had one who was admitted to hospital because the parents were thought to be responsible and the baby died suddenly in the ward.
My city was one of 10 areas that was aiding and assisting SIDs researchers. It is clear that some of the authors of these papers were actively involved in research in my own area at the time of my children’s deaths in fact at the time of all 40+ SIDS deaths. Is it coincidence that the post mortem files in relation to these children ‘cannot be found’?
It is also clear that parental involvement within the deaths in my own area was foremost in the minds of all professionals involved. I have data that shows that parental involvement in these deaths was investigated and signs and symptoms of abuse actively sought.
In 2 years in one city it is clear that there were other families that had suffered 2 SIDS deaths. (This is confirmed by ‘other sources’) Families that had little or no connection with each other and families that lived in separate parts of the city. The only real connection between them being that the majority of deaths were amongst the military community.
To say that the chance of 2 SIDs deaths is rare is disproved by events in my own city.
With regards to Ms Blakemore Brown’s response:
My own child died within 36 hours of having his vaccines. My first child died approx 2 weeks after vaccines. I know of one other family (in my own city) whose child died within 24 hours of having vaccines. The parents were convinced that their child died as a result of the vaccines and actually told the pathologist when he gave the cause of death as SIDS that they thought there had been a ‘cover up’.
I have recently had released to me vaccination records for my children, (records that have taken over 5+ years to get released, records whose very existence was denied 5+ years ago) these say that I gave permission for my child to have his vaccines 2 weeks after he died! Why would I give permission for a dead child to have vaccines? There are other worrying discrepancies.
I find it interesting that the majority of deaths within my own area occurred on or around the time of vaccines being due. I understand that one ‘batch’ of these vaccines would have been enough to vaccinate the children of my own city. Was this a ‘hot’ lot?
Maybe the authors of these papers need to look at these issues; I would be interested to know why the subject of vaccine involvement in SIDS is completely ignored in these papers.
What is clear is that the authors of these papers do not take kindly to parents asking questions re their children’s data. Preferring to completely ignore parental requests, concerns and questions. I have been effectively stone walled by these authors. Why is that I have to ask?
Surely if the system is now, yet again, being encouraged to think of mothers as murderers, the authors of these papers cannot be selective in their reporting nor can theses authors base their reporting on incomplete data. Mothers like me, who have lost babies, fully welcome any discussions and research into the causes of their deaths but please don’t demonise and patronise us. We just need the truth.
Many thanks
A mum
Devon
25.07.07
I would like to make an addition to my response:
Carpenter said in his 2005 paper:
Repeat sudden unexpected and unexplained infant deaths: natural or unnatural
http://www.firstcandle.org/FC-PDF4/Research_Recent%20Studies/Infanticide%20or%20SIDS.pdf
We studied all deaths in 6373 infants who had completed the CONI programme by December 1999
Carpenter clarifies this further in this paper:
The Care of Next Infant (CONI) scheme, which started in
1988, was available in 75% of health districts in England,
Wales, and Northern Ireland by 1994 and is currently
available in 91%.
My second child was enrolled in this programme pre birth pre 1988. 1 other surviving child was enrolled pre 1988. This 'programme' was certainly up and running pre 1988. The name of the programme changed over time.
It seems that the Carpenter et al paper also cannot be taken seriously, setting aside my earlier concerns above, Carpenter et al have apparently only included babies since 1988, when Emery’s original paper apparently included babies that had died much earlier (including my own). If this is supposed to be a serious reworking of Emery’s original paper then Carpenter et al cannot be selective in what they leave out. Omitting whole years of data calls into question the credibility of this paper.
Emery said in his 1993 paper:
Acta Paediatr. 1993 Oct;82(10):873-6. Links
Recurrence of unexpected infant death.
Wolkind S, Taylor EM, Waite AJ, Dalton M, Emery JL.
Maudsley Hospital, London, UK.
Families which had experienced two or more unexpected infant deaths were the subject of detailed confidential enquiries, including necropsy examination. Cases were derived from two main sources: first, deaths occurring during a nationwide programme of support for families with a subsequent baby (8 families) plus 2 families from a series of confidential enquiries in Sheffield, and second, direct referrals from paediatricians (17 families). Fifty-seven deaths were studied. Twenty-four families had experienced 2 and three had experienced 3 deaths; 11 deaths (19%) were found to be adequately explained by history or post-mortem findings; 7 (12%) were probably accidental; 31 (55%) were most probably due to an action by one of the parents (filicide); only 5 (9%) were considered to be true or idiopathic sudden infant death syndrome; in 3 (5%) cases there was insufficient information to draw a conclusion. Five (18%) of the families lived in circumstances of serious social deprivation. A history of psychiatric illness was present in one or both parents in 18 (67%) of the families.
I say that Emery included my children in this paper.
However if he did not then why not? If this is the case then these papers are indeed selective in the children they represent.
I cannot get the authors of these papers to confirm of deny that data from my children was used in ANY of these papers, they refuse to answer and prefer silence.
A simple confirmation or denial as to my children’s inclusion and their data by these authors would be nice; surely I am allowed to know what research my children were involved in?
Or is it that I have them between a rock and a hard place? To say that they did seek detailed data from my children would mean that I have been lied to (and can prove it), it would mean that data has been withheld from me and it would also mean that permission was NOT sought from myself to seek and include this data which would open these ‘authors’ up to litigation. Or,
If they didn’t seek this information then this opens up these papers to legitimate criticism.
As a further addendum:
I emailed Dr Bacon:
This is his response:Dear XXXXXXX Thank you for your email. What you've told me is most distressing, and I should certainly like to help you if I could. However I'm afraid I'm not in a position myself to provide the information you seek. In preparing our paper Dr Hey and I used only the information given in the report by Professor Carpenter. We didn't know the identity of any of the cases, and we didn't see any other medical records or notes. Professor Carpenter states that his team studied all the available information about each case, but I don't know whether this always included the medical records. He or XXXXXX, who was in the team, could best advise you on this. In the 1980s, when cases were used in research, copies of the medical records were sometimes made for the researchers, while the originals stayed in the hospital where the patient was treated. Or sometimes the original notes were loaned out to the researchers on the understanding that they'd be returned later. Parents are now entitled to see the hospital medical records (which would normally include any post-mortem reports) of their children unless it's considered against the children's interest. You've probablyalready approached the hospital where your babies were taken when they died, but if you haven't, that's certainly worth trying. There may be a problem if the records have gone astray or have been routinely destroyed after a certain period. I don't know when you were last in contact with XXXXX, who coordinates the CONI programme. Most parents find her very helpful, and I'm sending her a copy of our email correspondence so that she can advise you if you decide to approach her again. I hope that this is some help, and that you'll be able to find some respite from the distress you've had for so many years. Yours sincerely, Christopher Bacon I would like to thank Dr Bacon for his response; he is the only one that has responded. However it is clear that Dr Bacon was not in possession of the records in relation to these children he simply based his ‘report’ on the Carpenter paper. The question has to be asked, what ‘data’ did Carpenter et al base their ‘paper’ upon? Given the ‘evidence’ I have gathered it seems that Carpenter et al based their ‘paper’ on incomplete data? I have approached XXXXX at CONI, however I am told NOT to contact her again and only contact her ‘Risk Management Officer’. Her ‘Risk Management Officer’ refuses to acknowledge my requests let alone respond to them. Why this heavy handed treatment when all I ask is reasonable legitimate questions in relation to my children, surely I have a right to know? I have approached Prof Carpenter and the co authors of the paper, 2+ months later I am still awaiting an acknowledgement, let alone a response. What is clear is that the ‘authors’ of these papers do not like parents asking questions about their children’s ‘data’ and its inclusion in ‘research’. I am treated appallingly by the very people who profess to care for parents like myself, why? …….Because I am asking difficult questions.
What stands out when mothers are accused is that adverse reactions to vaccine are routinely NEVER included in the differential diagnosis. This is deeply worrying, as it is a well known form of iatrogenic abuse. However rare, it happens, but if we do not acknowledge that it happens, and could have happened to the child in question, then as all other possibilities fall away, the mother stands accused.
Over the last decade we have seen dramatic developments within legal circles when it was established that Professor Sir Roy Meadow gave a wrong statistic in the case of Sally Clark, the mother whose children died after vaccines were given. His 73 million to 1 statistic was applied to the possibility that the children could have died from natural causes. It shouted out the message that these were impossible odds, so the mother must have killed them. A possible link to vaccines was never even brought into the Court. Professor Meadow was struck off and then re-instated as Expert opinions are just opinions, after all.
Sally Clark has now died as well as two of her children and we now have another published paper by Hey and Bacon which has raised the issue again and appears to want to take us back to the old position that more mothers do kill their children, supporting Meadow's thinking, even though the statistic he used to back it up and the way in which he used it has been thoroughly discredited.
The recent Hey and Bacon BMJ (British Medical Journal) article was written about by various people and Nigel Hawkes at Times took up the story.
Times Online allows for comments and my own comment was published along with a medic who writes in support of Professor Sir Roy Meadow and the idea that murder is more common than recent legal cases and the media interpretations would have us believe.
A cynic might suggest that this was a clean up operation. A non cynic might say this was new research backing up Meadow's thinking about mothers and murder.
However, this was not new research and I was to discover that Hey and Bacon did not even have access to the records of the cases in the research by Carpenter et al.
I discovered this through information provided to me by a mother who also lost two sons to cot death following vaccines and whose children were in the research on which these various studies have been based. She was disturbed by this 'new' research and wrote to all of the authors of the original Carpenter paper and the more recent Bacon and Hey paper. Only Dr Bacon had the decency to reply. She also wrote to the Times Online.
Her lengthy, detailed and highly important contribution was not published.
She sent her letter to me and I am re-producing it below as it raises issues of enormous concern, not least the fact that ranks close in and parents are refused information about their children even though careers have been built on the data .
Dear Sir,
I write in response to Nigel Hawkes article in Times online
Cot Death Suspicions are revived
I am a mother who had 2 SIDS deaths many years ago and am shocked at this paper by Hey and Bacon as it leaves out far too much information to reach the position it reaches in its rather clumsy attempt to (yet again) blame mothers and exonerate medics. Perhaps I can help with some of the information that has been omitted. Perhaps the public might then start asking questions about this research.
I became aware many years after my children’s deaths that data in relation to them had been used in published research. I was taken aback by this as I had not been informed of their inclusion nor had the authors of these ‘papers’ sought permission from myself for their inclusion.
‘Data’ in relation to my children was apparently used in the original Emery paper.
This paper was revisited by Carpenter et al in 2005 – and discussed by Gornall.
Hey and Bacon’s recent paper is again a revisiting of Carpenter et al and the original paper.
I set about trying to discover exactly what apparent data in relation to my children had been used in these papers.
Initially I tried ‘locally’ to obtain records in relation to my children; I then discovered that records in relation to my children ‘could not be found’.
These included GP, Health Visitor, Clinic, Midwifery and Birth, Vaccination, Hospital admission, Outpatient and Ambulance records.
With regard to Post Mortem records, all that was available was a brief 2 page Official Coroners Record for each child, which gave scant details and a cause of death as SIDS for both children. I knew that there had to be a Post Mortem File in relation to each child which obviously contained specific details of my children’s Post Mortems i.e. tests carried out, date and time of PM, samples taken etc.
It later was confirmed that my children’s Post Mortem Files ‘could also not be found’.
There were 40+ SIDS deaths in my city area (including my own children) these 40+ deaths occurred within a total of 2 years. For a population of approx 250.000 this appeared to be a high incidence. In fact this is documented by a GP as being ‘a significant blip’.
I discovered that all 40+ SIDS victims Post Mortem Files apparently also ‘could not be found’. It was clear that Post Mortem samples and organs were retained from many of these SIDS victims (including my own). Though why this happened, what was being tested for and the results of these tests apparently ‘were not available’ or ‘could not be found’.
Given the ‘research’ being carried out in my area by SIDS researchers I find it impossible to believe records in relation to 40+ children apparently have simply ‘disappeared’.
My second child was enrolled pre birth in Care Of the Next Infant Programme.
I reasoned that as my children had apparently been included in Emery’s original paper and others, it was reasonable to assume that CONI and or the authors of these papers had access to the missing records in relation to my children.
To have apparently included my children in these papers without this data would be professional suicide and would mean the criticisms levied against these papers had great merit and warranted investigation.
This would also mean that Hey and Bacon’s recent paper could be open to the same criticism.
CONI researchers released to me the daily ‘tick’ charts (filled out by myself and my children’s father), they also released to me daily weight charts (again filled out by myself and my child’s father) and weekly Health Visitor Contact sheets along with a few other telephone and contact records.
I knew that to have apparently included my children in ‘research and these published papers’ the authors of these papers needed to have had more detailed information in relation to my children that that which was released.
However I was told in no uncertain terms that these were the only records held. I am astounded.
There was a clear protocol for a ‘death on CONI scheme’, (As outlined by Emery and others)
The original paper states:
We studied all deaths in 6373 infants who had completed the CONI programme by December, 1999. After a CONI death, we made detailed enquiries into the previous death and the CONI death, including a family interview, a review of autopsies, and case discussion.
My children died pre 1999 and so by default would have been included in this paper.
However those that released the few papers detailed above deny any involvement after my son’s death, they and the authors of these papers refuse to answer specific questions in relation to my children’s inclusion in these papers.
Those that released these scant records to me deny that any information in relation to my children’s deaths was obtained.
I find this hard to believe especially has I have already said that Emery had stated in ‘other papers’ that my children died from probable inborn metabolic disorder and or familial cause. How could he reach these conclusions WITHOUT these records?
Though the people that released these scant records deny obtaining any post mortem records or information in relation to my children, in the papers released to me by them there was one page of the Official Coroners record, this could only have been obtained either from the Pathologist or the Coroner, which tells me that CONI did indeed request/obtain records in relation to my children.
We were visited at home by one of the authors of these papers pre my son’s birth and post his death. (As per the protocol for birth and death on scheme.) Recruitment of my child’s GP, Health Visitor and Paediatricians was secured by this person in relation to co operation and participation in their research. (As per their own protocol).
If no records were obtained re my children’s deaths, then why the visit to us as per their own protocol, why the recruitment of the GP, Health Visitor and Paediatricians? Any data gathered would be useless as research, WITHOUT complete records in relation to my children’s lives and deaths. So far the person who visited has declined to answer.
John Emery, sadly now deceased, contacted the Pathologist on the day of my son’s Post Mortem. (Though researchers at CONI deny this contact took place, I have the evidence to show this contact did indeed take place)
If it is true that CONI/Emery did not contact the pathologist and that records were NOT collected in relation to my children, then my children’s apparent inclusion in these papers means that these papers are worthless as research, they are based on incomplete data, their own ‘protocols’ for a death on scheme were not followed and it also means that they could not possibly have reached the conclusions they did based on ‘evidence’.
I say it would also mean the revisiting of these papers by Carpenter et al and Bacon and Hey is based upon flawed data.
One has to ask how many other children’s data used in these papers is incomplete.
If they did indeed have this data in relation to my children, then this means that the authors of these papers are withholding this data from the parents of the children they have ‘researched’. Data that parents have a right to have, worse still, it maybe that this data may aid some parents in legal proceedings and that gross miscarriages of justice may have occurred. Data they are withholding.
As a parent this data is apparently not available locally in relation to my own children. Therefore it is reasonable to assume that there may be parents involved in legal proceedings whose records in relation to their children have also ‘gone missing’. These parents, like my self previously, may not be aware that this data is apparently held or at least accessible by the authors of these papers. I certainly would not have been aware of my children’s apparent inclusion in published papers if I had not set about this path in recent years. The authors of these papers certainly do not volunteer this information to parents.
As I have said if the authors of these papers did not have this data in relation to my children and included them in research papers without this data, then these papers are worthless as research and deserve the criticisms levied against them. If Bacon and Hey also used incomplete data then they too will deserve such criticisms.
They CANNOT have it both ways.
I have contacted the authors of these papers in recent months and put it to them that to have apparently included my children in these papers, the authors must have been in possession of the entire records in relation to my children. I put it to them that to have apparently included my children in these papers based on the scant records released by CONI would have been professional suicide.
I have asked the authors of these papers to confirm or deny that my children were included in any of these papers, to date they have not even acknowledged my request. I have been stone walled by these ‘authors’.
I also put it them that in relation to my own children ‘they made detailed enquiries into the previous death and the CONI death, including a family interview, a review of autopsies, and case discussions took place’. I put it too them that I could not believe that their own protocols were not followed in relation to my own child’s death. A family interview did indeed take place pre and post my child’s death. Was I really expected to believe that a review of autopsy, detailed enquiries and case discussions did not take place? I think not.
I asked the authors of these papers what form the detailed enquries into my children’s lives and deaths took, were records and samples obtained? I asked if a review of my own children’s autopsies had taken place and what this entailed, I asked if a case discussion had taken place in relation to my own children and what data was used in these ‘discussions’. I asked the authors of these papers to release to me any and all data that they had used in preparation of these papers in accordance with their own protocols, relating to my own children…….. 2 months later I am still awaiting a response.
Certain quarters have actually told me that they now refuse to acknowledge or answer my questions, concerns or requests.
The point is that the authors of these papers CANNOT have it both ways. They either have these records or they don’t.
They either based these papers on complete data or they didn’t.
They included my children or they didn’t.
I say that these papers are not open to scrutiny by the very parents of the children they include.
With regards to Professor Meadow being right or wrong, I have evidence to show that in my area the SIDS rate was relatively high, especially amongst the Royal Naval Community. In at least 3 military married quarter estates there were a higher percentage of SIDS deaths then amongst the civilian population. In one area alone there were over 6 SIDS deaths in just over 18 months.
I am in possession of a letter from a Pathologist which states:
These multiple SIDS cases are very worrying. We have had several down here of three’s and fours and despite every care it seems impossible to do anything about it. All of the investigations seem to turn out negative and we even had one who was admitted to hospital because the parents were thought to be responsible and the baby died suddenly in the ward.
My city was one of 10 areas that was aiding and assisting SIDs researchers. It is clear that some of the authors of these papers were actively involved in research in my own area at the time of my children’s deaths in fact at the time of all 40+ SIDS deaths. Is it coincidence that the post mortem files in relation to these children ‘cannot be found’?
It is also clear that parental involvement within the deaths in my own area was foremost in the minds of all professionals involved. I have data that shows that parental involvement in these deaths was investigated and signs and symptoms of abuse actively sought.
In 2 years in one city it is clear that there were other families that had suffered 2 SIDS deaths. (This is confirmed by ‘other sources’) Families that had little or no connection with each other and families that lived in separate parts of the city. The only real connection between them being that the majority of deaths were amongst the military community.
To say that the chance of 2 SIDs deaths is rare is disproved by events in my own city.
With regards to Ms Blakemore Brown’s response:
My own child died within 36 hours of having his vaccines. My first child died approx 2 weeks after vaccines. I know of one other family (in my own city) whose child died within 24 hours of having vaccines. The parents were convinced that their child died as a result of the vaccines and actually told the pathologist when he gave the cause of death as SIDS that they thought there had been a ‘cover up’.
I have recently had released to me vaccination records for my children, (records that have taken over 5+ years to get released, records whose very existence was denied 5+ years ago) these say that I gave permission for my child to have his vaccines 2 weeks after he died! Why would I give permission for a dead child to have vaccines? There are other worrying discrepancies.
I find it interesting that the majority of deaths within my own area occurred on or around the time of vaccines being due. I understand that one ‘batch’ of these vaccines would have been enough to vaccinate the children of my own city. Was this a ‘hot’ lot?
Maybe the authors of these papers need to look at these issues; I would be interested to know why the subject of vaccine involvement in SIDS is completely ignored in these papers.
What is clear is that the authors of these papers do not take kindly to parents asking questions re their children’s data. Preferring to completely ignore parental requests, concerns and questions. I have been effectively stone walled by these authors. Why is that I have to ask?
Surely if the system is now, yet again, being encouraged to think of mothers as murderers, the authors of these papers cannot be selective in their reporting nor can theses authors base their reporting on incomplete data. Mothers like me, who have lost babies, fully welcome any discussions and research into the causes of their deaths but please don’t demonise and patronise us. We just need the truth.
Many thanks
A mum
Devon
25.07.07
I would like to make an addition to my response:
Carpenter said in his 2005 paper:
Repeat sudden unexpected and unexplained infant deaths: natural or unnatural
http://www.firstcandle.org/FC-PDF4/Research_Recent%20Studies/Infanticide%20or%20SIDS.pdf
We studied all deaths in 6373 infants who had completed the CONI programme by December 1999
Carpenter clarifies this further in this paper:
The Care of Next Infant (CONI) scheme, which started in
1988, was available in 75% of health districts in England,
Wales, and Northern Ireland by 1994 and is currently
available in 91%.
My second child was enrolled in this programme pre birth pre 1988. 1 other surviving child was enrolled pre 1988. This 'programme' was certainly up and running pre 1988. The name of the programme changed over time.
It seems that the Carpenter et al paper also cannot be taken seriously, setting aside my earlier concerns above, Carpenter et al have apparently only included babies since 1988, when Emery’s original paper apparently included babies that had died much earlier (including my own). If this is supposed to be a serious reworking of Emery’s original paper then Carpenter et al cannot be selective in what they leave out. Omitting whole years of data calls into question the credibility of this paper.
Emery said in his 1993 paper:
Acta Paediatr. 1993 Oct;82(10):873-6. Links
Recurrence of unexpected infant death.
Wolkind S, Taylor EM, Waite AJ, Dalton M, Emery JL.
Maudsley Hospital, London, UK.
Families which had experienced two or more unexpected infant deaths were the subject of detailed confidential enquiries, including necropsy examination. Cases were derived from two main sources: first, deaths occurring during a nationwide programme of support for families with a subsequent baby (8 families) plus 2 families from a series of confidential enquiries in Sheffield, and second, direct referrals from paediatricians (17 families). Fifty-seven deaths were studied. Twenty-four families had experienced 2 and three had experienced 3 deaths; 11 deaths (19%) were found to be adequately explained by history or post-mortem findings; 7 (12%) were probably accidental; 31 (55%) were most probably due to an action by one of the parents (filicide); only 5 (9%) were considered to be true or idiopathic sudden infant death syndrome; in 3 (5%) cases there was insufficient information to draw a conclusion. Five (18%) of the families lived in circumstances of serious social deprivation. A history of psychiatric illness was present in one or both parents in 18 (67%) of the families.
I say that Emery included my children in this paper.
However if he did not then why not? If this is the case then these papers are indeed selective in the children they represent.
I cannot get the authors of these papers to confirm of deny that data from my children was used in ANY of these papers, they refuse to answer and prefer silence.
A simple confirmation or denial as to my children’s inclusion and their data by these authors would be nice; surely I am allowed to know what research my children were involved in?
Or is it that I have them between a rock and a hard place? To say that they did seek detailed data from my children would mean that I have been lied to (and can prove it), it would mean that data has been withheld from me and it would also mean that permission was NOT sought from myself to seek and include this data which would open these ‘authors’ up to litigation. Or,
If they didn’t seek this information then this opens up these papers to legitimate criticism.
As a further addendum:
I emailed Dr Bacon:
This is his response:Dear XXXXXXX Thank you for your email. What you've told me is most distressing, and I should certainly like to help you if I could. However I'm afraid I'm not in a position myself to provide the information you seek. In preparing our paper Dr Hey and I used only the information given in the report by Professor Carpenter. We didn't know the identity of any of the cases, and we didn't see any other medical records or notes. Professor Carpenter states that his team studied all the available information about each case, but I don't know whether this always included the medical records. He or XXXXXX, who was in the team, could best advise you on this. In the 1980s, when cases were used in research, copies of the medical records were sometimes made for the researchers, while the originals stayed in the hospital where the patient was treated. Or sometimes the original notes were loaned out to the researchers on the understanding that they'd be returned later. Parents are now entitled to see the hospital medical records (which would normally include any post-mortem reports) of their children unless it's considered against the children's interest. You've probablyalready approached the hospital where your babies were taken when they died, but if you haven't, that's certainly worth trying. There may be a problem if the records have gone astray or have been routinely destroyed after a certain period. I don't know when you were last in contact with XXXXX, who coordinates the CONI programme. Most parents find her very helpful, and I'm sending her a copy of our email correspondence so that she can advise you if you decide to approach her again. I hope that this is some help, and that you'll be able to find some respite from the distress you've had for so many years. Yours sincerely, Christopher Bacon I would like to thank Dr Bacon for his response; he is the only one that has responded. However it is clear that Dr Bacon was not in possession of the records in relation to these children he simply based his ‘report’ on the Carpenter paper. The question has to be asked, what ‘data’ did Carpenter et al base their ‘paper’ upon? Given the ‘evidence’ I have gathered it seems that Carpenter et al based their ‘paper’ on incomplete data? I have approached XXXXX at CONI, however I am told NOT to contact her again and only contact her ‘Risk Management Officer’. Her ‘Risk Management Officer’ refuses to acknowledge my requests let alone respond to them. Why this heavy handed treatment when all I ask is reasonable legitimate questions in relation to my children, surely I have a right to know? I have approached Prof Carpenter and the co authors of the paper, 2+ months later I am still awaiting an acknowledgement, let alone a response. What is clear is that the ‘authors’ of these papers do not like parents asking questions about their children’s ‘data’ and its inclusion in ‘research’. I am treated appallingly by the very people who profess to care for parents like myself, why? …….Because I am asking difficult questions.
Saturday, 21 July 2007
Friday, 20 July 2007
Dan Olmsted on 'the story of a lifetime'- environmentally induced autism
Dan has written 113 articles on this issue and even though this will be his last for UPI, he will not be stopping writing about Autism and its causes.
His concerns were raised early on when he found that there had been NO STUDIES of vaccinated versus unvaccinated children. WHY???
http://www.upi.com/inc/view.php?StoryID=20070717-103005-5761r
His concerns were raised early on when he found that there had been NO STUDIES of vaccinated versus unvaccinated children. WHY???
http://www.upi.com/inc/view.php?StoryID=20070717-103005-5761r
Sunday, 15 July 2007
MMR, Mercury and the Mystery surrounding my book
Tomorrow at the General Medical Council will start the case against Dr Andrew Wakefield and two other Doctors who raised concerns about children they assessed in the nineties, very worried that the problems they found were linked to adverse reactions to the MMR vaccine.
As there has been an almighty reaction by the Pharmaceutical lobby there has been NO public debate on exactly what has been going on.
In my book, Reweaving the Autistic Tapestry, having seen too many children with what I called 'tapestry impairments' many of which developed following the DTP and in fewer cases, the MMR, I suggested there may be a 'tapestry' causal effect with vaccines as one thread.
I mentioned Thimerosal and included some lawyers details here and in the US.
The launch of the book was at a CHADD conference in Anaheim California in October 2001. Eli Lilly were on the next stand and bought a copy of the book.
On my return to the UK there was no contact from the publisher.
Within weeks of my book being published parents were being told by Amazon that it was a 'rare book' and that it would take a year to get and would cost $79 plus post and packing!!!
There were none in the shops.
There were none in the warehouses of the retailers.
There were none in the Distributors.
The UK National Autistic Society carry all the books on Autism - except mine.
Probably nothing to do with my concerns about the vaccine, a small part of the book incidentally, or about my concern about the use of the label Munchausen Syndrome by proxy when children were genuinely ill - many had suffered reactions to vaccines. The fact that during the time my Editor was working on the book he was invited to change jobs and work on the MSBP/Factitious Illness Guidlelines at the RCPCH - Royal College of Paediatrics and Child Health, I am sure was total coincidence.
Guess I'm just paranoid when it comes to the things done by the powerful vaccine lobby and the need to protect the vaccine programme more than the public...
Prior to the documentary My Family and Autism being aired on the BBC, over a year after the trip to Anaheim, in which I am seen undertaking an assessment, I was able to at least get the book made more accessible.
If just one person is allowed to speak about their concerns without being leapt on from a great height, I might have confidence that the vaccine programme is safe - but I think they have gone too far and protested too much.
We all now want to know WHY???
As there has been an almighty reaction by the Pharmaceutical lobby there has been NO public debate on exactly what has been going on.
In my book, Reweaving the Autistic Tapestry, having seen too many children with what I called 'tapestry impairments' many of which developed following the DTP and in fewer cases, the MMR, I suggested there may be a 'tapestry' causal effect with vaccines as one thread.
I mentioned Thimerosal and included some lawyers details here and in the US.
The launch of the book was at a CHADD conference in Anaheim California in October 2001. Eli Lilly were on the next stand and bought a copy of the book.
On my return to the UK there was no contact from the publisher.
Within weeks of my book being published parents were being told by Amazon that it was a 'rare book' and that it would take a year to get and would cost $79 plus post and packing!!!
There were none in the shops.
There were none in the warehouses of the retailers.
There were none in the Distributors.
The UK National Autistic Society carry all the books on Autism - except mine.
Probably nothing to do with my concerns about the vaccine, a small part of the book incidentally, or about my concern about the use of the label Munchausen Syndrome by proxy when children were genuinely ill - many had suffered reactions to vaccines. The fact that during the time my Editor was working on the book he was invited to change jobs and work on the MSBP/Factitious Illness Guidlelines at the RCPCH - Royal College of Paediatrics and Child Health, I am sure was total coincidence.
Guess I'm just paranoid when it comes to the things done by the powerful vaccine lobby and the need to protect the vaccine programme more than the public...
Prior to the documentary My Family and Autism being aired on the BBC, over a year after the trip to Anaheim, in which I am seen undertaking an assessment, I was able to at least get the book made more accessible.
If just one person is allowed to speak about their concerns without being leapt on from a great height, I might have confidence that the vaccine programme is safe - but I think they have gone too far and protested too much.
We all now want to know WHY???
Florida Today on Weldon's victory to take Mercury out of flu vaccines " Mercury is a neurotoxin"
"Mercury is a neurotoxin considered harmful to the developing central nervous system of fetuses and infants."
http://www.floridatoday.com/apps/pbcs.dll/article?AID=/20070713/BUSINESS/707130334/1003
http://www.floridatoday.com/apps/pbcs.dll/article?AID=/20070713/BUSINESS/707130334/1003
Monday, 9 July 2007
'Chemical exposure' linked to autism - MERCURY IN VACCINES???
At last it seems to be dawning on the very slow UK autism specialists and the media - myself excluded, as I have been saying this for years - that there is a much higher rate of autism than ever before - 1 in 58 now, yet 1 in 10,000 not so long ago. That represents AN EPIDEMIC of a totally debilitating disorder often accompanied by serious immune system impairments and painful bowel conditions. Asthma and ADHD are often part of what I have termed the 'tapestry' of disorders on the rise in our so called civilised Western world.
You cannot have genetic epidemics, so this is something else - and it is too rapid and large an increase to just be better diagnosis, especially in a country where politicians have tried to prevent diagnoses of autism by various means.
Simon Baron-C0hen who has inherited the genetic condition of sitting on the fence until the dust dies down - unlike his cousin Sasha - nevertheless is willing to whisper that maaayyybbbeee.... chemical exposure through pollutants could have something to do with this massive increase.
At last we have at least ONE answer which fits with concerns about certain vaccines and their effect on the developing system. Deadly toxic MERCURY, astonishingly, has been used in vaccines since 1930.
It forms 49.6% of the preservative THIMEROSAL.
This preservative was used by Eli Lilly in 1928 after it was found that children were dying after using multi-dose vials of vaccine. So bacteria was being spread from one to the other. The multi-dose vials were used to SAVE MONEY and MAKE MORE PROFITS FOR THE SHAREHOLDERS.
Ok. So clearly something had to be done. The choice:
1. Give single vaccines
2. Give multi-dose vaccines but use a preservative to kill off the bacteria.
Number 1 would have cost more, so Number 2 was chosen. It still is chosen, for flu vaccines and the Third World, whose millions don't have a clue what's happening, just as we didn't.
The trial of the vaccines containing this preservative was used on 22 dying meningitis patients.
Not surprisingly, it was not possible to fully test whether the product was dangerous, because the subjects were dying anyway. This confounding factor would have made it impossible to establish whether they died earlier than they should because of the vaccine, or because of the meningitis.
Political protection of Eli Lilly and indeed the vaccine industry as a whole in the West has ensured that this little story has never properly been told to the public, nor has Thimerosal in vaccines ever been tested properly.
But the concerns about the toxicity of this product have never subsided - albeit away from the public eye and usually quickly dismissed or mocked by Big Pharma shills if anything did sneak out.
If Baron-Cohen is right and chemical exposure can cause damage to people - and this is not rocket science - and this damage could lead to neurodevelopmental disorders which could include autism - then we are home and dry. MERCURY is the second most deadliest toxic metal on this earth - WHY WAS IT EVER PUT IN VACCINES?
Autism was first described a few years after Mercury was used in vaccines, when suddenly Kanner and Asperger, working across the world from each other in Austria and the US, began to see the same thing in the late 1930's.
The numbers remained much the same over the decades and autism was regarded as a rare disorder. Our focus was on diagnosis, education and forms of treatment. The National Autistic Society, set up by concerned parents in the 1960's, had its priorities right then. But, the message was always - "We don't know what causes this condition". Or " It's wholly genetic, don't have any more children". Tapestry thinking was a million miles away.
When my own interests in autism began in the 1970's, it was extremely rare. When you mentioned an autistic child to people they thought you were saying 'artistic' and no-one knew anything about it. When you say it now, everyone knows someone who has an autistic child.
This massive increase, now clear in these very late reports, shifted from a condition which came into professional consciousness in the 30's after the Mercury vaccine programme began in earnest across the West, and rapidly rose after the 1980's.
It is not a co-incidence that in the 1980's there was an accelerated Thimerosal containing DTP (Diptheria, Tetanus and Pertussis (Whooping Cough) ) programme which meant that babies were getting much more Mercury than they had previously been getting.
The shots were given to much younger infants, with obviously weaker immune systems, and the time between each vaccine was shortened.
US children were also given a shot on the first day of birth and more shots within the first few months of life, so they have seen an even more rapid rise in autism.
So much spin and big money given to those that weave it has blocked what is alarmingly obvious:
MERCURY IS A TOXIC METAL - A DEADLY POISON - AND HAS BEEN IN VACCINES SINCE 1930.
WHY?
What has it done to us all?
Why is public discussion prevented?
http://www.telegraph.co.uk/news/main.jhtml;jsessionid=WKK4IKDPVRDPVQFIQMGSFGGAVCBQWIV0?xml=/news/2007/07/08/nautism108.xml
You cannot have genetic epidemics, so this is something else - and it is too rapid and large an increase to just be better diagnosis, especially in a country where politicians have tried to prevent diagnoses of autism by various means.
Simon Baron-C0hen who has inherited the genetic condition of sitting on the fence until the dust dies down - unlike his cousin Sasha - nevertheless is willing to whisper that maaayyybbbeee.... chemical exposure through pollutants could have something to do with this massive increase.
At last we have at least ONE answer which fits with concerns about certain vaccines and their effect on the developing system. Deadly toxic MERCURY, astonishingly, has been used in vaccines since 1930.
It forms 49.6% of the preservative THIMEROSAL.
This preservative was used by Eli Lilly in 1928 after it was found that children were dying after using multi-dose vials of vaccine. So bacteria was being spread from one to the other. The multi-dose vials were used to SAVE MONEY and MAKE MORE PROFITS FOR THE SHAREHOLDERS.
Ok. So clearly something had to be done. The choice:
1. Give single vaccines
2. Give multi-dose vaccines but use a preservative to kill off the bacteria.
Number 1 would have cost more, so Number 2 was chosen. It still is chosen, for flu vaccines and the Third World, whose millions don't have a clue what's happening, just as we didn't.
The trial of the vaccines containing this preservative was used on 22 dying meningitis patients.
Not surprisingly, it was not possible to fully test whether the product was dangerous, because the subjects were dying anyway. This confounding factor would have made it impossible to establish whether they died earlier than they should because of the vaccine, or because of the meningitis.
Political protection of Eli Lilly and indeed the vaccine industry as a whole in the West has ensured that this little story has never properly been told to the public, nor has Thimerosal in vaccines ever been tested properly.
But the concerns about the toxicity of this product have never subsided - albeit away from the public eye and usually quickly dismissed or mocked by Big Pharma shills if anything did sneak out.
If Baron-Cohen is right and chemical exposure can cause damage to people - and this is not rocket science - and this damage could lead to neurodevelopmental disorders which could include autism - then we are home and dry. MERCURY is the second most deadliest toxic metal on this earth - WHY WAS IT EVER PUT IN VACCINES?
Autism was first described a few years after Mercury was used in vaccines, when suddenly Kanner and Asperger, working across the world from each other in Austria and the US, began to see the same thing in the late 1930's.
The numbers remained much the same over the decades and autism was regarded as a rare disorder. Our focus was on diagnosis, education and forms of treatment. The National Autistic Society, set up by concerned parents in the 1960's, had its priorities right then. But, the message was always - "We don't know what causes this condition". Or " It's wholly genetic, don't have any more children". Tapestry thinking was a million miles away.
When my own interests in autism began in the 1970's, it was extremely rare. When you mentioned an autistic child to people they thought you were saying 'artistic' and no-one knew anything about it. When you say it now, everyone knows someone who has an autistic child.
This massive increase, now clear in these very late reports, shifted from a condition which came into professional consciousness in the 30's after the Mercury vaccine programme began in earnest across the West, and rapidly rose after the 1980's.
It is not a co-incidence that in the 1980's there was an accelerated Thimerosal containing DTP (Diptheria, Tetanus and Pertussis (Whooping Cough) ) programme which meant that babies were getting much more Mercury than they had previously been getting.
The shots were given to much younger infants, with obviously weaker immune systems, and the time between each vaccine was shortened.
US children were also given a shot on the first day of birth and more shots within the first few months of life, so they have seen an even more rapid rise in autism.
So much spin and big money given to those that weave it has blocked what is alarmingly obvious:
MERCURY IS A TOXIC METAL - A DEADLY POISON - AND HAS BEEN IN VACCINES SINCE 1930.
WHY?
What has it done to us all?
Why is public discussion prevented?
http://www.telegraph.co.uk/news/main.jhtml;jsessionid=WKK4IKDPVRDPVQFIQMGSFGGAVCBQWIV0?xml=/news/2007/07/08/nautism108.xml
Sunday, 1 July 2007
"All drugs have side effects" Glaxo Smith Kline quote
As we know, the political spin machine has woven a story that there is no such thing as an adverse reaction or a side effect to a drug or vaccine, in order to slam the door shut of children damaged in such an iatrogenic way being recognised and compensated for it.
Knowing how that spin has resulted in smear campaigns and whitewashed reports masquerading as science and taken to similarly compromised Journals and Courts - all paid for by the pharmaceutical industry - makes this story all the more interesting.
http://seroxatsecrets.wordpress.com/2007/06/30/can-you-believe-they-really-said-this%E2%80%A6-reprise/
Knowing how that spin has resulted in smear campaigns and whitewashed reports masquerading as science and taken to similarly compromised Journals and Courts - all paid for by the pharmaceutical industry - makes this story all the more interesting.
http://seroxatsecrets.wordpress.com/2007/06/30/can-you-believe-they-really-said-this%E2%80%A6-reprise/
Thursday, 28 June 2007
Professor Gordon Stewart's warnings about DTP in the 1980's
Professor Gordon Stewart was Emeritus Professor of Public Health into the eighties at the University of Glasgow when he began to have very serious concerns about the DTP vaccine. He was particularly worried about increasing reports of adverse reactions including convulsions and white shock after the vaccine in some children and death in some others. Professor Stewart worked with committees looking at these reactions, thought to be linked to the live pertussis antigen.
He was to be shocked when others in the committee were making public announcements that the vaccine was perfectly safe. He knew this was simply not the case.
Time moves on and political spin has whipped up a veritable confection trying to convince the public that there are no reactions to vaccine, even saying that reported adverse reactions are simply co-incidences.
Biological studies (see Dish of the Day below) on Thimerosal with its 49.6% Mercury content show the damage it can do to cells, the retina and to the way it collects in certain organs. Mercury's potential to draw live viruses to it as well as other vaccine ingredients is never even mentioned to the public.
Did Mercury draw the pertussis antigen to it, or did it act alone/separately? How will we know if the lies and spin continue despite the vast evidence of adverse reactions in VAERS in the US, the Yellow Card scheme in the UK, the Brighton Collaboration spanning both and through the work and warnings of men of high integrity such as Professor Gordon Stewart?
Read the recent Spectator article about the tragic case of Sally Clark whose children had just had vaccines when they died.
Other cases known to me of babies whose deaths followed the DTP ( and in some cases the MMR) also involved parents having to take the blame.
Professors who have remained completely silent on the issue of vaccines even when stood in Court speaking on Oath and who have led the way in this blame game, also sat on Adverse Reactions to Vaccination Committees. One of these is Professor Sir Roy Meadow who said there was a 73 million to 1 chance that Sally Clark's two babies died 'naturally'. Meaning that she must have killed them. No mention of the vaccines.
Professor David Southall has also been involved in studies linked to CONI schemes - Care of the Next Infant, run by the FSID (Foundation for the Study of Infant Deaths) - after a baby died. Many died after a vaccine but he never mentions that either.
Could it be that for 25 years certain powerful individals have crafted theories to blame parents for the evidence of adverse reactions to vaccines set down right before their eyes? whilst others battled in vain to protect the public by raising concerns?
Will a new British Government headed by Gordon Brown, now, finally, protect the public and expose what has been happening to so many children ?
http://www.spectator.co.uk/archive/30630/what-killed-sally-clarks-child.thtml
He was to be shocked when others in the committee were making public announcements that the vaccine was perfectly safe. He knew this was simply not the case.
Time moves on and political spin has whipped up a veritable confection trying to convince the public that there are no reactions to vaccine, even saying that reported adverse reactions are simply co-incidences.
Biological studies (see Dish of the Day below) on Thimerosal with its 49.6% Mercury content show the damage it can do to cells, the retina and to the way it collects in certain organs. Mercury's potential to draw live viruses to it as well as other vaccine ingredients is never even mentioned to the public.
Did Mercury draw the pertussis antigen to it, or did it act alone/separately? How will we know if the lies and spin continue despite the vast evidence of adverse reactions in VAERS in the US, the Yellow Card scheme in the UK, the Brighton Collaboration spanning both and through the work and warnings of men of high integrity such as Professor Gordon Stewart?
Read the recent Spectator article about the tragic case of Sally Clark whose children had just had vaccines when they died.
Other cases known to me of babies whose deaths followed the DTP ( and in some cases the MMR) also involved parents having to take the blame.
Professors who have remained completely silent on the issue of vaccines even when stood in Court speaking on Oath and who have led the way in this blame game, also sat on Adverse Reactions to Vaccination Committees. One of these is Professor Sir Roy Meadow who said there was a 73 million to 1 chance that Sally Clark's two babies died 'naturally'. Meaning that she must have killed them. No mention of the vaccines.
Professor David Southall has also been involved in studies linked to CONI schemes - Care of the Next Infant, run by the FSID (Foundation for the Study of Infant Deaths) - after a baby died. Many died after a vaccine but he never mentions that either.
Could it be that for 25 years certain powerful individals have crafted theories to blame parents for the evidence of adverse reactions to vaccines set down right before their eyes? whilst others battled in vain to protect the public by raising concerns?
Will a new British Government headed by Gordon Brown, now, finally, protect the public and expose what has been happening to so many children ?
http://www.spectator.co.uk/archive/30630/what-killed-sally-clarks-child.thtml
The Tapestry of disorders is becoming all too obvious
In the early nineties I began to see that the usual approaches to diagnosis with black and white diagnostic methods were not that helpful. So many children then emerging fell through the net.
That is because they were increasingly complex. They had a complex interweave of conditions - such as the Autism, ADHD and Asthma Generation Rescue finds as being higher in vaccinated boys. It was then that I began to use the metaphor of the Tapestry.
There also seemed at that stage to probably be a complex interweave of causes and certainly there need to be a complex interweave of interventions to maximise the chances of success so the metaphor worked on various levels of explanation.
Tragically and astonishingly, the system has done all in its power to deny this tapestry, and to play games with diagnosis and indeed with those doing the diagnosing.
Once respectable professionals now take the stand one after the other against children to talk about studies with clear conflicts of interest as a glance at the transcripts in the Cedillo case now running in New York will show. Shame on them.
It all started with that tapestry of corruption - Big Pharma in bed with Governments and now we have a tapestry of crippling life-long disorders in the lucky ones who survive adverse reactions to vaccinations. But until the tapestry of disorders and the causes are fully understood by the public, the majority of these children will continue to suffer as we have not even begun to address their complex needs as we should in our so called advanced society.
That is because they were increasingly complex. They had a complex interweave of conditions - such as the Autism, ADHD and Asthma Generation Rescue finds as being higher in vaccinated boys. It was then that I began to use the metaphor of the Tapestry.
There also seemed at that stage to probably be a complex interweave of causes and certainly there need to be a complex interweave of interventions to maximise the chances of success so the metaphor worked on various levels of explanation.
Tragically and astonishingly, the system has done all in its power to deny this tapestry, and to play games with diagnosis and indeed with those doing the diagnosing.
Once respectable professionals now take the stand one after the other against children to talk about studies with clear conflicts of interest as a glance at the transcripts in the Cedillo case now running in New York will show. Shame on them.
It all started with that tapestry of corruption - Big Pharma in bed with Governments and now we have a tapestry of crippling life-long disorders in the lucky ones who survive adverse reactions to vaccinations. But until the tapestry of disorders and the causes are fully understood by the public, the majority of these children will continue to suffer as we have not even begun to address their complex needs as we should in our so called advanced society.
Thursday, 14 June 2007
The FIVE YEAR STRUGGLE for parents to get this to Court
This schedule provides a glimpse at the struggle parents have been put through and the extraordinary lengths the system will go to in order to prevent the public becoming aware of a well known phenomenon - adverse reactions to vaccinations in some children.
http://www.uscfc.uscourts.gov/OSM/AutismDocket.htm
http://www.uscfc.uscourts.gov/OSM/AutismDocket.htm
Wednesday, 13 June 2007
Madeleine McCann - another victim
The Official Website to find Madeleine McCann
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Madeleine McCann---Missing---
'Madeleine's Fund : Leaving No Stone Unturned '
The balance on 11/06/07, the fund account current stands at £721,748.84.
Home
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Website updated 11 hours ago. Can you Help? Click Here to find out how.Portuguese Police on 00351 282 405 400Crimestoppers on 0800 555 111International Crimestoppers on 00 44 18 83 73 13 36
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Dutch paper tipped off about Madeleine McCann
Radio Netherlands Worldwide
13/06/2007
Moroccan support for missing Madeleine
New Zealand Herald
12/06/2007
Madeleine Parents to go through Period of Reflection
Christian Today
12/06/2007
UK police to post photos of Maddie on Second Life
Middle East Times
12/06/2007
We Think Madeleine Is Still Alive
SKY News
12/06/2007
Martin Brunt In Rabat As Search Continues
SKY News
12/06/2007
Madeleine McCann Still Alive Parents Believe
National Ledger
12/06/2007
If Shes There, They Will Find Her
SKY News
12/06/2007
Hunt for Madeleine reaches Morocco
Scotsman
11/06/2007
The route kidnappers could have used to spirit her to Morocco
Daily Mail
11/06/2007
McCanns begin final leg of Madeleine campaign
Guardian Unlimited
11/06/2007
Parents to stay in Portugal for summer
Inthenews
11/06/2007
Madeleine parents to take time off search
Inthenews
10/06/2007
Madeleine is more than a news story, she symbolises the dangers all children face
Sunday Herald
10/06/2007
Madeleine McCann Family Harassed by Portuguese Police
National Ledger
10/06/2007
Search continues for Madeleine McCann
Herald Sun, Australia
09/06/2007
Madeleine phone call is dismissed
IC Liverpool
08/06/2007
Capital gets ready for Madeleine church service
Scotsman
08/06/2007
Argentina link to Madeleine?
The Herald
08/06/2007
Children raise cash for Madeleine search
Lancashire Evening Post
08/06/2007
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Madeleine McCann---Missing---
'Madeleine's Fund : Leaving No Stone Unturned '
The balance on 11/06/07, the fund account current stands at £721,748.84.
Home
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Dutch paper tipped off about Madeleine McCann
Radio Netherlands Worldwide
13/06/2007
Moroccan support for missing Madeleine
New Zealand Herald
12/06/2007
Madeleine Parents to go through Period of Reflection
Christian Today
12/06/2007
UK police to post photos of Maddie on Second Life
Middle East Times
12/06/2007
We Think Madeleine Is Still Alive
SKY News
12/06/2007
Martin Brunt In Rabat As Search Continues
SKY News
12/06/2007
Madeleine McCann Still Alive Parents Believe
National Ledger
12/06/2007
If Shes There, They Will Find Her
SKY News
12/06/2007
Hunt for Madeleine reaches Morocco
Scotsman
11/06/2007
The route kidnappers could have used to spirit her to Morocco
Daily Mail
11/06/2007
McCanns begin final leg of Madeleine campaign
Guardian Unlimited
11/06/2007
Parents to stay in Portugal for summer
Inthenews
11/06/2007
Madeleine parents to take time off search
Inthenews
10/06/2007
Madeleine is more than a news story, she symbolises the dangers all children face
Sunday Herald
10/06/2007
Madeleine McCann Family Harassed by Portuguese Police
National Ledger
10/06/2007
Search continues for Madeleine McCann
Herald Sun, Australia
09/06/2007
Madeleine phone call is dismissed
IC Liverpool
08/06/2007
Capital gets ready for Madeleine church service
Scotsman
08/06/2007
Argentina link to Madeleine?
The Herald
08/06/2007
Children raise cash for Madeleine search
Lancashire Evening Post
08/06/2007
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Dish of the Day: Red Herrings stuffed with Thimerosal - guaranteed 49.5% Mercury. Lisa Blakemore Brown 5th March 2005 British Medical Journal
Dish of the Day: Red Herrings stuffed with Thiomersal - guaranteed 49.5% Mercury.
5 March 2005
Lisa C Blakemore-Brown, Psychologist UK based
Send response to journal: Re: Dish of the Day: Red Herrings stuffed with Thiomersal - guaranteed 49.5% Mercury.
Thiomersal/Thimerosal, a preservative developed in the late 1920's was manufactured by Eli Lilly and has been routinely used in vaccines and many other products since that time.
Thiomersal/Thimerosal contains 49.5% ethyl mercury. Methyl mercury is known to accumulate in fish and for this reason there is a safe daily limit for the amount of mercury adults are advised to not exceed. This is 0.1 mcg of Methyl Mercury per kilogram of weight. Babies have been given 25 microgrammes in each of the following vaccines: whole cell DTP and Hib, and the Hep B in the US. During this same period many very small premature babies have survived whereas in the past they would not have done so.
Over the course of the last century, individuals were given single vaccines with single amounts of mercury, but with the introduction of triple vaccines the amount of mercury contained within the preservative was multiplied and the cumulative effects are only just now being discovered by the public. Early papers on autism and battered baby syndrome appeared following the introduction of vaccines containing this preservative in the 30's and 40's and following the introduction of triple vaccines there has been an epidemic of autism - and genetic epidemics do not occur without some outside influence. It is also interesting that the Shaken Baby Syndrome and parent blame theories for odd medical presentations, have also vastly increased since these triple vaccines were brought in.
Thiomersal is still used in flu vaccines and other products but has been phased out in many childhood vaccines, but only very recently. For the UK it was August 2004 when the announcement was made.
Public Health agencies around the world have known about concerns with this neurotoxin for some years, and certainly since 1997 when the US Congress passed the FDA Modernization Act requiring the FDA to review all drugs that contained Mercury and determine their effect on humans. (3)
In 2000, recognising the cumulative amount of mercury in the triple vaccines, the FDA stated that children were receiving levels of mercury via this preservative far in excess of the 'safe' guidelines. Rough estimates suggested a child could be injected with 40 times the amount of mercury considered safe (3)
Despite the expected red herring arguments of the defensive, and the collaborative efforts of many countries to handle worrying data, many lab studies have explored the toxic effects of Thiomersal in humans and animals.
Evidence that Thiomersal can create changes at cellular level is rife in the literature (6,7,14,17,18.)A recent study concluded 'thimerosal is genotoxic in the cytochalasin B block micronucleus test with human lymphocytes. These data raise some concern on the widespread use of thimerosal.'(12)
Changes to phenotypes have been recognised (13) and the tapestry model allows for these various synergistic effects. For instance, it has been consistently shown that Thiomersal(Thimerosal) is a neurotoxin which is linked to the depletion of the protective anti-oxidant, glutathione (1,13,14,15,18,19)and that some individuals are more susceptible than others to such effects (4,16) Autistic individuals have been found to have lowered levels of glutathione and to have greater difficulties excreting mercury.
It is not impossible that earlier generations of constitutionally susceptible individuals were affected by the Mercury in their very early vaccinations, phenotypes were altered and in turn their offspring increased their risk factors for susceptibility to mercury damage.
Such susceptibilities, combined with an already weak immune system - in a baby. a medically vulnerable individual or an elderly person - further increase the risk factors.
As the changes triggered by Thiomersal appear at cellular level, including cell death and increased cellular permeability, it is not surprising that many forms of impairment are found.
'Exposure to organic mercury leads to primarily neurologic effects but a number of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal.' (2) Travis Haws has discussed Louis Reik's Disseminated Vasculomyelinopathy:an Immune Complex Disease relating to the multiple effects of infection once the immune system has been compromised. (20)
Effects of the preservative in preparations have found retinal (21) and corneal damage. (22)
The consistent reference to allergic effects and immune system interference (4, 5) maps onto my own findings that early vaccines seemed to trigger various allergies and intolerances in some children (See CASE ONE 2004 ebmj as an example taken directly from the medical notes)
My very early observations during the mid to late 1990's was that it was these medically vulnerable and allergic individuals who were more likely to have reacted to the MMR - which contains no Thiomersal. (23) Unfortunately because of Red Herring arguments and denial of what is known, we have yet to fully explore in a scientific way, why so many children reacted to vaccines.
In 2000 a meeting held in Simpsonwood US, revealed significant findings in a study by Verstraeten in relation to the emergence of a variety of neurodevelopmental disorders including tics, ADHD, speech and language and motor impairments - and Thiomersal. It has taken the Freedom of Information Act to expose what was shown in that meeting - and the steps taken to cover it up.
The epidemic of health and developmental problems in so called advanced countries is now undeniable. 1 in 10 children suffer from gastrointestinal disorders, 1 in 4 have asthma. A colleague last week mentioned that out of 16 children on a school trip involving his child, 15 had asthma. Children are arriving at school unable to use a knife and fork, pay attention or understand their social worlds, highly sensitised to all aspects of the real world.
When we have removed the Red Herrings - and those who cook them up - we might begin to take responsibility again for the health of millions across the world.
Refs:
1: Neurotoxicology. 2005 Jan;26(1):1-8.
Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors.
James SJ, Slikker W 3rd, Melnyk S, New E, Pogribna M, Jernigan S.
Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, USA. jamesjill@uams.edu
Thimerosol is an antiseptic containing 49.5% ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Environmental methyl mercury has been shown to be highly neurotoxic, especially to the developing brain. Because mercury has a high affinity for thiol (sulfhydryl (-SH)) groups, the thiol-containing antioxidant, glutathione (GSH), provides the major intracellular defense against mercury-induced neurotoxicity. Cultured neuroblastoma cells were found to have lower levels of GSH and increased sensitivity to thimerosol toxicity compared to glioblastoma cells that have higher basal levels of intracellular GSH. Thimerosal-induced cytotoxicity was associated with depletion of intracellular GSH in both cell lines. Pretreatment with 100 microM glutathione ethyl ester or N-acetylcysteine (NAC), but not methionine, resulted in a significant increase in intracellular GSH in both cell types. Further, pretreatment of the cells with glutathione ethyl ester or NAC prevented cytotoxicity with exposure to 15 microM Thimerosal. Although Thimerosal has been recently removed from most children's vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries. The potential protective effect of GSH or NAC against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccinations.
2: Toxicol Ind Health. 2002 Apr;18(3):109-60.
Organic mercury compounds: human exposure and its relevance to public health.
Risher JF, Murray HE, Prince GR.
Agency for Toxic Substances and Disease Registry, Division of Toxicology, Toxicology Information Branch, Clifton Road, Atlanta, Georgia 30333, USA.
Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes, and the effects of such exposure depend upon both the type of mercury to which exposed and the magnitude of the exposure. In general, the effects of exposure to organic mercury are primarily neurologic, while a host of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal. While the primary source of exposure to organic mercury for most populations is the consumption of methylmercury-contaminated fish and shellfish, there are a number of other organomercurials to which humans might be exposed. The antibacterial and antifungal properties of organomercurials have resulted in their long use as topical disinfectants (thimerosal and merbromin) and preservatives in medical preparations (thimerosal) and grain products (both methyl and ethyl mercurials). Phenylmercury has been used in the past in paints, and dialkyl mercurials are still used in some industrial processes and in the calibration of certain analytical laboratory equipment. The effects of exposure to different organic mercurials by different routes of exposure are summarized in this article.
3. Trade Off: Vaccine Maker Profits and Autism. Evelyn Pringle . Independent News Media. 4th March 2005
4: Med Pr. 2001;52(1):45-51.
[Genetic polymorphism of glutathione s-transferase as a factor predisposing to allergic dermatitis]
[Article in Polish]
Lutz W, Tarkowski M, Nowakowska E.
Zakladu Diagnostyki Laboratoryjnej, Instytutu Medycyny Pracy, Lodzi.
In the inductive phase of contact allergic dermatitis, simple chemical compounds (haptens) produce together with epidermic proteins adducts presented by Langerhans cells to T lymphocytes. Binding to protein carrier is a necessary condition of transforming a low-molecular allergen into immunogenic one and evoking immunological reaction. The production of allergen adducts with proteins is conditioned by the presence of electrophilic groups in their molecules, or their acquiring during biotransformation phase I. Active allergen metabolites undergo further alterations during biotransformation phase II which leads most frequently to the decline in their chemical activity and more rapid excretion from the body. The number of reactive metabolites (reactive allergens) available for producing adducts with proteins keeps the balance between activation and deactivation reactions. Glutathione S-transferases play a particular role in the allergens (or their metabolites) deactivation process in biotransformation phase II. These enzymes catalyse reactions responsible for the declined electrophilic potential of allergens (or their metabolites), and thus for the decrease in the number of allergen molecules able to produce protein covalent bindings (adducts). Glutathione S-transferases, occurring in the human cellular cytoplasm belong to five classes: alpha(GST A), mu(GST M), theta(GST P), pi(GST T) and Z(GST Z), as well as to one class present in microsomes. The study indicated the presence of isoenzymes GST T1 and GST M1 in the skin. Both isoforms participate in the process of low-molecular allergen biotransformation. Carriers of defective genes GST T1 and/or GST M1 are more vulnerable to allergenic effect of some allergens, e.g. thimerosal, which is associated with the absence of or decrease in the activity of isoenzymes GST T1 and GST M1.
5: Cell Biol Toxicol. 1999 Feb;15(1):57-62.
Mechanisms of drug-induced allergic contact dermatitis.
Lebrec H, Bachot N, Gaspard I, Kerdine S, Guinnepain MT, Laurent J, Pallardy M.
INSERM U 461, Faculte de Pharmacie Paris Sud, Chatenay-Malabry, France. hlebrec@infobiogen.fr
Allergic contact dermatitis is induced by a wide variety of drugs that trigger specific immune responses following topical exposure. Identified chemical structures involved in such reactions include the mercuric and thiosalicylic acid groups of thimerosal, the diphenylketone group of the anti- inflammatory drug ketoprofen, the amide or ester structure of local anesthetics, and the side-chain and thiazolidine ring of beta-lactams. The T cell responses to such compounds involve CD4+ and CD8+ alphabeta+ T lymphocytes and also CD4 /CD8 gammadelta+ T cells. Although "T helper 2" cytokine production by drug- specific human T cells from patients with allergic contact dermatitis has been described, T helper 1-like and T cytotoxic 1-like responses clearly play key roles in this cutaneous reaction.
6. Int J Biochem. 1994 Jan;26(1):93-6.
Effect of thimerosal on cytosolic calcium and phosphatidylserine synthesis in Jurkat T cells.
Pelassy C, Breittmayer JP, Ticchioni M, Aussel C.
INSERM U343, Faculte de Medecine, Nice, France.
1. We investigated the effect of the thiol reagent, thimerosal on calcium movements in the Jurkat T cell line. 2. Thimerosal induced a rise in cytosolic Ca2+ concentration due both to a release of Ca2+ from intracellular stores and a Ca2+ influx. 3. Thimerosal, released Ca2+ from the same intracellular stores than CD3 mAb and ionomycin. 4. Emptying the Ca2+ intracellular stores was accompanied by a marked decrease of phosphatidylserine synthesis indicating that phosphatidylserine synthesis occurs within or close to the endoplasmic reticulum Ca(2+)-stores as previously described in CD3-, ionomycin- or Ca(2+)-ATPase inhibitor-treated lymphocytes.
7. Biochim Biophys Acta. 1992 Oct 19;1111(1):65-74.
Effect of the sulfhydryl reagent thimerosal on cytosolic free Ca2+ and membrane potential of thymocytes.
Gukovskaya AS, Trepakova ES, Zinchenko VP, Korystov YN, Bezuglov VV.
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region.
The sulfhydryl reagent thimerosal at concentrations 5-100 microM has been found to induce a variety of changes in ion transport in rat thymocytes. In particular, [Ca2+]i increases about 10-fold from the basal level. The [Ca2+]i response to thimerosal displays a two-stage time course, with the main [Ca2+]i rise during the second stage. Evidence has been obtained for the depletion of intracellular Ca2+ pools in thimerosal-treated cells, however, Ca2+ mobilization from intracellular stores does not contribute significantly into [Ca2+]i rise. Thimerosal elicits permeability not only for Ca2+, but also for Mn2+ and Ni2+, which is Ca(2+)-dependent. We failed to get any evidence on thimerosal- induced inhibition of the plasma membrane Ca(2+)-ATPase. The induction of Ca2+ influx, rather than inhibition of Ca(2+)-ATPase, accounts for the disturbance of [Ca2+]i homeostasis in thimerosal-treated cells. Thimerosal also elicits changes in monovalent ion fluxes resulting in marked depolarization. The latter seems unrelated to the changes in [Ca2+]i and is suggested to be mediated both by increased permeability for Na+ and a decreased one for K+. Thimerosal significantly stimulates AA release from thymocytes. Evidence has been presented that AA metabolite(s), probably, LO product(s), may mediate the changes in the transport of mono- and divalent cations elicited by the sulfhydryl reagent. Prolonged treatment of thymocytes with thimerosal resulted in cell death.
8. Lancet. 1991 Aug 3;338(8762):315-6.
Ecotoxicol Environ Saf. 1985 Oct;10(2):150-8.
Effect of organomercurial poisoning on the peripheral blood and metabolite levels of a freshwater fish.
Gill TS, Pant JC.
This work evaluated the hematological and biochemical changes in the fish, Puntius conchonius, under experimental organomercurial poisoning. Long- term (8 weeks) exposure to 3.63 and 6.03 mg/liter methoxyethyl mercuric chloride (MEMC) (0.2 and 0.33 fractions of 96-hr LC50) led to morphological aberrations in mature erythrocytes including nuclear and cytoplasmic deterioration, vacuolation, chromatin condensation, and hypochromia. Immature erythrocytes showing membrane leakage were also encountered. Erythrocyte count and hemoglobin (Hb) were significantly lowered after 1 and 3 weeks followed by a marginal rise persisting upto 8 weeks. Differential leucocyte counts revealed significant thrombocytopenia, lymphocytosis, and neutropenia. Collateral evaluation of blood glucose and tissue glycogen levels revealed significant hyperglycemia as well as glycogen depletion in liver and brain. Heart glycogen content evinced a substantial increase after 5 and 8 weeks exposure.
9. Rev Neurol (Paris). 1979;135(11):827-33.
[Morvan's fibrillary chorea]
[Article in French]
de Bray JM, Emile J, Basle M, Morer T, Bastard J.
Two cases of Morvan's chorea are reported. One of the patients presented the characteristic of having had two attacks, the first after organic mercury preparations, and the second after gold salts for inflammatory rheumatism. The second case had facial fibrillations only, and this was followed by a regressive polyradiculoneuritis one month later. This latter case raises certain diagnostic problems. The existence of a particular type of immuno-allergic tendency could be validly related to a triggering effect of various etiological agents (metals such as mercury or gold salts, or infective agents). The absence of hypotonia, and a regressive course appear to be the characteristics that distinguish fibrillary chorea from the continuous activity syndrome of the muscle fibers described by Isaacs.
10. Contact Dermatitis. 1980 Jun;6(4):241-5.
Merthiolate hypersensitivity and vaccination.
Forstrom L, Hannuksela M, Kousa M, Lehmuskallio E.
Epicutaneous tests with 0.1% merthiolate in petrolatum showed hypersensitivity in 96 of 4647 eczema patients (2.0%) and in seven of 105 healthy recruits (7%). There was a marked preponderance of young age classes in the eczema group. Twelve of 41 merthiolate-positive patients tested reacted to mercury alone, three to thiosalicylic acid alone and one to both. The remaining 25 patients reacted to neither of the individual components although the merthiolate complex as a whole gave a positive test result. Forty-five of the merthiolate- positive patients were tested subcutaneously with 0.5 ml of a 0.01% merthiolate solution, i.e. a dose equal to that contained in one shot of tetanus toxoid, for example. Nine patients developed a local reaction at the site of the injection, and the area became eczematous in four cases. In one of the patients the eczema spread over the body, causing fever. Since merthiolate-sensitive patients also react to merthiolate administered intracutaneously, the vaccinator should avoid the use of a needle whose outer surface has been contaminated when the vaccine was aspirated from the bottle. However, even when this precautionary measure is taken, local reactions can be expected in such a high percentage of merthiolate-sensitive persons that merthiolate in vaccines should be replaced by another antibacterial agent.
11. Contact Dermatitis. 1986 Nov;15(5):309-10.
Reactions to merthiolate in infants.
Novak M, Kvicalova E, Friedlanderova B.
12. Arch Toxicol. 2003 Jan;77(1):50-5. Epub 2002 Nov 06.
Thimerosal induces micronuclei in the cytochalasin B block micronucleus test with human lymphocytes.
Westphal GA, Asgari S, Schulz TG, Bunger J, Muller M, Hallier E.
Department of Occupational Health, Georg-August-University Gottingen, Waldweg 37, 37073 Gottingen, Germany. gwestph@gwdg.de
Thimerosal is a widely used preservative in health care products, especially in vaccines. Due to possible adverse health effects, investigations on its metabolism and toxicity are urgently needed. An in vivo study on chronic toxicity of thimerosal in rats was inconclusive and reports on genotoxic effects in various in vitro systems were contradictory. Therefore, we reinvestigated thimerosal in the cytochalasin B block micronucleus test. Glutathione S-transferases were proposed to be involved in the detoxification of thimerosal or its decomposition products. Since the outcome of genotoxicity studies can be dependent on the metabolic competence of the cells used, we were additionally interested whether polymorphisms of glutathione S-transferases (GSTM1, GSTT1, or GSTP1) may influence the results of the micronucleus test with primary human lymphocytes. Blood samples of six healthy donors of different glutathione S-transferase genotypes were included in the study. At least two independent experiments were performed for each blood donor. Significant induction of micronuclei was seen at concentrations between 0.05-0.5 micro g/ml in 14 out of 16 experiments. Thus, genotoxic effects were seen even at concentrations which can occur at the injection site. Toxicity and toxicity-related elevation of micronuclei was seen at and above 0.6 micro g/ml thimerosal. Marked individual and intraindividual variations in the in vitro response to thimerosal among the different blood donors occurred. However, there was no association observed with any of the glutathione S-transferase polymorphism investigated. In conclusion, thimerosal is genotoxic in the cytochalasin B block micronucleus test with human lymphocytes. These data raise some concern on the widespread use of thimerosal.
13. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.
Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal.
Muller M, Westphal G, Vesper A, Bunger J, Hallier E.
Department of Occupational and Social Medicine, Georg-August- University Gottingen, D-37073 Gottingen, Germany. mmuelle3@gwdg.de
We have investigated the interaction of thimerosal, a widely used antiseptic and preservative, with the human erythrocytic GST T1 (glutathione-S- transferase T1). This detoxifying enzyme is expressed in the erythrocytes of solely the human species and it displays a genetic polymorphism. Due to this polymorphism about 25% of the individuals of the caucasian population lack this activity ("non-conjugators"), while 75% show it ("conjugators") (Hallier, E., et al., 1993). Using our newly developed HPLC-fluorescence detection assay (Muller, M., et al., 2001) we have profiled the kinetics of enzyme inhibition in erythrocyte lysates of two individuals previously identified as "normal conjugator" (medium enzyme activity) and "super-conjugator" (very high activity). For the normal conjugator we have determined a 2.77 mM thimerosal concentration to inhibit 50% of the GST T1 activity. In the case of the super-conjugator a 2.3 mM thimerosal concentration causes a 50% inhibition of the enzyme activity. For both phenotypes a 14.8 mM thimerosal concentration results in residual enzyme activities equal to those typically detected in non-conjugator lysates. Thus, sufficiently high doses of thimerosal may be able to change the phenotypic status of an individual--at least in vitro--by inhibition of the GST T1 enzyme.
14. Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.
Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization.
Westphal GA, Schnuch A, Schulz TG, Reich K, Aberer W, Brasch J, Koch P, Wessbecher R, Szliska C, Bauer A, Hallier E.
Abteilung fur Arbeits- und Sozialmedizin, Georg-August-Universitat Gottingen, Germany. gwestph@gwdg.de
OBJECTIVE: Thimerosal is an important preservative in vaccines and ophthalmologic preparations. The substance is known to be a type IV sensitizing agent. High sensitization rates were observed in contact-allergic patients and in health care workers who had been exposed to thimerosal-preserved vaccines. There is evidence for the involvement of the glutathione system in the metabolism of thimerosal or its decomposition products (organomercury alkyl compounds). Thus detoxification by polymorphically expressed glutathione S-transferases such as GSTT1 and GSTM1 might have a protective effect against sensitization by these substances. METHODS: To address this question, a case control study was conducted, including 91 Central European individuals with a positive patch-test reaction to thimerosal. This population was compared with 169 healthy controls and additionally with 114 individuals affected by an allergy against para-substituted aryl compounds. The latter population was included in order to test whether possible associations were due to substance-specific effects, or were a general feature connected with type IV immunological diseases. Homozygous deletions of GSTT1 and GSTM1 were determined by polymerase chain reaction. RESULTS: Glutathione S-transferase M1 deficiency was significantly more frequent among patients sensitized to thimerosal (65.9%, P = 0.013) compared with the healthy control group (49.1%) and the "para-compound" group (48%, P = 0.034). Glutathione S-transferase T1 deficiency in the thimerosal/mercury group (19.8%) was barely elevated versus healthy controls (16.0%) and the "para-compound" group (14.0%). The combined deletion (GSTT1-/GSTM1-) was markedly more frequent among thimerosal-sensitized patients than in healthy controls (17.6% vs. 6.5%, P = 0.0093) and in the "para- compound" group (17.6% vs. 6.1%, P =0.014), revealing a synergistic effect of these enzyme deficiencies (healthy controls vs. thimerosal GSTM1 negative individuals, OR = 2.0 [CI = 1.2-3.4], GSTT1-, OR = 1.2 [CI = 0.70-2.1], GSTM1/T1-, OR = 3.1 [CI = 1.4-6.5]). CONCLUSIONS: Since the glutathione-dependent system was repeatedly shown to be involved in the metabolism of thimerosal decomposition products, the observed association may be of functional relevance.
PMID: 11007341 [PubMed - indexed for MEDLINE]
15 Toxicol In Vitro. 2004 Oct;18(5):563-9.
Property of thimerosal-induced decrease in cellular content of glutathione in rat thymocytes: a flow cytometric study with 5-chloromethylfluorescein diacetate.
Ueha-Ishibashi T, Tatsuishi T, Iwase K, Nakao H, Umebayashi C, Nishizaki Y, Nishimura Y, Oyama Y, Hirama S, Okano Y.
Laboratory of Cellular Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Minami-Jyosanjima 1-1, Tokushima 770-8502, Japan.
There is a concern on the part of public health community that adverse health consequences by thimerosal, a preservative in vaccines for infants, may occur among infants during immunization schedule. Therefore, the effect of thimerosal on cellular content of glutathione was examined on thymocytes obtained from 4-week-old rats using a flow cytometer and 5-chloromethylfluorescein diacetate. Thimerosal at concentrations ranging from 1 to 10 microM reduced the cellular content of glutathione in a concentration-dependent manner, and the complete depletion of cellular glutathione was observed when the cells were treated with 30 microM thimerosal. L-Cysteine significantly attenuated the actions of thimerosal to reduce the glutathione content and to increase the intracellular Ca2+ concentration. Prolonged incubation (24 h) with 1-3 microM thimerosal induced the apoptosis. The cytotoxic action of thimerosal was greatly augmented when the cells suffered oxidative stress induced by H2O2. It may be unlikely that thimerosal exerts potent cytotoxic action under the in vivo condition because the blood concentration of thimerosal after receiving vaccines does not seem to reach micromolar range and nonprotein thiols at micromolar concentrations are present in the blood.
16: J Invest Dermatol. 2003 Nov;121(5):1039-44.
Thiol antioxidants block the activation of antigen-presenting cells by contact sensitizers.
Bruchhausen S, Zahn S, Valk E, Knop J, Becker D.
Department of Dermatology, University of Mainz, Mainz, Germany.
Strong contact sensitizers are able to induce signal transduction mechanisms such as tyrosine phosphorylation and activation of MAP kinases in antigen-presenting cells. We studied the capacity of different antioxidants (ascorbic acid, alpha-tocopherol, pyrrolidine dithiocarbamate, N- acetylcysteine, and glutathione) to block the increase in tyrosine phosphorylation in human monocytes seen after stimulation with strong contact sensitizers. Human peripheral blood mononuclear cells were stimulated with 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone in the presence or absence of these antioxidants. The total amount of membrane-associated phosphotyrosine in CD14+ cells was quantified using flow cytometric techniques. Complete inhibition of tyrosine phosphorylation was noticed when cells were stimulated in the presence of N-acetylcysteine or glutathione. Using N-acetylcysteine as inhibitor similar results were obtained for cells stimulated with formaldehyde, thimerosal methyldibromoglutaronitrile, diphenylcyclopropenone, p-phenylenediamine, toluene-2,5-diamine, and 2,4-dinitrofluorobenzene. By use of a trinitrophenyl-specific monoclonal antibody it was shown that N-acetylcysteine as well as cysteine prevents the binding of 2,4,6-trinitrochlorobenzene to proteins in monocytes and monocyte-derived mature dendritic cells. Furthermore, the capacity of N-acetylcysteine to block the activation of p38 and ERK1/2 MAP kinases by 2,4,6-trinitrochlorobenzene was demonstrated. The radical scavengers ascorbic acid and alpha-tocopherol as well as the nuclear factor kappaB inhibitor pyrrolidine dithiocarbamate failed to prevent the increase in tyrosine phosphorylation. Our data present evidence that reactive oxygen species as well as transcription factor nuclear factor kappaB seem to be unimportant for the induction of tyrosine phosphorylation by contact sensitizers. On the other hand, protection of thiol groups using compounds with free sulfhydryl groups is very effective to block this process. This finding may have implications for prevention of occupational sensitization to strong contact allergens.
17. 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 T, Oyama Y, Nakao H, Umebayashi C, Nishizaki Y, Tatsuishi T, Iwase K, Murao K, Seo 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.
18: Genes Immun. 2002 Aug;3(5):270-8.
Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway.
Makani S, Gollapudi S, Yel L, Chiplunkar S, Gupta S.
Cellular and Molecular Immunology Laboratories, Division of Basic and Clinical Immunology, University of California, Irvine 92697, USA.
The major source of thimerosal (ethyl mercury thiosalicylate) exposure is childhood vaccines. It is believed that the children are exposed to significant accumulative dosage of thimerosal during the first 2 years of life via immunization. Because of health-related concerns for exposure to mercury, we examined the effects of thimerosal on the biochemical and molecular steps of mitochondrial pathway of apoptosis in Jurkat T cells. Thimerosal and not thiosalcylic acid (non-mercury component of thimerosal), in a concentration-dependent manner, induced apoptosis in T cells as determined by TUNEL and propidium iodide assays, suggesting a role of mercury in T cell apoptosis. Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. Furthermore, thimerosal enhanced intracellular reactive oxygen species and reduced intracellular glutathione (GSH). Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. These data suggest that thimerosal induces apoptosis in T cells via mitochondrial pathway by inducing oxidative stress and depletion of GSH.
19. Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.
Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization.
Westphal GA, Schnuch A, Schulz TG, Reich K, Aberer W, Brasch J, Koch P, Wessbecher R, Szliska C, Bauer A, Hallier E.
Abteilung fur Arbeits- und Sozialmedizin, Georg-August-Universitat Gottingen, Germany. gwestph@gwdg.de
OBJECTIVE: Thimerosal is an important preservative in vaccines and ophthalmologic preparations. The substance is known to be a type IV sensitizing agent. High sensitization rates were observed in contact-allergic patients and in health care workers who had been exposed to thimerosal-preserved vaccines. There is evidence for the involvement of the glutathione system in the metabolism of thimerosal or its decomposition products (organomercury alkyl compounds). Thus detoxification by polymorphically expressed glutathione S-transferases such as GSTT1 and GSTM1 might have a protective effect against sensitization by these substances. METHODS: To address this question, a case control study was conducted, including 91 Central European individuals with a positive patch-test reaction to thimerosal. This population was compared with 169 healthy controls and additionally with 114 individuals affected by an allergy against para-substituted aryl compounds. The latter population was included in order to test whether possible associations were due to substance-specific effects, or were a general feature connected with type IV immunological diseases. Homozygous deletions of GSTT1 and GSTM1 were determined by polymerase chain reaction. RESULTS: Glutathione S-transferase M1 deficiency was significantly more frequent among patients sensitized to thimerosal (65.9%, P = 0.013) compared with the healthy control group (49.1%) and the "para-compound" group (48%, P = 0.034). Glutathione S-transferase T1 deficiency in the thimerosal/mercury group (19.8%) was barely elevated versus healthy controls (16.0%) and the "para-compound" group (14.0%). The combined deletion (GSTT1-/GSTM1-) was markedly more frequent among thimerosal-sensitized patients than in healthy controls (17.6% vs. 6.5%, P = 0.0093) and in the "para- compound" group (17.6% vs. 6.1%, P =0.014), revealing a synergistic effect of these enzyme deficiencies (healthy controls vs. thimerosal GSTM1 negative individuals, OR = 2.0 [CI = 1.2-3.4], GSTT1-, OR = 1.2 [CI = 0.70-2.1], GSTM1/T1-, OR = 3.1 [CI = 1.4-6.5]). CONCLUSIONS: Since the glutathione-dependent system was repeatedly shown to be involved in the metabolism of thimerosal decomposition products, the observed association may be of functional relevance.
20. Travis Haws Re:Re:Re:Re: A Fatal Misdiagnosis. bmj. February 18th 2005.
21, J Neurosci Res. 1996 Apr 15;44(2):149-56.
Pharmacological characterization of inositol-1,4,5,-trisphosphate binding to membranes from retina and retinal cultures.
Lopez-Colome AM, Lee I.
Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico.
Light and excitatory amino acids (EAA) stimulate the phosphoinositide cycle in the vertebrate retina. The regulation of Ca2+ release from intracellular stores by inositol-1,4, 5-trisphosphate (IP3) involves an interaction of this compound with specific receptors. By means of [3H]IP3-specific binding, we studied the kinetic and pharmacological properties of IP3 receptors in the chick retina as well as in primary cultures of neurons and glia from this tissue. The equilibrium time for the binding reaction was 15 min and was optimal at alkaline pH (8.3). IP3 receptor displayed high affinity (K(B) approximately 40 nM) and selectivity for D-IP3, compared to D-IP4 > L-IP3 > D-IP2 > D- IP1. These characteristics were the same in subcellular fractions from outer (P1) and thinner (P2) plexiform layers, binding sites being more abundant in P2 (2.65 pmol/mg protein). IP3 receptors were present in both neuronal and glial cultures, but were concentrated in neuronal cultures. Binding was not affected by ryanodine, or caffeine, related to calcium-induced calcium release (CICR)channels, nor by the endoplasmic reticulum Ca2+ ATPase inhibitor thapsigargin, while heparin affectively inhibited IP3 binding. GSSG and thimerosal increased the affinity of [3H]IP3 binding from IC50 approximately 80 nM to IC50 approximately 40 nM; this effect was reversed by DTT. Binding in zero Ca2+ was decreased by low concentrations of Ca2+ (350 nM). These results suggest that actions of IP3 in the retina are regulated by physiological changes in intracellular pH and Ca2+ concentrations, as well as by the oxidation state of the receptor. Additionally, the presence of IP3 receptors in Muller glia opens the possibility of IP3 participation in nonsynaptic signalling through Ca2+ waves in glial cells.
22. Invest Ophthalmol Vis Sci. 1977 Apr;16(4):273-80.
Effect of the ophthalmic preservative thimerosal on rabbit and human corneal endothelium.
Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R, Pederson HF.
Widespread use of the mercurial-containing preservative thimerosal as an antibacterial agent in ophthalmic drugs and solutions warranted an investigation into its possible cytotoxic effects on the functional and ultrastructural integrity of the corneal endothelium. No changes in corneal thickness were observed during 5 hours' perfusion of the endothelium of rabbit and human corneas with 0.0001 and 0.0005 percent thimerosal in glutathione bicarbonate Ringer's solution (GBR). Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) of the endothelium of the 0.0001 percent group revealed normal ultrastructure. SEM and TEM of the endothelium of corneas perfused with 0.0005 percent thimerosal for 5 hours revealed condensed mitochondria, cytoplasmic vacuoles, and cytoplasmic flaps at the apical end of the cellular junctions. Perfusion of higher concentrations (0.001 and 0.005 perecnt) of thimerosal in GBR resulted in increases in corneal thickness after 2 hours and irreversible ultrastructural damage to the endothelial cells by 5 hours. Corneas perfused with 0.01 and 0.1 percent thimerosal in GBR showed a rapid and immediate increase in corneal thickness and endothelial cell death and necrosis within 1 hour. It is postulated that the mercury in thimerosal becomes bound to the cell membrane protein sulfhydryl groups, causing an increase in cellular permeability; These results suggest that the prolonged exposure of the corneal endothelium to thimerosal in the accepted antimicrobial dosage of 0.005 to 0.001 percent may result in functional and structural damage to the endothelium.
23. Blakemore-Brown Reweaving the Autistic Tapestry. Jessica Kingsley Publishers London 2002.
Competing interests: Expert in Autism and associated tapestry impairments
5 March 2005
Lisa C Blakemore-Brown, Psychologist UK based
Send response to journal: Re: Dish of the Day: Red Herrings stuffed with Thiomersal - guaranteed 49.5% Mercury.
Thiomersal/Thimerosal, a preservative developed in the late 1920's was manufactured by Eli Lilly and has been routinely used in vaccines and many other products since that time.
Thiomersal/Thimerosal contains 49.5% ethyl mercury. Methyl mercury is known to accumulate in fish and for this reason there is a safe daily limit for the amount of mercury adults are advised to not exceed. This is 0.1 mcg of Methyl Mercury per kilogram of weight. Babies have been given 25 microgrammes in each of the following vaccines: whole cell DTP and Hib, and the Hep B in the US. During this same period many very small premature babies have survived whereas in the past they would not have done so.
Over the course of the last century, individuals were given single vaccines with single amounts of mercury, but with the introduction of triple vaccines the amount of mercury contained within the preservative was multiplied and the cumulative effects are only just now being discovered by the public. Early papers on autism and battered baby syndrome appeared following the introduction of vaccines containing this preservative in the 30's and 40's and following the introduction of triple vaccines there has been an epidemic of autism - and genetic epidemics do not occur without some outside influence. It is also interesting that the Shaken Baby Syndrome and parent blame theories for odd medical presentations, have also vastly increased since these triple vaccines were brought in.
Thiomersal is still used in flu vaccines and other products but has been phased out in many childhood vaccines, but only very recently. For the UK it was August 2004 when the announcement was made.
Public Health agencies around the world have known about concerns with this neurotoxin for some years, and certainly since 1997 when the US Congress passed the FDA Modernization Act requiring the FDA to review all drugs that contained Mercury and determine their effect on humans. (3)
In 2000, recognising the cumulative amount of mercury in the triple vaccines, the FDA stated that children were receiving levels of mercury via this preservative far in excess of the 'safe' guidelines. Rough estimates suggested a child could be injected with 40 times the amount of mercury considered safe (3)
Despite the expected red herring arguments of the defensive, and the collaborative efforts of many countries to handle worrying data, many lab studies have explored the toxic effects of Thiomersal in humans and animals.
Evidence that Thiomersal can create changes at cellular level is rife in the literature (6,7,14,17,18.)A recent study concluded 'thimerosal is genotoxic in the cytochalasin B block micronucleus test with human lymphocytes. These data raise some concern on the widespread use of thimerosal.'(12)
Changes to phenotypes have been recognised (13) and the tapestry model allows for these various synergistic effects. For instance, it has been consistently shown that Thiomersal(Thimerosal) is a neurotoxin which is linked to the depletion of the protective anti-oxidant, glutathione (1,13,14,15,18,19)and that some individuals are more susceptible than others to such effects (4,16) Autistic individuals have been found to have lowered levels of glutathione and to have greater difficulties excreting mercury.
It is not impossible that earlier generations of constitutionally susceptible individuals were affected by the Mercury in their very early vaccinations, phenotypes were altered and in turn their offspring increased their risk factors for susceptibility to mercury damage.
Such susceptibilities, combined with an already weak immune system - in a baby. a medically vulnerable individual or an elderly person - further increase the risk factors.
As the changes triggered by Thiomersal appear at cellular level, including cell death and increased cellular permeability, it is not surprising that many forms of impairment are found.
'Exposure to organic mercury leads to primarily neurologic effects but a number of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal.' (2) Travis Haws has discussed Louis Reik's Disseminated Vasculomyelinopathy:an Immune Complex Disease relating to the multiple effects of infection once the immune system has been compromised. (20)
Effects of the preservative in preparations have found retinal (21) and corneal damage. (22)
The consistent reference to allergic effects and immune system interference (4, 5) maps onto my own findings that early vaccines seemed to trigger various allergies and intolerances in some children (See CASE ONE 2004 ebmj as an example taken directly from the medical notes)
My very early observations during the mid to late 1990's was that it was these medically vulnerable and allergic individuals who were more likely to have reacted to the MMR - which contains no Thiomersal. (23) Unfortunately because of Red Herring arguments and denial of what is known, we have yet to fully explore in a scientific way, why so many children reacted to vaccines.
In 2000 a meeting held in Simpsonwood US, revealed significant findings in a study by Verstraeten in relation to the emergence of a variety of neurodevelopmental disorders including tics, ADHD, speech and language and motor impairments - and Thiomersal. It has taken the Freedom of Information Act to expose what was shown in that meeting - and the steps taken to cover it up.
The epidemic of health and developmental problems in so called advanced countries is now undeniable. 1 in 10 children suffer from gastrointestinal disorders, 1 in 4 have asthma. A colleague last week mentioned that out of 16 children on a school trip involving his child, 15 had asthma. Children are arriving at school unable to use a knife and fork, pay attention or understand their social worlds, highly sensitised to all aspects of the real world.
When we have removed the Red Herrings - and those who cook them up - we might begin to take responsibility again for the health of millions across the world.
Refs:
1: Neurotoxicology. 2005 Jan;26(1):1-8.
Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors.
James SJ, Slikker W 3rd, Melnyk S, New E, Pogribna M, Jernigan S.
Department of Pediatrics, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, USA. jamesjill@uams.edu
Thimerosol is an antiseptic containing 49.5% ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Environmental methyl mercury has been shown to be highly neurotoxic, especially to the developing brain. Because mercury has a high affinity for thiol (sulfhydryl (-SH)) groups, the thiol-containing antioxidant, glutathione (GSH), provides the major intracellular defense against mercury-induced neurotoxicity. Cultured neuroblastoma cells were found to have lower levels of GSH and increased sensitivity to thimerosol toxicity compared to glioblastoma cells that have higher basal levels of intracellular GSH. Thimerosal-induced cytotoxicity was associated with depletion of intracellular GSH in both cell lines. Pretreatment with 100 microM glutathione ethyl ester or N-acetylcysteine (NAC), but not methionine, resulted in a significant increase in intracellular GSH in both cell types. Further, pretreatment of the cells with glutathione ethyl ester or NAC prevented cytotoxicity with exposure to 15 microM Thimerosal. Although Thimerosal has been recently removed from most children's vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries. The potential protective effect of GSH or NAC against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccinations.
2: Toxicol Ind Health. 2002 Apr;18(3):109-60.
Organic mercury compounds: human exposure and its relevance to public health.
Risher JF, Murray HE, Prince GR.
Agency for Toxic Substances and Disease Registry, Division of Toxicology, Toxicology Information Branch, Clifton Road, Atlanta, Georgia 30333, USA.
Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes, and the effects of such exposure depend upon both the type of mercury to which exposed and the magnitude of the exposure. In general, the effects of exposure to organic mercury are primarily neurologic, while a host of other organ systems may also be involved, including gastrointestinal, respiratory, hepatic, immune, dermal, and renal. While the primary source of exposure to organic mercury for most populations is the consumption of methylmercury-contaminated fish and shellfish, there are a number of other organomercurials to which humans might be exposed. The antibacterial and antifungal properties of organomercurials have resulted in their long use as topical disinfectants (thimerosal and merbromin) and preservatives in medical preparations (thimerosal) and grain products (both methyl and ethyl mercurials). Phenylmercury has been used in the past in paints, and dialkyl mercurials are still used in some industrial processes and in the calibration of certain analytical laboratory equipment. The effects of exposure to different organic mercurials by different routes of exposure are summarized in this article.
3. Trade Off: Vaccine Maker Profits and Autism. Evelyn Pringle . Independent News Media. 4th March 2005
4: Med Pr. 2001;52(1):45-51.
[Genetic polymorphism of glutathione s-transferase as a factor predisposing to allergic dermatitis]
[Article in Polish]
Lutz W, Tarkowski M, Nowakowska E.
Zakladu Diagnostyki Laboratoryjnej, Instytutu Medycyny Pracy, Lodzi.
In the inductive phase of contact allergic dermatitis, simple chemical compounds (haptens) produce together with epidermic proteins adducts presented by Langerhans cells to T lymphocytes. Binding to protein carrier is a necessary condition of transforming a low-molecular allergen into immunogenic one and evoking immunological reaction. The production of allergen adducts with proteins is conditioned by the presence of electrophilic groups in their molecules, or their acquiring during biotransformation phase I. Active allergen metabolites undergo further alterations during biotransformation phase II which leads most frequently to the decline in their chemical activity and more rapid excretion from the body. The number of reactive metabolites (reactive allergens) available for producing adducts with proteins keeps the balance between activation and deactivation reactions. Glutathione S-transferases play a particular role in the allergens (or their metabolites) deactivation process in biotransformation phase II. These enzymes catalyse reactions responsible for the declined electrophilic potential of allergens (or their metabolites), and thus for the decrease in the number of allergen molecules able to produce protein covalent bindings (adducts). Glutathione S-transferases, occurring in the human cellular cytoplasm belong to five classes: alpha(GST A), mu(GST M), theta(GST P), pi(GST T) and Z(GST Z), as well as to one class present in microsomes. The study indicated the presence of isoenzymes GST T1 and GST M1 in the skin. Both isoforms participate in the process of low-molecular allergen biotransformation. Carriers of defective genes GST T1 and/or GST M1 are more vulnerable to allergenic effect of some allergens, e.g. thimerosal, which is associated with the absence of or decrease in the activity of isoenzymes GST T1 and GST M1.
5: Cell Biol Toxicol. 1999 Feb;15(1):57-62.
Mechanisms of drug-induced allergic contact dermatitis.
Lebrec H, Bachot N, Gaspard I, Kerdine S, Guinnepain MT, Laurent J, Pallardy M.
INSERM U 461, Faculte de Pharmacie Paris Sud, Chatenay-Malabry, France. hlebrec@infobiogen.fr
Allergic contact dermatitis is induced by a wide variety of drugs that trigger specific immune responses following topical exposure. Identified chemical structures involved in such reactions include the mercuric and thiosalicylic acid groups of thimerosal, the diphenylketone group of the anti- inflammatory drug ketoprofen, the amide or ester structure of local anesthetics, and the side-chain and thiazolidine ring of beta-lactams. The T cell responses to such compounds involve CD4+ and CD8+ alphabeta+ T lymphocytes and also CD4 /CD8 gammadelta+ T cells. Although "T helper 2" cytokine production by drug- specific human T cells from patients with allergic contact dermatitis has been described, T helper 1-like and T cytotoxic 1-like responses clearly play key roles in this cutaneous reaction.
6. Int J Biochem. 1994 Jan;26(1):93-6.
Effect of thimerosal on cytosolic calcium and phosphatidylserine synthesis in Jurkat T cells.
Pelassy C, Breittmayer JP, Ticchioni M, Aussel C.
INSERM U343, Faculte de Medecine, Nice, France.
1. We investigated the effect of the thiol reagent, thimerosal on calcium movements in the Jurkat T cell line. 2. Thimerosal induced a rise in cytosolic Ca2+ concentration due both to a release of Ca2+ from intracellular stores and a Ca2+ influx. 3. Thimerosal, released Ca2+ from the same intracellular stores than CD3 mAb and ionomycin. 4. Emptying the Ca2+ intracellular stores was accompanied by a marked decrease of phosphatidylserine synthesis indicating that phosphatidylserine synthesis occurs within or close to the endoplasmic reticulum Ca(2+)-stores as previously described in CD3-, ionomycin- or Ca(2+)-ATPase inhibitor-treated lymphocytes.
7. Biochim Biophys Acta. 1992 Oct 19;1111(1):65-74.
Effect of the sulfhydryl reagent thimerosal on cytosolic free Ca2+ and membrane potential of thymocytes.
Gukovskaya AS, Trepakova ES, Zinchenko VP, Korystov YN, Bezuglov VV.
Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Pushchino, Moscow Region.
The sulfhydryl reagent thimerosal at concentrations 5-100 microM has been found to induce a variety of changes in ion transport in rat thymocytes. In particular, [Ca2+]i increases about 10-fold from the basal level. The [Ca2+]i response to thimerosal displays a two-stage time course, with the main [Ca2+]i rise during the second stage. Evidence has been obtained for the depletion of intracellular Ca2+ pools in thimerosal-treated cells, however, Ca2+ mobilization from intracellular stores does not contribute significantly into [Ca2+]i rise. Thimerosal elicits permeability not only for Ca2+, but also for Mn2+ and Ni2+, which is Ca(2+)-dependent. We failed to get any evidence on thimerosal- induced inhibition of the plasma membrane Ca(2+)-ATPase. The induction of Ca2+ influx, rather than inhibition of Ca(2+)-ATPase, accounts for the disturbance of [Ca2+]i homeostasis in thimerosal-treated cells. Thimerosal also elicits changes in monovalent ion fluxes resulting in marked depolarization. The latter seems unrelated to the changes in [Ca2+]i and is suggested to be mediated both by increased permeability for Na+ and a decreased one for K+. Thimerosal significantly stimulates AA release from thymocytes. Evidence has been presented that AA metabolite(s), probably, LO product(s), may mediate the changes in the transport of mono- and divalent cations elicited by the sulfhydryl reagent. Prolonged treatment of thymocytes with thimerosal resulted in cell death.
8. Lancet. 1991 Aug 3;338(8762):315-6.
Ecotoxicol Environ Saf. 1985 Oct;10(2):150-8.
Effect of organomercurial poisoning on the peripheral blood and metabolite levels of a freshwater fish.
Gill TS, Pant JC.
This work evaluated the hematological and biochemical changes in the fish, Puntius conchonius, under experimental organomercurial poisoning. Long- term (8 weeks) exposure to 3.63 and 6.03 mg/liter methoxyethyl mercuric chloride (MEMC) (0.2 and 0.33 fractions of 96-hr LC50) led to morphological aberrations in mature erythrocytes including nuclear and cytoplasmic deterioration, vacuolation, chromatin condensation, and hypochromia. Immature erythrocytes showing membrane leakage were also encountered. Erythrocyte count and hemoglobin (Hb) were significantly lowered after 1 and 3 weeks followed by a marginal rise persisting upto 8 weeks. Differential leucocyte counts revealed significant thrombocytopenia, lymphocytosis, and neutropenia. Collateral evaluation of blood glucose and tissue glycogen levels revealed significant hyperglycemia as well as glycogen depletion in liver and brain. Heart glycogen content evinced a substantial increase after 5 and 8 weeks exposure.
9. Rev Neurol (Paris). 1979;135(11):827-33.
[Morvan's fibrillary chorea]
[Article in French]
de Bray JM, Emile J, Basle M, Morer T, Bastard J.
Two cases of Morvan's chorea are reported. One of the patients presented the characteristic of having had two attacks, the first after organic mercury preparations, and the second after gold salts for inflammatory rheumatism. The second case had facial fibrillations only, and this was followed by a regressive polyradiculoneuritis one month later. This latter case raises certain diagnostic problems. The existence of a particular type of immuno-allergic tendency could be validly related to a triggering effect of various etiological agents (metals such as mercury or gold salts, or infective agents). The absence of hypotonia, and a regressive course appear to be the characteristics that distinguish fibrillary chorea from the continuous activity syndrome of the muscle fibers described by Isaacs.
10. Contact Dermatitis. 1980 Jun;6(4):241-5.
Merthiolate hypersensitivity and vaccination.
Forstrom L, Hannuksela M, Kousa M, Lehmuskallio E.
Epicutaneous tests with 0.1% merthiolate in petrolatum showed hypersensitivity in 96 of 4647 eczema patients (2.0%) and in seven of 105 healthy recruits (7%). There was a marked preponderance of young age classes in the eczema group. Twelve of 41 merthiolate-positive patients tested reacted to mercury alone, three to thiosalicylic acid alone and one to both. The remaining 25 patients reacted to neither of the individual components although the merthiolate complex as a whole gave a positive test result. Forty-five of the merthiolate- positive patients were tested subcutaneously with 0.5 ml of a 0.01% merthiolate solution, i.e. a dose equal to that contained in one shot of tetanus toxoid, for example. Nine patients developed a local reaction at the site of the injection, and the area became eczematous in four cases. In one of the patients the eczema spread over the body, causing fever. Since merthiolate-sensitive patients also react to merthiolate administered intracutaneously, the vaccinator should avoid the use of a needle whose outer surface has been contaminated when the vaccine was aspirated from the bottle. However, even when this precautionary measure is taken, local reactions can be expected in such a high percentage of merthiolate-sensitive persons that merthiolate in vaccines should be replaced by another antibacterial agent.
11. Contact Dermatitis. 1986 Nov;15(5):309-10.
Reactions to merthiolate in infants.
Novak M, Kvicalova E, Friedlanderova B.
12. Arch Toxicol. 2003 Jan;77(1):50-5. Epub 2002 Nov 06.
Thimerosal induces micronuclei in the cytochalasin B block micronucleus test with human lymphocytes.
Westphal GA, Asgari S, Schulz TG, Bunger J, Muller M, Hallier E.
Department of Occupational Health, Georg-August-University Gottingen, Waldweg 37, 37073 Gottingen, Germany. gwestph@gwdg.de
Thimerosal is a widely used preservative in health care products, especially in vaccines. Due to possible adverse health effects, investigations on its metabolism and toxicity are urgently needed. An in vivo study on chronic toxicity of thimerosal in rats was inconclusive and reports on genotoxic effects in various in vitro systems were contradictory. Therefore, we reinvestigated thimerosal in the cytochalasin B block micronucleus test. Glutathione S-transferases were proposed to be involved in the detoxification of thimerosal or its decomposition products. Since the outcome of genotoxicity studies can be dependent on the metabolic competence of the cells used, we were additionally interested whether polymorphisms of glutathione S-transferases (GSTM1, GSTT1, or GSTP1) may influence the results of the micronucleus test with primary human lymphocytes. Blood samples of six healthy donors of different glutathione S-transferase genotypes were included in the study. At least two independent experiments were performed for each blood donor. Significant induction of micronuclei was seen at concentrations between 0.05-0.5 micro g/ml in 14 out of 16 experiments. Thus, genotoxic effects were seen even at concentrations which can occur at the injection site. Toxicity and toxicity-related elevation of micronuclei was seen at and above 0.6 micro g/ml thimerosal. Marked individual and intraindividual variations in the in vitro response to thimerosal among the different blood donors occurred. However, there was no association observed with any of the glutathione S-transferase polymorphism investigated. In conclusion, thimerosal is genotoxic in the cytochalasin B block micronucleus test with human lymphocytes. These data raise some concern on the widespread use of thimerosal.
13. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.
Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal.
Muller M, Westphal G, Vesper A, Bunger J, Hallier E.
Department of Occupational and Social Medicine, Georg-August- University Gottingen, D-37073 Gottingen, Germany. mmuelle3@gwdg.de
We have investigated the interaction of thimerosal, a widely used antiseptic and preservative, with the human erythrocytic GST T1 (glutathione-S- transferase T1). This detoxifying enzyme is expressed in the erythrocytes of solely the human species and it displays a genetic polymorphism. Due to this polymorphism about 25% of the individuals of the caucasian population lack this activity ("non-conjugators"), while 75% show it ("conjugators") (Hallier, E., et al., 1993). Using our newly developed HPLC-fluorescence detection assay (Muller, M., et al., 2001) we have profiled the kinetics of enzyme inhibition in erythrocyte lysates of two individuals previously identified as "normal conjugator" (medium enzyme activity) and "super-conjugator" (very high activity). For the normal conjugator we have determined a 2.77 mM thimerosal concentration to inhibit 50% of the GST T1 activity. In the case of the super-conjugator a 2.3 mM thimerosal concentration causes a 50% inhibition of the enzyme activity. For both phenotypes a 14.8 mM thimerosal concentration results in residual enzyme activities equal to those typically detected in non-conjugator lysates. Thus, sufficiently high doses of thimerosal may be able to change the phenotypic status of an individual--at least in vitro--by inhibition of the GST T1 enzyme.
14. Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.
Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization.
Westphal GA, Schnuch A, Schulz TG, Reich K, Aberer W, Brasch J, Koch P, Wessbecher R, Szliska C, Bauer A, Hallier E.
Abteilung fur Arbeits- und Sozialmedizin, Georg-August-Universitat Gottingen, Germany. gwestph@gwdg.de
OBJECTIVE: Thimerosal is an important preservative in vaccines and ophthalmologic preparations. The substance is known to be a type IV sensitizing agent. High sensitization rates were observed in contact-allergic patients and in health care workers who had been exposed to thimerosal-preserved vaccines. There is evidence for the involvement of the glutathione system in the metabolism of thimerosal or its decomposition products (organomercury alkyl compounds). Thus detoxification by polymorphically expressed glutathione S-transferases such as GSTT1 and GSTM1 might have a protective effect against sensitization by these substances. METHODS: To address this question, a case control study was conducted, including 91 Central European individuals with a positive patch-test reaction to thimerosal. This population was compared with 169 healthy controls and additionally with 114 individuals affected by an allergy against para-substituted aryl compounds. The latter population was included in order to test whether possible associations were due to substance-specific effects, or were a general feature connected with type IV immunological diseases. Homozygous deletions of GSTT1 and GSTM1 were determined by polymerase chain reaction. RESULTS: Glutathione S-transferase M1 deficiency was significantly more frequent among patients sensitized to thimerosal (65.9%, P = 0.013) compared with the healthy control group (49.1%) and the "para-compound" group (48%, P = 0.034). Glutathione S-transferase T1 deficiency in the thimerosal/mercury group (19.8%) was barely elevated versus healthy controls (16.0%) and the "para-compound" group (14.0%). The combined deletion (GSTT1-/GSTM1-) was markedly more frequent among thimerosal-sensitized patients than in healthy controls (17.6% vs. 6.5%, P = 0.0093) and in the "para- compound" group (17.6% vs. 6.1%, P =0.014), revealing a synergistic effect of these enzyme deficiencies (healthy controls vs. thimerosal GSTM1 negative individuals, OR = 2.0 [CI = 1.2-3.4], GSTT1-, OR = 1.2 [CI = 0.70-2.1], GSTM1/T1-, OR = 3.1 [CI = 1.4-6.5]). CONCLUSIONS: Since the glutathione-dependent system was repeatedly shown to be involved in the metabolism of thimerosal decomposition products, the observed association may be of functional relevance.
PMID: 11007341 [PubMed - indexed for MEDLINE]
15 Toxicol In Vitro. 2004 Oct;18(5):563-9.
Property of thimerosal-induced decrease in cellular content of glutathione in rat thymocytes: a flow cytometric study with 5-chloromethylfluorescein diacetate.
Ueha-Ishibashi T, Tatsuishi T, Iwase K, Nakao H, Umebayashi C, Nishizaki Y, Nishimura Y, Oyama Y, Hirama S, Okano Y.
Laboratory of Cellular Signaling, Faculty of Integrated Arts and Sciences, The University of Tokushima, Minami-Jyosanjima 1-1, Tokushima 770-8502, Japan.
There is a concern on the part of public health community that adverse health consequences by thimerosal, a preservative in vaccines for infants, may occur among infants during immunization schedule. Therefore, the effect of thimerosal on cellular content of glutathione was examined on thymocytes obtained from 4-week-old rats using a flow cytometer and 5-chloromethylfluorescein diacetate. Thimerosal at concentrations ranging from 1 to 10 microM reduced the cellular content of glutathione in a concentration-dependent manner, and the complete depletion of cellular glutathione was observed when the cells were treated with 30 microM thimerosal. L-Cysteine significantly attenuated the actions of thimerosal to reduce the glutathione content and to increase the intracellular Ca2+ concentration. Prolonged incubation (24 h) with 1-3 microM thimerosal induced the apoptosis. The cytotoxic action of thimerosal was greatly augmented when the cells suffered oxidative stress induced by H2O2. It may be unlikely that thimerosal exerts potent cytotoxic action under the in vivo condition because the blood concentration of thimerosal after receiving vaccines does not seem to reach micromolar range and nonprotein thiols at micromolar concentrations are present in the blood.
16: J Invest Dermatol. 2003 Nov;121(5):1039-44.
Thiol antioxidants block the activation of antigen-presenting cells by contact sensitizers.
Bruchhausen S, Zahn S, Valk E, Knop J, Becker D.
Department of Dermatology, University of Mainz, Mainz, Germany.
Strong contact sensitizers are able to induce signal transduction mechanisms such as tyrosine phosphorylation and activation of MAP kinases in antigen-presenting cells. We studied the capacity of different antioxidants (ascorbic acid, alpha-tocopherol, pyrrolidine dithiocarbamate, N- acetylcysteine, and glutathione) to block the increase in tyrosine phosphorylation in human monocytes seen after stimulation with strong contact sensitizers. Human peripheral blood mononuclear cells were stimulated with 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone in the presence or absence of these antioxidants. The total amount of membrane-associated phosphotyrosine in CD14+ cells was quantified using flow cytometric techniques. Complete inhibition of tyrosine phosphorylation was noticed when cells were stimulated in the presence of N-acetylcysteine or glutathione. Using N-acetylcysteine as inhibitor similar results were obtained for cells stimulated with formaldehyde, thimerosal methyldibromoglutaronitrile, diphenylcyclopropenone, p-phenylenediamine, toluene-2,5-diamine, and 2,4-dinitrofluorobenzene. By use of a trinitrophenyl-specific monoclonal antibody it was shown that N-acetylcysteine as well as cysteine prevents the binding of 2,4,6-trinitrochlorobenzene to proteins in monocytes and monocyte-derived mature dendritic cells. Furthermore, the capacity of N-acetylcysteine to block the activation of p38 and ERK1/2 MAP kinases by 2,4,6-trinitrochlorobenzene was demonstrated. The radical scavengers ascorbic acid and alpha-tocopherol as well as the nuclear factor kappaB inhibitor pyrrolidine dithiocarbamate failed to prevent the increase in tyrosine phosphorylation. Our data present evidence that reactive oxygen species as well as transcription factor nuclear factor kappaB seem to be unimportant for the induction of tyrosine phosphorylation by contact sensitizers. On the other hand, protection of thiol groups using compounds with free sulfhydryl groups is very effective to block this process. This finding may have implications for prevention of occupational sensitization to strong contact allergens.
17. 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 T, Oyama Y, Nakao H, Umebayashi C, Nishizaki Y, Tatsuishi T, Iwase K, Murao K, Seo 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.
18: Genes Immun. 2002 Aug;3(5):270-8.
Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway.
Makani S, Gollapudi S, Yel L, Chiplunkar S, Gupta S.
Cellular and Molecular Immunology Laboratories, Division of Basic and Clinical Immunology, University of California, Irvine 92697, USA.
The major source of thimerosal (ethyl mercury thiosalicylate) exposure is childhood vaccines. It is believed that the children are exposed to significant accumulative dosage of thimerosal during the first 2 years of life via immunization. Because of health-related concerns for exposure to mercury, we examined the effects of thimerosal on the biochemical and molecular steps of mitochondrial pathway of apoptosis in Jurkat T cells. Thimerosal and not thiosalcylic acid (non-mercury component of thimerosal), in a concentration-dependent manner, induced apoptosis in T cells as determined by TUNEL and propidium iodide assays, suggesting a role of mercury in T cell apoptosis. Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. Furthermore, thimerosal enhanced intracellular reactive oxygen species and reduced intracellular glutathione (GSH). Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. These data suggest that thimerosal induces apoptosis in T cells via mitochondrial pathway by inducing oxidative stress and depletion of GSH.
19. Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.
Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization.
Westphal GA, Schnuch A, Schulz TG, Reich K, Aberer W, Brasch J, Koch P, Wessbecher R, Szliska C, Bauer A, Hallier E.
Abteilung fur Arbeits- und Sozialmedizin, Georg-August-Universitat Gottingen, Germany. gwestph@gwdg.de
OBJECTIVE: Thimerosal is an important preservative in vaccines and ophthalmologic preparations. The substance is known to be a type IV sensitizing agent. High sensitization rates were observed in contact-allergic patients and in health care workers who had been exposed to thimerosal-preserved vaccines. There is evidence for the involvement of the glutathione system in the metabolism of thimerosal or its decomposition products (organomercury alkyl compounds). Thus detoxification by polymorphically expressed glutathione S-transferases such as GSTT1 and GSTM1 might have a protective effect against sensitization by these substances. METHODS: To address this question, a case control study was conducted, including 91 Central European individuals with a positive patch-test reaction to thimerosal. This population was compared with 169 healthy controls and additionally with 114 individuals affected by an allergy against para-substituted aryl compounds. The latter population was included in order to test whether possible associations were due to substance-specific effects, or were a general feature connected with type IV immunological diseases. Homozygous deletions of GSTT1 and GSTM1 were determined by polymerase chain reaction. RESULTS: Glutathione S-transferase M1 deficiency was significantly more frequent among patients sensitized to thimerosal (65.9%, P = 0.013) compared with the healthy control group (49.1%) and the "para-compound" group (48%, P = 0.034). Glutathione S-transferase T1 deficiency in the thimerosal/mercury group (19.8%) was barely elevated versus healthy controls (16.0%) and the "para-compound" group (14.0%). The combined deletion (GSTT1-/GSTM1-) was markedly more frequent among thimerosal-sensitized patients than in healthy controls (17.6% vs. 6.5%, P = 0.0093) and in the "para- compound" group (17.6% vs. 6.1%, P =0.014), revealing a synergistic effect of these enzyme deficiencies (healthy controls vs. thimerosal GSTM1 negative individuals, OR = 2.0 [CI = 1.2-3.4], GSTT1-, OR = 1.2 [CI = 0.70-2.1], GSTM1/T1-, OR = 3.1 [CI = 1.4-6.5]). CONCLUSIONS: Since the glutathione-dependent system was repeatedly shown to be involved in the metabolism of thimerosal decomposition products, the observed association may be of functional relevance.
20. Travis Haws Re:Re:Re:Re: A Fatal Misdiagnosis. bmj. February 18th 2005.
21, J Neurosci Res. 1996 Apr 15;44(2):149-56.
Pharmacological characterization of inositol-1,4,5,-trisphosphate binding to membranes from retina and retinal cultures.
Lopez-Colome AM, Lee I.
Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico.
Light and excitatory amino acids (EAA) stimulate the phosphoinositide cycle in the vertebrate retina. The regulation of Ca2+ release from intracellular stores by inositol-1,4, 5-trisphosphate (IP3) involves an interaction of this compound with specific receptors. By means of [3H]IP3-specific binding, we studied the kinetic and pharmacological properties of IP3 receptors in the chick retina as well as in primary cultures of neurons and glia from this tissue. The equilibrium time for the binding reaction was 15 min and was optimal at alkaline pH (8.3). IP3 receptor displayed high affinity (K(B) approximately 40 nM) and selectivity for D-IP3, compared to D-IP4 > L-IP3 > D-IP2 > D- IP1. These characteristics were the same in subcellular fractions from outer (P1) and thinner (P2) plexiform layers, binding sites being more abundant in P2 (2.65 pmol/mg protein). IP3 receptors were present in both neuronal and glial cultures, but were concentrated in neuronal cultures. Binding was not affected by ryanodine, or caffeine, related to calcium-induced calcium release (CICR)channels, nor by the endoplasmic reticulum Ca2+ ATPase inhibitor thapsigargin, while heparin affectively inhibited IP3 binding. GSSG and thimerosal increased the affinity of [3H]IP3 binding from IC50 approximately 80 nM to IC50 approximately 40 nM; this effect was reversed by DTT. Binding in zero Ca2+ was decreased by low concentrations of Ca2+ (350 nM). These results suggest that actions of IP3 in the retina are regulated by physiological changes in intracellular pH and Ca2+ concentrations, as well as by the oxidation state of the receptor. Additionally, the presence of IP3 receptors in Muller glia opens the possibility of IP3 participation in nonsynaptic signalling through Ca2+ waves in glial cells.
22. Invest Ophthalmol Vis Sci. 1977 Apr;16(4):273-80.
Effect of the ophthalmic preservative thimerosal on rabbit and human corneal endothelium.
Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R, Pederson HF.
Widespread use of the mercurial-containing preservative thimerosal as an antibacterial agent in ophthalmic drugs and solutions warranted an investigation into its possible cytotoxic effects on the functional and ultrastructural integrity of the corneal endothelium. No changes in corneal thickness were observed during 5 hours' perfusion of the endothelium of rabbit and human corneas with 0.0001 and 0.0005 percent thimerosal in glutathione bicarbonate Ringer's solution (GBR). Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) of the endothelium of the 0.0001 percent group revealed normal ultrastructure. SEM and TEM of the endothelium of corneas perfused with 0.0005 percent thimerosal for 5 hours revealed condensed mitochondria, cytoplasmic vacuoles, and cytoplasmic flaps at the apical end of the cellular junctions. Perfusion of higher concentrations (0.001 and 0.005 perecnt) of thimerosal in GBR resulted in increases in corneal thickness after 2 hours and irreversible ultrastructural damage to the endothelial cells by 5 hours. Corneas perfused with 0.01 and 0.1 percent thimerosal in GBR showed a rapid and immediate increase in corneal thickness and endothelial cell death and necrosis within 1 hour. It is postulated that the mercury in thimerosal becomes bound to the cell membrane protein sulfhydryl groups, causing an increase in cellular permeability; These results suggest that the prolonged exposure of the corneal endothelium to thimerosal in the accepted antimicrobial dosage of 0.005 to 0.001 percent may result in functional and structural damage to the endothelium.
23. Blakemore-Brown Reweaving the Autistic Tapestry. Jessica Kingsley Publishers London 2002.
Competing interests: Expert in Autism and associated tapestry impairments
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