Author Archives: The Refusers

CNN iReport on CDC Whistleblower Spreads like Wildfire, then Censored

by Jon Rappoport of No More Fake News Aug 24, 2014

CensorshipOn August 22, a user named Bobby Dee posted a CNN iReport about the CDC whistleblower who states he cooked data to hide a vaccine-autism connection.

CNN iReports aren’t official CNN stories. They’re “user generated news…opinions belong to the submitter.”

Well, Bobby’s submission, as Celia Farber reports at, rocketed to 45,232 views in a matter of hours. 178 comments, 17 thousand shares.

Story 1

Story 2

Then it was axed, removed, deleted.

printed the usual tired explanation. The iReport had been “flagged.” It was “in violation of iReport’s policy.”

Translation: Lots of people cared about the report, wanted to read it, it was getting more action than a great deal of what CNN calls news—and it implied something was wrong in the Holy Temple of the Vaccine.

So CNN axed it.

It’s gone.

CNN claims that when an iReport goes “virish,” they then “vet” the report to make sure it’s accurate. Look around and see if you can find examples where this has taken place. So far, I don’t see any—except for Bobby Dee’s report.


Here is what Bobby Dee posted on CNN’s iReport, before it was taken down:

“William W Thompson, PhD, Senior Scientist, National Center of Birth Defects and Development Disabilities, has stepped forward and admitted the 2004 paper [which found no link between the MMR vaccine and autism] was a fraud.

“Dr. Thompson has admitted the 340% increase [in autism] in boys receiving the MMR vaccine ‘on time’ as opposed to delayed was buried by himself, Dr. DeStefano, Dr. Bhasin, Dr. Yeargin-Allsopp, and Dr. Boyle [all co-authors of the 2004 paper]…”

CNN makes up the news as it goes along and as it receives marching orders from its “reliable sources,” but a citizen with actual news must be stopped.

An editor at CNN told Bobby Dee she would contact Brian Hooker, who played a central role in bringing whistleblower Thompson’s confession forward to the public—but so far, she hasn’t.

CNN: the most trusted name in twisted information.

CNN headquarters are right down the street in Atlanta from the CDC, where the MMR vaccine data were cooked, stepped on, and buried.

I guess it’s just too much trouble for a reporter or editor to hop in a cab and go over there and ask a few tough questions.

Well, there are really no questions to ask, are there? CNN and the CDC are the “already asked and answered” dancing twins, who can read each other’s minds.

Vaccines? Never met one they didn’t love. Adverse effects? Damage? Never heard of such a thing.

“What do you want to be when you grow up, Jimmy?”

“I want to be a mouthpiece for the vaccine cartel, Daddy.”

“That’s wonderful, son. Try CNN.”

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Revealed: CDC Whistleblower Who Falsified MMR/Autism Safety Study

The CDC scientist who faked MMR/autism data at the request of CDC bosses is revealed in this excellent video: William Thompson CDC.

Brian Hooker PhD: “He has released quite compelling information regarding fraud and malfeasance in the CDC.”

William Thompson CDC: “It’s the lowest point of my career that I went along with that paper … we didn’t report significant findings.”

William Thompson CDC: “The higher ups wanted to do certain things and I went along with it.”

William Thompson CDC: “I’m completely ashamed of what I did … I have great shame now when I meet families with kids with autism because I have been part of the problem.”

William Thompson CDC: “Oh my God, I cannot believe we did what we did.”

William Thompson CDC: “I have stopped lying.”


Fraudulent Thompson/CDC study: MMR vaccination and autism: is there a link? DeStefano F, Thompson WW.

Fraudulent Thompson/CDC study: MMR vaccine and autism: an update of the scientific evidence. DeStefano F1, Thompson WW.

New PubMed study by Brian Hooker re-examining original MMR/autism data concealed by CDC

PubMed.Gov - Measles-mumps-rubella vaccination timing and autism among young african american boys: a reanalysis of CDC data. August 8, 2014 

Background: A significant number of children diagnosed with autism spectrum disorder suffer a loss of previously-acquired skills, suggesting neurodegeneration or a type of progressive encephalopathy with an etiological basis occurring after birth. The purpose of this study is to investigate the effect of the age at which children got their first Measles-Mumps-Rubella (MMR) vaccine on autism incidence. This is a reanalysis of the data set, obtained from the U.S. Centers for Disease Control and Protection (CDC), used for the Destefano et al. 2004 publication on the timing of the first MMR vaccine and autism diagnoses.

Conclusions: The present study provides new epidemiologic evidence showing that African American males receiving the MMR vaccine prior to 24 months of age or 36 months of age are more likely to receive an autism diagnosis.


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More Flu Vaccine Cockamamie – Dr. Brownstein MD

MB Comment: The biggest flaw in this ridiculous study sponsored by vaccine manufacturer Sanofi is there was no unvaccinated control group. Without that information, the vaccinated could have a HIGHER rate of flu than the unvaccinated

By Dr. David Brownstein MD August 20, 2014

Researchers reported in the New England Journal of Medicine (August 14, 2014) that a high dose flu vaccine was more effective than the standard flu vaccine for seniors. The vaccine is called Fluzone High Dose vaccine. Of course, the media jumped on this report. In the Healthday article, the chief medical office for Sanofi-Pasteur—the Big Pharma company who funded the study—stated, “The study demonstrated a 24 percent reduction in influenza illness among the participants who received the high-dose vaccine compared to those who received the standard dose.”

To date, no flu vaccine has shown any significant efficacy in seniors. A 24 percent reduction in influenza illness in seniors would certainly be something to celebrate.

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When medical students and residents rotate through my office, the first thing I do is hand them an article and ask them to explain the statistical methods used by the researchers. Over the years, I have had one student/doctor who understood statistics enough to understand how research articles are reported. I always tell the students/doctors that if they don’t know how to properly read the original research articles, they cannot make a proper decision on whether the particular therapy is useful or not.

After seeing the media article, I pulled the flu research article and read it. Here are the results: 31,989 participants were enrolled form 126 research centers in the U.S. and Canada. Half were given the standard flu vaccine and half given the high dose vaccine.

1.4% of the seniors who received the high dose vaccine became ill with the flu and 1.9% of the seniors who received the standard flu vaccine developed the flu.

(I hope you are not laughing as I did when I read that.)

How in the world did they report a 24% lowered incidence of the flu with the use of the high-dose vaccine? Simply dividing 1.4% by 1.9% gives the relative risk reduction of 24%. However, this is a relative risk reduction—a useless number to use when deciding whether a therapy is good for any patient.

A better analysis of this data involves calculating the absolute risk. The absolute risk, according the New England Journal of Medicine, is better to use when deciding whether a particular therapy is warranted for an individual patient. The absolute risk is the difference between the treated and untreated group. What is the absolute risk difference in this study? 1.9 percent minus 1.4 percent which equals 0.5 percent or 0.005. That means that, according to this study, 200 seniors (1/.005) would have to be vaccinated with the high-dose flu vaccine to prevent one case of the flu. Here’s my interpretation of this study:  This study shows that the high dose flu vaccine is a colossal failure as the results indicate that 99.5 percent of seniors who get this vaccine will not receive any benefit.

So, 200 seniors must receive a vaccine to prevent one case of the flu. What is the cost of that? I called my local CVS and was told that the cost of the flu vaccine was $32.00/dose. Multiplying the numbers reveals that it costs $6,400 dollars to vaccinate all those people.

What a waste of money. That amount of money could buy a lot of vitamin C which would not only help the immune system but also provide the body with an essential nutrient.

What is the take-away? Just say “no” to the flu vaccine.

Folks, don’t be fooled here. This study was another failed flu vaccine study. The flu vaccine has never been shown to protect the elderly from getting the flu, dying from the flu, or developing complications from the flu. The elderly would be better served by eating a better diet, maintaining hydration and taking vitamin C.

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Junking Down Our Food Supply With Monsanto Herbicide

Dr. Thierry Vrain - Common Ground – June 8

• Dr. Thierry Vrain, a former soil biologist and genetic scientist, worked for Agriculture Canada for 30 years. He was the designated spokesperson to assure the public of the safety of GMO crops. Since retiring 10 years ago from Agriculture Canada, Dr. Vrain now warns of the dangers of GMOs.

It is high time to change the debate from the safety of engineering food to the pesticides that are inside the food. The technology is essentially about spraying a weed killer on the crops and the herbicide RoundUp is an integral part of the technology – the engineered crops are called RoundUp Ready. Farmers everywhere have been assured complete safety, higher yields and savings of herbicide. When these promises don’t quite pan out, the farmers don’t have much of an opportunity to do something different. It turns out the technology has been incredibly successful, so much so that there is not much of a market for non-engineered seeds now. Monsanto has a monopoly and has cornered the seed supply of much of the planet.

Click PLAY to hear Refusers song Let’s Roundup Monsanto

Since all engineered foods come from crops sprayed with RoundUp, they all contain residues of RoundUp. And it turns out other crops are also sprayed with this herbicide, but much later, just before harvest, because it kills the plants and they are dried fast to make harvesting easier for the farmers. This is commonly done with sugar cane, beans, grains, potatoes and many other crops. I usually say in my lectures that if you want to avoid any residue of RoundUp herbicide in your food, go organic. That is the only choice.

A bit of history to show why RoundUp should be avoided: in the early 60’s, a small chemical company was testing new molecules that could be used to clean industrial pipes and boilers of mineral deposits – just like the kettle in your home that makes mineral deposits after a few months or years. In 1964, the company, called Stauffer Chemicals, patented their best molecule. It was named glyphosate and described as a strong and very broad spectrum descaling agent. A descaling agent is a chelator in chemistry and biology lingo. A chelator is a molecule that can grab onto and hold metal ions.

Within a few years, the descaling agent was also found to kill plants very effectively. It was then bought and patented in 1969 as an exceptionally broad spectrum herbicide by a bigger chemical corporation named Monsanto. The 70’s were the years of my graduate work in North Carolina and I remember RoundUp being touted as the new wonder herbicide. Allegedly, it was non-toxic to animals, had no effect on the environment and biodegraded rapidly. It was a really effective weed killer that grew very popular very fast.

Starting with the first two engineered crops, corn and soybean, engineered to survive being doused with the weed killer, the spread of the technology since 1996 has been nothing but revolutionary. This is seen as high-tech agriculture – a gene revolution after the green revolution. In 2013, there were about 500-million acres of engineered crops and 90% of them were doused liberally with close to two billion pounds of glyphosate. The molecule is so ubiquitous, it is now found in our food, our drinking water, the rain and most importantly, in our bodies.

Life is movement and movement is an activity that only one kind of molecule can perform in living cells. Proteins are the only molecules that can move. Their movement relies on metal ions that are an integral part of the protein molecules. Proteins with metal ions are called metallo-proteins, also known as enzymes. All enzymes of all living cells rely on their metal cofactors for proper function. If the metal ions are not available, the protein molecules cannot function, the cells malfunction, the organs slow down and show disease symptoms.

So in one corner we have all living cells – which include bacteria, fungi, plants and animals – that must find metal micronutrients in their food to have a normal function. And in the other corner we have nearly two billion pounds of a chemical that functions by grabbing onto metal ions and holding on – making them bio-unavailable. If you find the imagery disturbing, read on. In 2010, glyphosate was also patented as an antibiotic by Monsanto. Obviously, the plan was to use it in hospitals and pharmacies. The patent contains a very long list of bacteria killed by this chemical; this is a very broad spectrum antibiotic and indeed damages the microbiome of animals. It does not affect many human pathogenic bacteria, but it certainly kills a lot of bacteria.

In case you did not notice that word, microbiome, I will say a few words about this organ. It turns out all animals – even the bees – are symbiotic organisms with thousands of species of bacteria in their digestive system. We humans have about one hundred trillion bacteria in our intestine. Aside from riding with us and getting fed, this complex bacterial community actually controls many of our organs. Our immune system, our brain and many other organs are completely “influenced” (if you do not like the word control). We humans may think we are on top, but we are in a very dependent and symbiotic relationship with these bacteria. Firstly, they make most of the serotonin in your body. A small malfunction and a small decrease in serotonin and you are depressed. They make most of the other neurotransmitters too and your vitamins and half of the building blocks of your own proteins – too complex for your bodies to make. The microbiome is like a second brain. That is how important it is.

When you eat engineered food – by definition, depleted of metal micronutrients because it contains residues of a strong chelator – your microbiome and your intestine are, of course, first in line. After a few years of eating depleted food, other organs start to show symptoms. This is shown in the statistics of both the Centre for Disease Control in Atlanta Georgia and the US Department of Agriculture, put together by Dr. Nancy Swanson for the US. I wish somebody would do the same compilation in Canada. The statistics show a very probable link between the amount of glyphosate sprayed on crops and the number of people coming down with gastrointestinal problems, kidney inflammation, liver damage and a host of other degenerative (read inflammation) diseases. These are very similar to the symptoms we have seen for the last 10 years in published studies of rats fed engineered food. Calorie rich and nutrient depleted, isn’t that the definition of junk food?

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New Study Claiming Vaccines Are Safe Has Suspicious Origins

By Health Sciences Institute  July 17, 2014

Vaccine alert: Don’t be tricked by this deceptive new ‘study’

memeStilllWaitingForMainstreamMediaIt’s a shameful example of corporate propaganda dressed up as a scientific study.

And the media moles bought it hook, line and sinker.

You probably saw some of the news coverage — it was everywhere.

Stories with headlines that said “Large study confirms that childhood vaccinations are safe.” Or this one from USA Today: “Study finds vaccine side effects extremely rare.”

This latest “research” is meant to “give parents some reassurance,” and counter all that “misinformation out there about vaccines” said the authors.

But even they couldn’t hide all of the facts.

And that’s how I discovered the shocking truth about the “study” that’s behind all the headlines.

Big Pharma knows its vaccination ship is sinking. And it’s doing whatever it can to try and keep it afloat.

That’s because more and more parents are questioning the safety of these shots.

And what was just published in the journal Pediatrics is a brazen attempt to turn things around for vaccine makers. But when you look at the real story, suddenly what these people are saying holds about as much water as a leaky bucket.

The researchers set out to “reassure” parents on the safety of vaccines, as that’s “critical for population health.” And to do that, they pulled data from published studies, vaccine makers, the CDC and reports by other federal agencies.

And their conclusion, the one that made all the headlines, is that “vaccines are very safe.”

But hold on. There are some tidbits here that throw that conclusion right out the window.

To begin with these researchers started with 20,000 studies, but only used 67 for their report. Talk about cherry-picking your data!

But here’s what makes the whole thing a joke. And if it weren’t so serious we could all have a good laugh over it.

They omitted all the reports sent to VAERS — the Vaccine Adverse Event Reporting System!

Are you kidding me? These researchers are doing a study on vaccine safety and they don’t even bother to include reports of vaccine side effects sent into this federal program!

VAERS was set up, and is run by the CDC and FDA, to collect data about adverse reactions from vaccines. Also, vaccine manufacturers, by law, must report any side effects they are aware of to VAERS.

The program receives over 30,000 reports annually. And it says that 13 percent of those are “serious.” Things like disability, life-threatening illness…and death. Since it started collecting data in 1990, it’s received over 200,000 such reports.

And magically, none of those reports made it into this “study.”

Click PLAY to hear Refusers song Unavoidably Unsafe

But the researchers wanted to make sure it looked like they were doing their job. That is if you don’t look too far.

So they included a brief mention of what they called “rare but actual side effects.” Things like the MMR shot causing seizures, or the flu vaccine causing diarrhea, or the rotavirus vaccine giving some kids a serious bowel disorder.

Well that’s certainly “reassuring!”

But here’s the icing on the cake — and it will explain a lot.

Nine out of 10 of the authors of this study come from the RAND Corporation. That’s the mostly federally funded “think tank” that produces “official” studies to support its sponsors.

And two big RAND “clients” are GlaxoSmithKline and Merck.

Unfortunately that news won’t make it into the headlines. Because if it did, those headlines would read something like this:

“Study sponsored by Big Pharma claims its vaccines are safe. Ignores over 200,000 reports of adverse effects.”

And if it said that, I doubt we ever would have seen the story.


“Vaccine side effects are very, very rare” July 2, 2014, The Huffington Post,

RAND Corporation annual report 2013,

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Tetanus Shot: How Do We Know That It Works? ~ By Tetyana Obukhanych, PhD

International Medical Council on Vaccination      July 10, 2014

By Tetyana Obukhanych, PhD


Although a major disease in tropical under-developed countries, tetanus in the USA has been very rare. In the past, tetanus occurred primarily in poor segments of the population in southern states and in Mexican migrants in California. It was swiftly diminishing with each decade prior to the 1950s (in the pre-vaccination era), as inferred from tetanus mortality records and similar case-fatality ratios (about 67-70%) in the early 20th century[8] versus the mid-20th century).[9] The tetanus vaccine was introduced in the USA in 1947 without performing any placebo-controlled clinical trials in the segment of the population (children or adults), where it is now routinely used …

Severe and even deadly tetanus is known to occur in recently vaccinated people with high levels of serum antitoxin.[11] Although the skeptic might say that no vaccine is effective 100% of the time, the situation with the tetanus vaccine is quite different. In these cases of vaccine-unpreventable tetanus, vaccination was actually very effective in inducing serum antitoxin, but serum antitoxin did not appear to have helped preventing tetanus in these unfortunate individuals.

The occurrence of tetanus despite the presence of antitoxin in the serum should have raised a red flag regarding the rationale of the tetanus vaccination program. But such reports were invariably interpreted as an indication that higher than previously thought levels of serum antitoxin must be maintained to protect from tetanus, hence the need for more frequent, if not incessant, boosters. Then how much higher “than previously thought” do serum levels of antitoxin need to be to ensure protection from tetanus?

Crone & Reder (1992) have documented a curious case of severe tetanus in a 29-year old man with no pre-existing conditions and no history of drug abuse, typical among modern-day tetanus victims in the USA. In addition to the regular series of tetanus immunization and boosters ten years earlier during his military service, this patient had been hyper-immunized (immunized with the tetanus toxoid to have extremely high serum antitoxin) as a volunteer for the purposes of the commercial TIG production. He was monitored for the levels of antitoxin in his serum and, as expected, developed extremely high levels of antitoxin after the hyper-immunization procedure. Nevertheless, he incurred severe tetanus 51 days after the procedure despite clearly documented presence of serum antitoxin prior to the disease. In fact, upon hospital admission for tetanus treatment his serum antitoxin levels measured about 2,500 times higher than the level deemed protective. His tetanus was severe and required more than five weeks of hospitalization with life-saving measures. This case demonstrated that serum antitoxin has failed to prevent severe tetanus even in the amounts 2,500 times higher than what is considered sufficient for tetanus prevention in adults.



Severe and even deadly tetanus is known to occur in recently vaccinated people with high levels of serum antitoxin.[11] Although the skeptic might say that no vaccine is effective 100% of the time, the situation with the tetanus vaccine is quite different. In these cases of vaccine-unpreventable tetanus, vaccination was actually very effective in inducing serum antitoxin, but serum antitoxin did not appear to have helped preventing tetanus in these unfortunate individuals.

The occurrence of tetanus despite the presence of antitoxin in the serum should have raised a red flag regarding the rationale of the tetanus vaccination program. But such reports were invariably interpreted as an indication that higher than previously thought levels of serum antitoxin must be maintained to protect from tetanus, hence the need for more frequent, if not incessant, boosters. Then how much higher “than previously thought” do serum levels of antitoxin need to be to ensure protection from tetanus?

Crone & Reder (1992) have documented a curious case of severe tetanus in a 29-year old man with no pre-existing conditions and no history of drug abuse, typical among modern-day tetanus victims in the USA. In addition to the regular series of tetanus immunization and boosters ten years earlier during his military service, this patient had been hyper-immunized (immunized with the tetanus toxoid to have extremely high serum antitoxin) as a volunteer for the purposes of the commercial TIG production. He was monitored for the levels of antitoxin in his serum and, as expected, developed extremely high levels of antitoxin after the hyper-immunization procedure. Nevertheless, he incurred severe tetanus 51 days after the procedure despite clearly documented presence of serum antitoxin prior to the disease. In fact, upon hospital admission for tetanus treatment his serum antitoxin levels measured about 2,500 times higher than the level deemed protective. His tetanus was severe and required more than five weeks of hospitalization with life-saving measures. This case demonstrated that serum antitoxin has failed to prevent severe tetanus even in the amounts 2,500 times higher than what is considered sufficient for tetanus prevention in adults.

Ascorbic acid in tetanus treatment

Anti-serum is not the only therapeutic measure tried in tetanus treatment. Ascorbic acid (Vitamin C) has also been tried. Early research on ascorbic acid has demonstrated that it too could neutralize the tetanus toxin.[12]

In a clinical study of tetanus treatment conducted in Bangladesh in 1984, the administration of conventional procedures, including the anti-tetanus serum, to patients who contracted tetanus left 74% of them dead in the 1-12 age group and 68% dead in the 13-30 age group. In contrast, daily co-administration of one gram of ascorbic acid intravenously had cut down this high mortality to 0% in the 1-12 age group, and to 37% in the 13-30 age group.[13] The older patients were treated with the same amount of ascorbic acid without adjustments for their body weight …

Natural resistance to tetanus

In the early 20th century, investigators Drs. Carl Tenbroeck and Johannes Bauer pursued a line of laboratory research, which was much closer to addressing natural resistance to tetanus than the typical laboratory research on antitoxin in their days. Omitted from immunologic textbooks and the history of immunologic research, their tetanus protection experiments in guinea pigs, together with relevant serological and bacteriological data in humans, nevertheless provide a good explanation for tetanus being a rather rare disease in many countries around the world …

In 1926, already being aware that oral exposure to tetanus spores does not lead to clinical tetanus, Drs. Tenbroeck and Bauer set out to determine whether feeding research animals with tetanus spores could provide protection from tetanus induced by an appropriate laboratory method of spore injection. In their experiment, several groups of guinea pigs were given food containing distinct strains of C. tetani. A separate group of animals were used as controls—their diet was free of any C. tetani. After six months, all groups were injected under the skin with spores premixed with aleuronat. The groups that were previously exposed to spores orally did not develop any symptoms of tetanus upon such tetanus-prone spore injection, whereas the control group did. The observed protection was strain-specific, as animals still got tetanus if injected with spores from a mismatched strain—a strain they were not fed with. But when fed multiple strains, they developed protection from all of them.

Quite striking, the protection from tetanus established via spore feeding did not have anything to do with the levels of antitoxin in the serum of these animals. Instead, the protection correlated with the presence of another type of antibody called agglutinin—so named due to its ability to agglutinate (clump together) C. tetani spores in a test tube. Just like the observed protection was strain-specific, agglutinins were also strain-specific. These data are consistent with the role of strain-specific agglutinins, not of antitoxin, in natural protection from tetanus. The mechanism thereby strain-specific agglutinins have caused, or correlated with, tetanus protection in these animals has remained unexplored …

How do these experimental data in research animals relate to humans? In the early 20th century, not only animals but also humans were found to be intestinal carriers of C. tetani without developing tetanus. About 33% of tested human subjects living around Beijing, China were found to be C. tetani carriers without any prior or current history of tetanus disease.[15] Bauer & Meyer (1926) cite other studies, which have reported around 25% of tested humans being healthy C. tetani carriers in other regions of China, 40% in Germany, 16% in England, and on average 25% in the USA, highest in central California and lowest on the southern coast. Based on the California study, age, gender, or occupation denoting the proximity to horses did not appear to play a role in the distribution of human C. tetani carriers.

Another study was performed back in the 1920s in San Francisco, CA.[16] About 80% of the examined subjects had various levels of agglutinins to as many as five C. tetani strains at a time, although no antitoxin could be detected in the serum of these subjects. C. tetani organisms could not be identified in the stool of these subjects either. It is likely that tetanus spores were in their gut transiently in the past, leaving serological evidence of oral exposure, without germinating into toxin-producing organisms …

Regrettably, further research on naturally acquired agglutinins and on exactly how they are involved in the protection from clinical tetanus appears to have been abandoned in favor of more lucrative research on antitoxin and vaccines. If such research continued, it would have given us clear understanding of natural tetanus defenses we may already have by virtue of our oral exposure to ubiquitous inactive C. tetani spores.

Since the extent of our natural resistance to clinical tetanus is unknown due to the lack of modern studies, all we can be certain of is that preventing dormant tetanus spores from germinating into toxin-producing microorganisms is an extremely important measure in the management of potentially contaminated skin cuts and wounds. If this crucial stage of control—at the level of preventing spore germination—is missed and the toxin production ensues, the toxin must be neutralized before it manages to reach nerve endings.

Both antitoxin and ascorbic acid exhibit toxin-neutralizing properties in a test tube. In the body, however, vaccine-induced antitoxin is located in the blood, whereas the toxin might be focally produced in the skin or muscle injury. This creates an obvious physical impediment for toxin neutralization to happen effectively, if at all, by means of vaccine-induced serum antitoxin. Furthermore, no placebo-controlled trials have ever been performed to rule out the concern about such an impediment by providing clear empirical evidence for the effectiveness of tetanus shots in children and adults. Nevertheless, the medical establishment relies upon induction of serum antitoxin and withholds ascorbic acid in tetanus prevention and treatment.

When an old medical procedure of unknown effectiveness, such as the tetanus shot, has been the standard of medical care for a long time, finalizing its effectiveness via a modern rigorous placebo-controlled trial is deemed unethical in human research. Therefore, our only hope for the advancement of tetanus care is that further investigation of the ascorbic acid therapy is performed and that this therapy becomes available to tetanus patients around the world, if confirmed effective by rigorous bio-statistical standards.

Until then, may the blind faith in the tetanus shot help us!


1. Tenbroeck, C. & Bauer, J.H. The immunity produced by the growth of tetanus bacilli in the digestive tract. J Exp Med 43, 361-377 (1926).
2. Fishman, P.S., Matthews, C.C., Parks, D.A., Box, M. & Fairweather, N.F. Immunization does not interfere with uptake and transport by motor neurons of the binding fragment of tetanus toxin. J Neurosci Res 83, 1540-1543 (2006).
3. Schofield, F.D., Tucker, V.M. & Westbrook, G.R. Neonatal tetanus in New Guinea. Effect of active immunization in pregnancy. Br Med J 2, 785-789 (1961).
4. Newell, K.W., Dueñas Lehmann, A., LeBlanc, D.R. & Garces Osorio, N. The use of toxoid for the prevention of tetanus neonatorum. Final report of a double-blind controlled field trial. Bull World Health Organ 35, 863-871 (1966).
5. Demicheli, V., Barale, A. & Rivetti, A. Vaccines for women to prevent neonatal tetanus. Cochrane Database Syst Rev 5:CD002959 (2013).
6. Maselle, S.Y., Matre, R., Mbise, R. & Hofstad, T. Neonatal tetanus despite protective serum antitoxin concentration. FEMS Microbiol Immunol 3, 171-175 (1991).
7. Fox, S.B. & Khong, T.Y. Lack of innervation of human umbilical cord. An immunohistological and histochemical study. Placenta 11, 59-62 (1990).
8. Bauer, J.H. & Meyer, K.F. Human intestinal carriers of tetanus spores in California J Infect Dis 38, 295-305 (1926).
9. LaForce, F.M., Young, L.S. & Bennett, J.V. Tetanus in the United States (1965-1966): epidemiologic and clinical features. N Engl J Med 280, 569-574 (1969).
10. Editorial: Tetanus in the United States Army in World War II. N Engl J Med 237, 411-413 (1947).
11. Abrahamian, F.M., Pollack, C.V., Jr., LoVecchio, F., Nanda, R. & Carlson, R.W. Fatal tetanus in a drug abuser with “protective” antitetanus antibodies. J Emerg Med 18, 189-193 (2000).
Beltran, A. et al. A case of clinical tetanus in a patient with protective antitetanus antibody level. South Med J 100, 83 (2007).
Berger, S.A., Cherubin, C.E., Nelson, S. & Levine, L. Tetanus despite preexisting antitetanus antibody. JAMA 240, 769-770 (1978).
Crone, N.E. & Reder, A.T. Severe tetanus in immunized patients with high anti-tetanus titers. Neurology 42, 761-764 (1992).
Passen, E.L. & Andersen, B.R. Clinical tetanus despite a protective level of toxin-neutralizing antibody. JAMA 255, 1171-1173 (1986).
Pryor, T., Onarecker, C. & Coniglione, T. Elevated antitoxin titers in a man with generalized tetanus. J Fam Pract 44, 299-303 (1997).
12. Jungeblut, C.W. Inactivation of tetanus toxin by crystalline vitamin C (L-ascorbic acid). J Immunol 33, 203-214 (1937).
13. Jahan, K., Ahmad, K. & Ali, M.A. Effect of ascorbic acid in the treatment of tetanus. Bangladesh Med Res Counc Bull 10, 24-28 (1984).
14. Hemilä, H. & Koivula, T. Vitamin C for preventing and treating tetanus. Cochrane Database Syst Rev 2:CD006665 (2008).
15. Tenbroeck, C. & Bauer, J.H. The tetanus bacillus as an intestinal saprophyte in man. J Exp Med 36, 261-271 (1922).
16. Coleman, G.E. & Meyer, K.F. Study of tetanus agglutinins and antitoxin in human serums. J Infect Dis 39, 332-336 (1926).

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Fast Food Fever: The Impact Of Western Diet On Immunity – BioMed Central

This new study from the Nutrition Journal reviews how fast food and GMOs destroy immunity and how junk food DNA modifications are passed to children.

‘Poor dietary behaviors are encoded into both our DNA scaffolding and gut microbiome, and thus these harmful immune modifications are passed to our offspring during their most critical developmental window.’ 

Fast food fever: reviewing the impacts of the Western diet on immunity

Ian A Myles

Nutrition Journal    17 June 2014

Our over abundance of calories and the macronutrients that compose our diet may all lead to increased inflammation, reduced control of infection, increased rates of cancer, and increased risk for allergic and auto-inflammatory disease …

Obese individuals have fewer white blood cells to fight infection and those cells they do possess have reduced phagocytosis capability …

In vitro evidence suggest processed, simple sugars also reduce white blood cell phagocytosis and possibly increase inflammatory cytokine markers in the blood …

Evidence implicates saccharin and sucralose as contributors to Crohn’s and Ulcerative Colitis via interference with homeostatic inactivation of digestive proteases …

Recent focus and technologic advances have allowed accurate elucidation of the mechanisms by which our lifestyle impacts our microbiome and leads to dysbiosis. In the gut (and on the skin), there is an optimal, albeit not yet fully elucidated, balance of bacterial species. Some strains of bacteria are needed to digest dietary fibers [91] while others produce valuable nutrients like vitamin K [92]. Beneficial bacteria aide their hosts by occupying space and/or modifying the microenvironment in ways that prevent harmful bacteria from gaining a foothold [91]. More importantly, the commensal flora provides a type of training to the immune system. Like a sparing partner in boxing, the immune system’s interactions with the normal commensal flora provides an education that is indispensable when a pathogenic opponent is encountered …

What is perhaps of larger concern is that the harmful effects of diet can actually stretch across generations. A mother’s diet may potentially shape her child’s flavor preferences even before birth, potentially skewing their palette towards anything from vegetables to sugary sweets in ways that could influence subsequent propensity for obesity and/or unhealthy dieting [108]. In addition, children inherit their microbiome from their mother mostly through parturition but also during breast-feeding and development until the bacterial balance matures around two to four years of age [92,109]. However, recent evidence suggests that the microbiome may also be seeded into the unborn fetus while still in the womb [109,110] (Figure 1B). When the mother’s diet causes a harmful imbalance of her bacteria, she passes this imbalance on to her child and thus fails to present the ideal commensals for a proper immune education during her child’s most critical developmental window [52]. This developmental dysbiosis leaves the offspring’s immune system poorly trained to fight off infections and encourages autoimmune and allergic diseases [52] …

Genetically modified (GM) foods
It is a concerning finding that pesticides like glyphosate induces cellular death in human umbilical, placental, embryonic, and peripheral blood mononuclear cells at physiologic levels …

In animal models, the combination of pesticide-producing GM maize and pesticide-resistant GM soy led to increased rates of severe stomach inflammation …

However, an additional concern was raised when studies revealed that functional genes, from both industrial and natural sources, ingested by animals could be internalized by gut bacteria, these bacteria transcribe the engrafted genes into functional proteins, and the genetic changes could be inherited by offspring via microbiome transfer [215-218]. Human corollary was uncovered when researchers showed that an intact and functional industrial gene could be found in bacteria from the small bowel of patients with ileostomies …

Of potentially greatest concern, our poor dietary behaviors are encoded into both our DNA scaffolding and gut microbiome, and thus these harmful immune modifications are passed to our offspring during their most critical developmental window. Therefore, given the scope of influence, the vast economic impacts, and the potential for trans-generational inheritance, the dietary impacts on immune health should thus, at minimum, be afforded a level of attention equal to that given to the dietary impacts on cardiovascular health.

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Prescription painkillers kill more people than heroin and cocaine combined – Journal of Public Health

American Journal of Public Health June 17, 2014

First major review provides evidence of sharp increase in deaths from painkillers in US and Canada and leading causes.

The number of deaths involving commonly prescribed painkillers is higher than the number of deaths by overdose from heroin and cocaine combined, according to researchers at McGill University. In a first-of-its-kind review of existing research, the McGill team has put the spotlight on a major public health problem: the dramatic increase in deaths due to prescribed painkillers, which were involved in more than 16,000 deaths in 2010 in the U.S. alone. Currently, the US and Canada rank #1 and #2 in per capita opioid consumption.

“Prescription painkiller overdoses have received a lot of attention in editorials and the popular press, but we wanted to find out what solid evidence is out there,” says Nicholas King, of the Biomedical Ethics Unit in the Faculty of Medicine. In an effort to identify and summarize available evidence, King and his team conducted a systematic review of existing literature, comprehensively surveying the scientific literature and including only reports with quantitative evidence.

“We also wanted to find out why thousands of people in the U.S and Canada are dying from prescription painkillers every year, and why these rates have climbed steadily during the past two decades,” says Nicholas King, of the Biomedical Ethics Unit in the Faculty of Medicine. “We found evidence for at least 17 different determinants of increasing opioid-related mortality, mainly, dramatically increased prescription and sales of opioids; increased use of strong, long-acting opioids like Oxycontin and methadone; combined use of opioids and other (licit and illicit) drugs and alcohol; and social and demographic factors.”

“We found little evidence that Internet sales of pharmaceuticals and errors by doctors and patients — factors commonly cited in the media — have played a significant role,” Prof. King adds.

The findings point to a complicated “epidemic” in which physicians, users, the health care system, and the social environment all play a role, according to the researchers.

“Our work provides a reliable summary of the possible causes of the epidemic of opioid overdoses, which should be useful for clinicians and policy makers in North America in figuring out what further research needs to be done, and what strategies might or might not be useful in reducing future mortality,” says King. “And as efforts are made to increase access to prescription opioids outside of North America, our findings might be useful in preventing other countries from following the same path as the U.S. and Canada.”



American Journal of Public Health June 12, 2014

Determinants of Increased Opioid-Related Mortality in the United States and Canada, 1990–2013: A Systematic Review

Nicholas B. King is with the Biomedical Ethics Unit and the Department of Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, Quebec. Veronique Fraser is with the Biomedical Ethics Unit, McGill University. Constantina Boikos, Robin Richardson, and Sam Harper are with the Department of Epidemiology, Biostatistics, and Occupational Health, McGill University.


We found a complex, multifaceted, and geographically varied web of determinants of increased opioid-related mortality.

Prescriber Behavior
Our review identified 5 ways in which the behavior of opioid prescribers may have played a role in increased opioid-related mortality: prescribing more opioids, prescribing higher doses of opioids, prescribing oxycodone, prescribing methadone, and prescribing at high volumes.

Prescription and sales of opioids.
Since the early 1990s, prescription and sales of opioid analgesics have risen steeply. Between 1999 and 2010, sales of prescription painkillers to US hospitals, clinics, and pharmacies increased 4-fold, with an accompanying increase in opioid-related mortality.2 The number of opioid prescriptions dispensed from US retail pharmacies increased from 174.1 million in 2000 to 256.9 million in 2009.57 In 2006, Americans consumed 115 272 kilograms of opioids, more than twice as much as in 199710; in Canada, prescription opioid consumption doubled between 2000 and 2010.58 In 2008, a Utah Department of Health survey showed that 21% of adults had been prescribed an opioid pain medication in the preceding 12 months.59 Prescription of opioid analgesics for chronic noncancer pain in particular has increased.12 Between 1980 and 2000, US prescriptions of opioids for chronic musculoskeletal pain doubled, and rates for more potent opioids quadrupled.13 According to one estimate, 9.6 million to 11.5 million adults were on long-term opioid therapy in the United States during 2005.60 We found 8 studies1,2,14—19 providing evidence that increased prescriptions for opioids may have played a role in increased opioid-related mortality. Canadian studies showed correlations between mortality and consumption of 4 prescription opioids (fentanyl, morphine, oxycodone, and hydromorphone) in 2 provinces1 and correlations between opioid prescribing rates and mortality rates across Ontario counties.14 Similarly, in a study of North Carolina counties, there were correlations between opioid sales, emergency department visits for overdoses, and opioid-related mortality.16 A US study also demonstrated a state-level association between overall opioid consumption and drug poisoning mortality.17 Opioid dosage. As overall opioid prescriptions have increased, so too have prescribed dosages. For example, a study of workers’ compensation claims in the state of Washington showed that the average daily morphine-equivalent dose (MED) of long-acting opioids increased 50% between 1996 and 2002 and exceeded the recommended “red flag” dose by 2005.13 We found 7 studies5,12,20—24 providing evidence of the contribution of increased dosages to increased opioid-related mortality. A study of social assistance recipients in Ontario showed that, between 2003 and 2008, there were increases in the mean daily doses of oxycodone (increase of 27.4%) and fentanyl (increase of 14.2%) dispensed, whereas doses remained flat for other opioids.21 By 2008, one third of prescriptions for long-acting oxycodone exceeded clinical guidelines with respect to mean daily dose,21 and patients receiving higher doses had higher rates of overdose, opioid-related mortality, and all-cause mortality.21,22 A study of patients receiving opioids for chronic noncancer pain in a health maintenance organization in Washington State also showed that the risk of overdose increased with increased dosages.12 It was noted in this study that, although overdose risk was higher at high doses, most overdoses occurred at low to moderate doses because such doses are prescribed more frequently, suggesting that even the most frequently used dose regimens carry some risk. The importance of increased dosages is supported by evidence indicating a dose—response relationship between maximum daily prescribed dose and risk of death.12,20,22,24 However, there does not seem to be an evidence based threshold for what constitutes a dangerously high dose. Although some clinical guidelines suggest an MED of 200 milligrams per day as a “watchful dose,” studies in our sample showed overdose and mortality increases at doses ranging from 40 to 200 milligrams per day MED.12,20,22,24

Prescription of oxycodone.
Prescription of more potent opioids, particularly methadone and longacting formulations of oxycodone, has increased most rapidly, with associated increases in mortality. Before 1990, weaker opioids such as codeine and meperidine were used more frequently than stronger formulations.17 Between 1997 and 2006, US retail sales of methadone increased 1177%, sales of oxycodone increased 732%, and sales of fentanyl increased 479%, whereas sales of hydromorphone, hydrocodone, and morphine increased between 196% and 274% and sales of codeine and meperidine dropped 25% and 28%, respectively.10 Studies of workers’ compensation claims in Washington State between 1996 and 2002 showed that whereas overall opioid prescriptions increased 25%, prescriptions for the more potent Schedule II opioids increased by almost 250%, with an accompanying increase in opioid-related mortality.13,25 Similarly, a North Carolina study demonstrated significant increases in prescriptions of oxycodone (839%), methadone, (607%) and fentanyl (530%) and significant decreases in prescriptions of meperidene and codeine between 1997 and 2010.16 We found 7 studies5,17,18,21,23,26,27 that provided evidence for the contribution of prescription of oxycodone, particularly the longacting formulation OxyContin, to increased opioid-related mortality. Long-acting opioids such as Oxy-Contin may be particularly dangerous when used recreationally: crushing pills releases high doses of the drug, and repeated use to increase or maintain a narcotic effect may lead to overdose. In addition, recreational users may avoid formulations that include opioids along with acetaminophen because of hepatoxicity.17 A study of patients in the Ontario public drug plan between 2003 and 2008 showed that whereas prescription rates for long-acting oxycodone more than doubled, rates for all other opioids decreased or remained flat, and opioid-related mortality increased.21 Other Ontario studies showed that annual opioid-related mortality rates increased 41% and oxycodone-related mortality increased 416% after OxyContin was added to the provincial drug formulary5 and that oxycodone was involved in one third of all opioid-related deaths between 2006 and 2008.23

Prescription of methadone.
We found 14 studies17—19,26—36 that provided evidence for the contribution of methadone prescriptions to increased opioid-related mortality. Methadone’s unusual pharmacology poses particular challenges because of the small difference between therapeutic and toxic doses.34 There is also some evidence that prescribers may prefer methadone for economic rather than clinical reasons. Because methadone is a cheaper generic drug, private insurers, Medicaid, and individual clinicians may prefer it over more expensive, patent-protected alternatives, thus driving increases in methadone prescriptions.30,34,57 There is evidence that a high proportion of opioid-related deaths have involved methadone. Studies conducted in Washington State,30 Oklahoma,18 and West Virginia32 have shown that methadone is involved in higher numbers of deaths than any other opioid, and a US study revealed that methadone was involved in twice as many single-drug deaths as any other opioid.31 A US ecological study conducted in 2002 suggested that methadone (43%) and oxycodone (46%) explained a large proportion of the geographic variation in opioid related mortality.17 Although methadone has traditionally been prescribed to combat substance abuse in methadone maintenance programs, it is increasingly being used for its original purpose, pain relief. We found some evidence that the use of methadone for pain relief has played a role in increased mortality. A Vermont study showed that although the percentage of drug overdose deaths that were methadone related increased from 12% to 37% between 2001 and 2006, only 2 of 76 decedents were in a methadone maintenance program.33 A Utah study showed that, between 1997 and 2004, population-adjusted methadone prescription rates increased 727% and opioid-related mortality increased 1770%. During this period, rates of heroin abuse and admissions to substance abuse facilities remained unchanged, suggesting that the increased prescriptions and associated mortality resulted primarily from prescriptions for pain.19 By contrast, a New Mexico study revealed a slight decrease in methadone related deaths between 1998 and 2002 and a higher proportion of decedents with prescriptions related to methadone maintenance (45%).36

High-volume prescribing.
The possible contribution of high volume prescribing to opioidrelated mortality has received considerable attention in the media61 and scholarly literature.2,57 Some states report problems with so-called “pill mills,” which prescribe large quantities of opioids to patients with questionable diagnoses. 2 We found 1study37 providing evidence that high-volume prescribing may have played a role in increased opioid-related mortality. A study of Ontario family physicians showed that the top quintile of prescribers issued opioid prescriptions 4.5 times more frequently than the next quintile and wrote the final opioid prescription in 63% of opioid-related deaths. However, it is still unclear whether high-volume prescribing is a direct driver of increased mortality.


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San Diego pertussis epidemic in the fully vaccinated (85%)

By MB June 15, 2014

PertussisVaccineFailureWhooping cough (pertussis) is back in the headlines, with CNN and the LA Times trumpeting the 3,458 reported state cases so far this year vs. the total 9,163 cases reported in the last full epidemic year 2010.

The CA health department claims: ‘This is a problem of “epidemic proportions.”

It is an epidemic in the vaccinated. Neither the LA Times, CNN or other mainstream media sources report the vaccination status of those 3,458 cases.

For that you have to dig a little deeper, past the usual media admonishment to rush out and get vaccinated.

United Press International newswire is the only media source to report the vaccination status of CA pertussis cases, it is for a subset of the state data.

For the San Diego region 85% of pertussis cases were fully vaccinated. With 6 shots!

Got that? San Diego has an epidemic of pertussis in the vaccinated and the state is still recommending a failed vaccine.

Here is the California State Health Department recommendation on the pertussis vaccine: “We urge all pregnant women to get vaccinated,” said Dr. Ron Chapman, director of the California Department of Public Health. “We also urge parents to vaccinate infants as soon as possible.”

Here is the San Diego pertussis vaccination failure rate according to UPI.

‘Of the 621 people in San Diego County diagnosed with whooping cough this year, 85 percent were up to date with their pertussis immunizations, calling into question the effectiveness of the vaccine. California is currently on track for having the most cases of the disease since 2010, and state officials declared the recent increase of cases an epidemic. San Diego County has seen 621 cases of the bacterial disease since the beginning of 2014, way up from the 430 total cases in 2013. There have been 3,458 cases this year in the entire state. Of the 621 people who’ve had the disease in San Diego County this year, 527 had the six shots necessary to be up to date with their pertussis vaccine and 67 were not. Immunization status for 27 of the ill wasn’t known.’

Clearly, the pertussis vaccine is a failure in San Diego.

But that won’t stop pro-vaccine evangelists from blaming the California pertussis outbreak on the unvaccinated. Because they can never admit their vaccines are a flop. That would invalidate their indoctrination and life mission, to enforce the CDC vaccine schedule no matter what the data says about vaccine failure, or what the vaccine package insert shows about pertussis vaccine adverse reactions.

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CDC’s Vaccine Safety Research is Exposed as Flawed and Falsified – Biomed Research Journal

Press release: Read full journal study below.

Substantial Scientific Evidence Exists that Vaccine Ingredient is a Developmental Neurotoxin

WATCHUNG, N.J., June 13, 2014 /PRNewswire-iReach/ — Just months after U.S. Congressman Bill Posey compared the Center for Disease Control (CDC)’s vaccine safety studies to the SEC’s Bernie Madoff scandal, malfeasance in the CDC’s studies of thimerosal-containing vaccines has, for the first time, been documented in peer-reviewed scientific literature. While the CDC states on its website that “low doses of thimerosal in vaccines do not cause harm, and are only associated with minor local injection site reactions like redness and swelling at the injection site,” the journal BioMed Research International now provides direct evidence that the CDC’s safety assurances about the mercury-containing preservative are not fact-based, according to the article’s lead author, Brian Hooker, PhD.

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The paper opens by citing over 165 studies that have found Thimerosal to be harmful, including 16 studies that had reported outcomes in human infants and children of death, acrodynia, poisoning, allergic reaction, malformations, auto-immune reaction, Well’s syndrome, developmental delay and neurodevelopmental disorders including tics, speech delay, language delay, ADHD and autism. These findings by multiple independent research groups over the past 75+ years have consistently found thimerosal to be harmful. “Substantial scientific evidence exists and has existed for many years that the vaccine ingredient thimerosal is a developmental neurotoxin” says George Lucier, former Associate Director of the National Toxicology Program.

Studies showing harm from thimerosal sharply contradict published outcomes of six CDC coauthored and sponsored papers – the very studies that CDC relies upon to declare that thimerosal is “safe” for use in infant and maternal vaccines. Dr. Hooker, biochemist and vaccine industry watchdog, said of the six CDC studies, “Each of these papers is fatally flawed from a statistics standpoint and several of the papers represent issues of scientific malfeasance.  For example, important data showing a relationship between thimerosal exposure and autism are withheld from three of the publications (Price et al. 2010, Verstraeten et al. 2003 and Madsen et al. 2003).  This type of cherry-picking of data by the CDC in order to change the results of important research studies to support flawed and dangerous vaccination policies should not be tolerated.”

Dr. Boyd Haley, international expert in mercury toxicity and a co-author of the recently published paper said “There is no doubt that authorities in the CDC have initiated and participated in a cover-up of vaccine-induced damage from thimerosal to our children—-and this I consider criminal.” The paper, “Methodological Issues and Evidence of Malfeasance in Research Purporting to Show Thimerosal in Vaccines is Safe,” was published on June 6 and contains eight pages of evidence that the CDC has had knowledge of the vaccine preservative’s neurological risks, yet continues to cover them up.

The paper concludes, “five of the publications examined in this review were directly commissioned by the CDC, raising the possible issue of conflict of interests or research bias, since vaccine promotion is a central mission of the CDC. Conceivably, if serious neurological disorders are found to be related to Thimerosal in vaccines, such findings could possibly be viewed as damaging to the vaccine program.”

Dr. Hooker has submitted over 100 FOIA requests to the CDC over the past 10 years and has amassed thousands of pages of documents showing malfeasance in the CDC’s vaccine safety program.  Hooker revealed that one CDC document quoted a top official instructing CDC employees to “Review all correspondences and documents to see if there is ‘foreseeable harm’ to the agency if they were released” so the documents could be redacted by CDC attorneys prior to release.

Barry Segal, founder of the Focus Autism Foundation and former entrepreneur whose company sales peaked near $2 billion said, “We are in the process of exposing what may be the biggest federal scandal ever with immense damage to our economy and our people, especially our children who are the future of our country. Their health has been compromised by mercury in vaccines. We need Congress to take action now. Thimerosal must be banned.”

A more effective vaccine preservative “2PE” has replaced thimerosal in many other vaccines and possesses a much better safety profile according to Dr. Hooker.

The Focus Autism Foundation is dedicated to providing information to the public that exposes the cause or causes of the autism epidemic and the rise of chronic illnesses – focusing specifically on the role of vaccinations. To learn more, visit  A Shot of Truthis an educational campaign sponsored by Focus Autism.

Read the press release

BioMed Research International
Volume 2014 (2014), Article ID 247218, 8 pages
Review Article

Methodological Issues and Evidence of Malfeasance in Research Purporting to Show Thimerosal in Vaccines Is Safe

1Simpson University, 2211 College View Drive, Redding, CA 96001, USA
2Institute of Chronic Illness, Inc., 14 Redgate Court, Silver Spring, MD 20905, USA
3University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75235, USA
4University of Kentucky, Lexington, KY 40506, USA
5CoMeD, Inc., Silver Spring, MD, USA

Received 15 February 2014; Accepted 12 May 2014; Published 4 June 2014

Academic Editor: Jyutika Mehta

Copyright © 2014 Brian Hooker et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There are over 165 studies that have focused on Thimerosal, an organic-mercury (Hg) based compound, used as a preservative in many childhood vaccines, and found it to be harmful. Of these, 16 were conducted to specifically examine the effects of Thimerosal on human infants or children with reported outcomes of death; acrodynia; poisoning; allergic reaction; malformations; auto-immune reaction; Well’s syndrome; developmental delay; and neurodevelopmental disorders, including tics, speech delay, language delay, attention deficit disorder, and autism. In contrast, the United States Centers for Disease Control and Prevention states that Thimerosal is safe and there is “no relationship between [T]himerosal[-]containing vaccines and autism rates in children.” This is puzzling because, in a study conducted directly by CDC epidemiologists, a 7.6-fold increased risk of autism from exposure to Thimerosal during infancy was found. The CDC’s current stance that Thimerosal is safe and that there is no relationship between Thimerosal and autism is based on six specific published epidemiological studies coauthored and sponsored by the CDC. The purpose of this review is to examine these six publications and analyze possible reasons why their published outcomes are so different from the results of investigations by multiple independent research groups over the past 75+ years.

1. Introduction

Thimerosal is an organic-mercury (Hg) based compound, used as a preservative in many childhood vaccines, in the past and present. To date, there have been over 165 studies that focused on Thimerosal and found it to be harmful [12]. (A comprehensive list of these studies is shown at Of these studies, 16 were conducted to specifically examine the effects of Thimerosal on human infants and/or children [318]. Within these studies, which focused on human infants and/or children, the reported outcomes following Thimerosal exposure were (1) death [3]; (2) acrodynia [4]; (3) poisoning [5]; (4) allergic reaction [6]; (5) malformations [7]; (6) autoimmune reaction [8]; (7) Well’s syndrome [9]; (8) developmental delay [1013]; and (9) neurodevelopmental disorders, including tics, speech delay, language delay, attention deficit disorder, and autism [10111418].

However, the United States (US) Centers for Disease Control and Prevention (CDC) still insists that there is “no relationship between [T]himerosal[-]containing vaccines and autism rates in children” [19]. This is a puzzling conclusion because, in a study conducted directly by the CDC, epidemiologists assessed the risk for neurologic and renal impairment associated with past exposure to Thimerosal-containing vaccine (TCV) using automated data from the Vaccine Safety Datalink (VSD) and found a 7.6-fold increased risk of autism from exposure to Thimerosal during infancy [20]. The database for that study was “from four health maintenance organizations [HMOs] in Washington, Oregon, and California, containing immunization, medical visit, and demographic data on over 400,000 infants born between 1991 and 1997.” In that initial study, Verstraeten et al. [20] “categorized the cumulative ethyl-Hg exposure from [T]himerosal[-]containing vaccines after one month of life and assessed the subsequent risk of degenerative and developmental neurologic disorders and renal disorders before the age of six.” They “applied proportional hazard models adjusting for HMO, year of birth, and gender, and excluded premature babies.” The reported results showed that “the relative risk (RR) of developing a neurologic development disorder was 1.8 (95% confidence intervals [CI] 1.1–2.8) when comparing the highest exposure group at 1 month of age (cumulative dose > 25 μg) to the unexposed group.” Similarly, they “also found an elevated risk for the following disorders: autism (RR 7.6, 95% CI = 1.8–31.5), nonorganic sleep disorders (RR 5.0, 95% CI = 1.6–15.9), and speech disorders (RR 2.1, 95% CI = 1.1–4.0)” in the highest exposure group.


Considering the many peer-reviewed published research studies that have shown harm from Thimerosal, including studies in which Thimerosal exposure is associated with the subsequent diagnosis of neurodevelopmental disorders (16 studies) such as autism, and the just-described evidence from the CDCs own research, which found evidence of a relationship between the level of Thimerosal exposure and the risk of a subsequent autism diagnosis, how does the CDC conclude that there is no evidence of that relationship? The foundation for the CDC’s current stance apparently is based primarily on six specific published epidemiological studies that the CDC has completed, funded, and/or cosponsored, starting in the late 1990s. These studies include (1) the Madsen et al. [21] ecological study of autism incidence versus Thimerosal exposure in Denmark, (2) the Stehr-Green et al. [22] ecological study of autism incidence versus Thimerosal exposure in Denmark, Sweden, and California, (3) the Hviid et al. [23] study of autism incidence versus Thimerosal exposure in Denmark (also ecological), (4) the Andrews et al. [24] cohort study of autism incidence and Thimerosal exposure in the United Kingdom, (5) the published Verstraeten et al. [25] CDC cohort study of autism incidence and Thimerosal exposure in the United States, and (6) the more recent Price et al. [26] case-control study of autism incidence and Thimerosal exposure in the United States. Although the CDC cites several other publications to purport the safety of Thimerosal, only these six specifically consider its putative relationship to autism.

The purpose of this review is to examine these six publications [2126] which were “overseen” by the CDC and which claim that prenatal and early childhood vaccine-derived Thimerosal exposures are not related to the risk of a subsequent diagnosis of autism or autism spectrum disorder (ASD). This review analyzes possible reasons why their published outcomes are so different from the results of investigations by multiple independent research groups over the past 75+ years. The review begins with an examination of the Madsen et al. [21] study.

2. The Madsen et al. 2003 Study

The CDC-sponsored Madsen et al. [21] study examined whether discontinuing the use of TCVs in Denmark led to a decrease in the incidence of autism. Data were obtained from the Danish Psychiatric Central Research Register, which contains all psychiatric admissions since 1971 and all outpatient contacts in psychiatric departments in Denmark since 1995. The study authors examined the data from 1971 to 2000 and reported that rate of autism increased with the removal of Thimerosal from vaccines (starting in 1992, the year that Thimerosal-containing early childhood vaccines were phased out).

Although there are several concerns about the methodology used, the most serious concern involves diagnosis. As described in the paper, estimates of total autism cases in Denmark were only based on diagnoses occurring during inpatient visits from 1971 to 1994 and then during both inpatient and outpatient visits from 1995 to the last year of the study in 2000. Thus, the inclusion criteria are greatly expanded two years after the phaseout of Thimerosal from infant vaccines in Denmark, creating an “artificial increase” in autism prevalence. The authors conceded that “the proportion of outpatient to inpatient activities was about 4 to 6 times as many outpatients as inpatients with variations across time and age bands.” However, in an earlier publication by Madsen et al. [27], the same authors had stated regarding this same data, “in our cohort, 93.1% of the children were treated only as outpatients…” Unlike the statement in the Madsen et al. [21] study, the 2002 paper indicates that the ratio between outpatients and inpatients in the 1971–2000 dataset was 13.5 : 1, which would account for an even greater increase in cases diagnosed starting in 1995 (i.e., after the probable completion of the phaseout of TCVs that started in 1992).

In addition, the authors stated that the Danish registry which was used to count cases did not include a large Copenhagen clinic before 1993. This clinic accounted for as many as 20% of the autism cases nationwide, which would again artificially inflate the autism incidence observed in Denmark after the phaseout of TCVs was initiated in 1992. The authors do not mention this change in inclusion criteria (i.e., the addition of a new clinic in the registry) neither do they attempt to adjust their analysis in accordance with the anomaly. It was revealed, instead, in a similar paper by Stehr-Green et al. [22] where the authors state regarding the Denmark registry of autistic patients, “Prior to 1992, the data in the national register did not include cases diagnosed in one large clinic in Copenhagen (which accounts for approximately 20% of cases occurring nationwide).”

Also, the diagnosis criteria for “autism” changed within the course of the study. From 1971 to 1993, the ICD-8 standards for diagnosis (psychosis protoinfantilis 299.00 or psychosis infantilis 299.01) were used to measure autism incidence. However, from 1994 to 2000, the ICD-10 standard (infantile autism, F84.1) was used. Although the authors did not address the impact of the change in diagnostic criteria, this could result in as much as a 25-fold increase in cases as the instantaneous change in autism prevalence in Denmark, due to this change, went from a low of 1.2/10,000 to a high of 30.8/10,000 [28].

Another disconcerting methodological issue was that the 2001 data, which showed a strong downward trend in autism rates in at least two of the three age groups (continuing from 1999 through 2001), was not included in the final publication. This was apparent because when the paper was initially submitted for publication, it included the 2001 data. After the paper was rejected for publication by the Journal of the American Medical Association (JAMA) and the Lancet, it was submitted to the journal Pediatrics again including the 2001 data. As stated by one of the peer-reviewers of the Pediatrics submission, “The drop of incidence shown for the most recent years is perhaps the most dramatic feature of the figure, and is seen in the oldest age group as well as the youngest. The authors do not discuss whether incomplete ascertainment in the youngest children or delay in recording of data in the most recent years might play a role in this decline, or the possibility that this decrease might have come about through elimination of [T]himerosal” (January 23, 2003, communication between Dr. Poul Thorsen, Aarhus University, and Dr. Coleen Boyle, CDC scientist). In response to this criticism, the authors removed the 2001 incidence numbers. The authors’ decision to withhold these data resembles scientific malfeasance, especially when coupled with the previously discussed problematic methods for counting autism cases. If the scientists believed that downward trend between 1999 and 2001 was caused by some phenomenon unrelated to the phaseout of the TCVs, these scientists should have included those data and then explained the trend within the discussion of the data.

If the 2001 data had been included in the final publication, the results would have been consistent with a more recent CDC study [29] where a decreasing trend of autism prevalence in Denmark after the removal of Thimerosal in 1992 was reported. Instead of large increases in autism prevalence after 1992, the recent Danish study revealed that the autism spectrum disorder prevalence in Denmark fell steadily from a high of 1.5% in 1994-95 (when children receiving Thimerosal-free formulations were too young to receive an autism diagnosis and, because of the known offset in diagnosis, most of those being diagnosed had been born 4 to 8 years earlier [from 1985 to 1990]) to a low of 1.0% in 2002–2004 (more than 10 years after the phasein of the use of Thimerosal-free vaccine formulations was started in 1992).

3. The Stehr-Green et al. 2003 Study

The CDC’s Stehr-Green et al. [22] study compared the prevalence/incidence of autism in California, Sweden, and Denmark with average exposures to TCVs. Graph-based ecologic analyses were used to examine population data from the state of California (national immunization coverage surveys and counts of children diagnosed with autism-like disorders seeking special education services in California); Sweden (national inpatient data on autism cases, national vaccination coverage levels, and information on use of all vaccines and vaccine-specific amounts of Thimerosal); and Denmark (national registry of inpatient/outpatient-diagnosed autism cases, national vaccination coverage levels, and information on use of all vaccines and vaccine-specific amounts of Thimerosal).

The study followed and appeared to be conducted in response to California study data [30], which was presented to the Institute of Medicine’s Immunization Safety Review Committee. The California data showed that increased uptake of Thimerosal-containing vaccines in California during the 1990s correlated with a corresponding increase in autism diagnoses. In the Stehr-Green et al. [22] study, the researchers stated that the reliability of the autism prevalence data, citing that the California data included autism spectrum disorder diagnoses such as pervasive development disorder (PDD), could account for the increase. However, in a published response to this paper, Blaxill and Stehr-Green [31] stated that the California prevalence rates were reported based solely on autism cases.

In the Stehr-Green paper, the Sweden autism prevalence data showed an increase in autism rates from 5- 6 cases per 100,000 in 1980–82 to a peak of 9.2 cases per 100,000 in 1993. In Sweden, TCVs were phased out starting in 1987. Denmark’s autism prevalence data was identical to that reported in the Madsen et al. [21] study critiqued previously. For Denmark, the authors reported an astounding 20-fold increase in autism prevalence between 1990 and 1999, despite the phaseout of TCVs that started in 1992.

In addition, the data from Sweden were based on inpatient (hospital) visits only. This limitation (counting a small fraction of the total number of cases) likely accounted for the erratic swings in the annual numbers of autism cases reported in that country. Also, the Thimerosal exposure level based on the Swedish vaccination schedule during this time period was much less (a nominal maximum of 75 μg of Hg by two years of age) than that possible in California (and the United States as a whole) where developing children nominally received up to 237.5 μg of Hg by 18 months of age through the standard immunization schedule. In conclusion, the Stehr-Green et al. study was problematic in its attempt to combine ecological data from three different countries that, relative to each other, demonstrated different vaccination policies and widely different Thimerosal exposure levels.

4. The Hviid et al. (2003) Study

The Hviid et al. [23] population-based cohort study, widely cited by the CDC, compared rates of autism prevalence among individuals who received Thimerosal-free vaccines to those receiving TCVs. The authors report that there was no evidence of increased autism prevalence with Thimerosal exposure.

The study authors stated that the mean age of autism diagnosis within their population was 4.7 years with a standard deviation of 1.7 years. However, cases and controls as young as 1 year of age were included within the analysis. Accordingly, controls that were less than the mean age of diagnosis minus two standard deviations (1.3 years) from that age had a 97.5% probability of actually being individuals who will later develop autism and are therefore possibly misclassified. Similarly, in this study, the mean age for an ASD diagnosis was 6.0 years with a standard deviation of 1.9 years. Thus, the study methodology is questionable because it appears to have underascertained the number of cases diagnosed with autism and ASD.

In addition, rather than counting persons within the cohort, the authors counted “person-years of follow up.” With this technique, each age group (one-year-olds, two-year-olds, etc.) was considered equally, despite the fact that younger age groups were much less likely to receive an autism diagnosis. This again contributed to the undercounting of the cases with a diagnosis of autism and ASD and biased the study towards the null hypothesis (that there is no statistically significant Thimerosal exposure effect on the outcomes observed).

5. The Andrews et al. (2004) Study

The Andrews et al. [24] study was a retrospective cohort study completed using records from a database in the United Kingdom, where autism prevalence rates were compared for children receiving Thimerosal-containing DTaP and DT vaccines. In the Andrews et al. [24] study, Cox’s proportional-hazards ratios were used to evaluate periods of followup in the cohort examined by the investigators using the records in the general practitioner research database (GPRD), a database that was known to have a significant level of errors. These investigators reported that increased organic-Hg exposure from TCVs was associated with a significantly reduced risk for diagnosed general developmental disorders and for unspecified developmental delay (although there was a significantly higher risk for diagnosed tics).

Considering that there are several studies conducted by independent investigators that have found that exposure to Thimerosal is a risk factor for neurodevelopmental delay and disorders [101116], the reduced rate of neurodevelopmental delay and disorders with Thimerosal exposure found in the Andrews et al. [24] study suggests possible methodological issues.

This result may have occurred, in part, because other studies examined cohorts with significantly different childhood vaccine schedules and with different diagnostic criteria for outcomes. This difference may also exist because these other studies that found Thimerosal to be a risk factor for neurodevelopmental delay and disorders employed different epidemiological methods, especially with respect to the issue of follow-up period for individuals in the cohorts examined. The method used to measure follow-up period for individuals is a critical issue in all studies examining the relationship between exposures and the subsequent risk of a neurodevelopmental disorder diagnosis, especially in those instances where the postexposure periods for all of the participants in the study are essentially the same. This is because the risk of an individual being diagnosed with a neurodevelopmental disorder is not uniform throughout his/her lifetime. As observed in the present study, the initial mean age for any neurodevelopmental disorder diagnosis was 2.62 years old, and the standard deviation of mean age of the initial diagnosis of neurodevelopmental disorder was 1.58 years old. These findings are highly problematic because (1) any follow-up method that fails to consider the lag time between birth and age of initial neurodevelopmental disorder diagnosis will likely not be able to observe the true relationship between exposure and the subsequent risk of a neurodevelopmental disorder diagnosis and (2) statistically, the mean and standard deviation age of diagnosis as reported lead to the nonsensical result that a significant portion (2.5%) of the children in this study were diagosed with a neurodevelopmental disorder more than six months before they were born (i.e., the mean age minus two standard deviations, 2.62 − [2 × 1.58] = −0.54 years of age).

Another issue with this study is that the authors used a nontransparent, multivariate regression technique to analyze vaccine uptake and autism prevalence data. The study included one dependent variable (autism) and multiple independent variables, including two independent variables (Thimerosal exposure levels and year of birth) that were “correlated” with each other, since Thimerosal exposures increased with time. Thus, the researchers did not report a statistical analysis of the effect of Thimerosal exposure on autism incidence, despite the fact that the authors stated that no such effect was observed. Moreover, the methods used in this study can create a problem in regression known as “multicolinearity.” In this case, since the time variable and the vaccine exposure variable are correlated, they actually compete to explain the outcome effect. Inclusion of the time variable reduces the significance of the exposure variable. Yet, the authors did not explain why they included a time variable that competes with the exposure variable. Unfortunately, the authors of this study never released the raw data so that a valid single-variable analysis could be conducted to ascertain the probability of an association between Thimerosal exposure and the risk of autism.

It is also important to note that the UK Thimerosal exposure (a maximum of 75 μg of Hg by 4 months of age) was not comparable to that in the United States (a maximum of 75 μg of Hg by 2 months of age and 187.5 μg of Hg by 6 months of age). Thus, this study should not be extrapolated to the probability of an autism-Thimerosal association based on the US vaccination schedule.

6. The Verstraeten et al. (2003) Study

The CDC’s published Verstraeten et al. [25] study consists of a cohort analysis of a subset of records from the medical records databases for several of the HMOs whose records were maintained in a central data repository, the Vaccine Safety Datalink (VSD). This study was conducted in at least five separate phases. In the final phase (i.e., the results reported in the publication), the authors stated that there was no relationship between Thimerosal exposure in vaccines and autism incidence. However, no data are reported in the published study to support this conclusion.

Results from the first phase of the study released in an internal presentation abstract by Verstraeten et al. [20] (mentioned earlier) using records from four (4) HMOs showed that infants who were exposed to greater than 25 μg of Hg in vaccines and immunoglobulins at the age of one month were 7.6 times more likely to have an autism diagnosis than those not exposed to any vaccine-derived organic Hg. Within the same abstract, Verstraeten reports that the risk for any neurodevelopmental disorder was 1.8, the risk for speech disorder was 2.1, and the risk for nonorganic sleep disorder was 5.0. All relative risks were statistically significant.

In the second phase of the study, a different approach was taken: exposure was compared at 3 months of age, rather than one month. Results of this phase showed that children exposed to the maximum amount of organic Hg in infant vaccines (62.5 μg) were 2.48 times more likely to have autism diagnosis compared to those exposed to less than 37.5 μg of Hg in vaccines. These results were also statistically significant. No assessment against a “no exposure” control was apparently completed in this study phase.

In the third phase of the study, in which more data stratification methods and different inclusion/exclusion criteria were applied to the analysis, the relative risk of autism for children at three months of Thimerosal exposure dropped to 1.69. At this point, evidence in an email from Verstraeten, the lead investigator, written to a colleague outside of the CDC (obtained by the authors via the US Freedom of Information Act of 1950 as amended), suggests that Verstraeten could have been receiving pressure within the CDC to apply unsound statistical methods to deny a causal relationship between Thimerosal and autism. In this email, Verstraeten states (Figure 1), “I do not wish to be the advocate of the anti-vaccine lobby and sound like being convinced that thimerosal is or was harmful, but at least I feel we should use sound scientific argumentation and not let our standards be dictated by our desire to disprove an unpleasant theory.”

Figure 1: July 14, 2000, email from Verstraeten to Philippe Grandjean regarding the risk of harm due to Thimerosal (obtained by the authors via the US Freedom of Information Act of 1950 as amended).

The fourth and fifth phase of the study used records from only two of the original HMOs and incorporated a third HMO, Harvard Pilgrim, into the analysis. Some critics of the study questioned the use of Harvard Pilgrim, as this HMO appeared to be riddled with uncertain record keeping practices, and the state of Massachusetts had been forced to take it over after it declared bankruptcy. In addition, the HMO used different diagnostic codes than the other two HMOs used in phases 2 and 3. Other criticisms include that the study used younger children, from 0 to 3 years of age, even though the average age for an autism diagnosis at the time was 4.4 years. Since half of the children receiving an autism diagnosis would be over 4.4 years of age, far greater than the maximum age in the study at 3 years, this analysis excluded more than 50% of all autism cases from this HMO. Also, the cohort from this HMO contained 7 times fewer individuals than the main cohort from the previous study (i.e., HMO B), and there was no apparent attempt to assess the power of this HMO to show any statistically significant effect.

Also of note is the lack of variability within strata among the different HMOs in the Verstraeten et al. [25] study. By design, a cohort study seeking to assess the effect of some treatment on a subsequent outcome should be designed to maximize the range of the independent “treatment” variable (Thimerosal exposure in this instance) in order to determine if there is indeed an “effect” in the dependent postexposure outcome variable (neurological disorders in this study). However, the authors knowingly stratified the analysis based on the participants’ gender, year of birth, month of birth, and clinic most often visited. This effectively reduced the variability of Thimerosal exposure within the strata to the point that it reduced the capability of the final analysis to find any but the “strongest” Thimerosal exposure-related outcome effects. The problems with such “overmatching” practices have been discussed in detail in peer-reviewed scientific literature and will be treated in greater detail in the forthcoming review of the CDC’s Price et al. [26] paper.

Another methodological concern about the Verstraeten et al. [25] study is related to the issue of the minimum follow-up period required for individuals in the cohorts examined to ensure that all the cases in the cohort will have been identified with a high degree of certainty. This issue has been mentioned as a problem in the previous studies. As mentioned earlier, the method used to determine the minimum follow-up period for individuals is a critical issue in all studies examining the relationship between exposures and the subsequent risk of a neurodevelopmental disorder diagnosis, especially in those instances where the exposures to all participants in the study are the same or essentially the same. This is the case because the risk of an individual being diagnosed with a neurodevelopmental disorder is not uniform throughout his/her lifetime. Any follow-up method that fails to consider the lag time between birth and age of initial neurodevelopmental disorder diagnosis will likely not be able to observe the true relationship between exposure and the subsequent risk of a neurodevelopmental disorder diagnosis. Verstraeten et al. [25] included children in the control group who were too young (down to “0” years of age) to receive a neurodevelopmental disorder diagnosis.

Within this study, Verstraeten et al. [25] still found significantly increased risk ratios for tics and language delay. However, the authors stated that, because these results were not consistent between the HMOs tested, these significantly increased risk ratios could not be used to make a determination of the potential adverse consequences of organic-Hg exposure from TCVs.

7. The Price et al. 2010 Study

In 2010, the CDC published another epidemiology study on Thimerosal and autism [26]. This case-control study was conducted using the records from three managed care organizations (MCOs) consisting of 256 children with an ASD diagnosis and 752 controls that were matched by birth year, gender, and MCO to the children with an ASD diagnosis. Exposure to Thimerosal in vaccines and immunoglobulin preparations was determined from electronic immunization registries, medical charts, and parent interviews. Conditional logistic regression was used to assess associations between ASD, autistic disorder (AD), and ASD with regression and exposure to ethyl-Hg during prenatal, birth-to-1-month, birth-to-7-month, and birth-to-20-month periods. Their published finding was that prenatal and infant Thimerosal exposure from TCVs and Thimerosal-containing immunoglobulin posed no statistically significant risk of autism.

As mentioned earlier, in case-control studies, the main methodological concern is the phenomenon called “overmatching.” This concern for overmatching in the Price et al. [26] study was voiced previously by DeSoto and Hitlan [32]. In their comprehensive analysis of overmatching errors specific to the Price paper, DeSoto and Hitlan [32] stated that “Matching cannot—or should not—be done in a way that artificially increases the chance that within[-] strata exposure is the same; this happens when a matching variable is a significant predictor of exposure and is called overmatching.”

Cases were matched with controls of the same age and sex, within the same HMO and essentially the same vaccination schedule, using the same vaccine manufacturers. DeSoto and Hitlan then state further, regarding the lack of variability of Thimerosal exposure in the Price study, “Across the different years, the average cumulative exposure varies from 42.3 μg to 125.46 μg; while within the birth year stratas (sic), the mean exposures do not vary by more than 15 micrograms.” In other words, the maximum level of variation in Thimerosal exposure in the cases and controls being compared was 15 μg of Hg, as compared to the “83” μg of Hg range for the average cumulative exposures in the cohort studies. Moreover, this range is much less than the range of Thimerosal exposures that could have been used to determine risk including (a) 0 to 50 μg of Hg for one-month exposures, (b) 0 to 190 μg of Hg for seven-month exposures, and (c) 0 to 300 μg of Hg for 20-month exposures. Finally, regarding the Price study, DeSoto and Hitlan [32] concluded, “this paper is flawed. Unfortunately, there is not an analytic fix for overmatching: it is [a] design flaw.”

Prenatal Thimerosal exposure for the children within the study arose from the Thimerosal-preserved inactivated-influenza vaccine given during pregnancy and the Rho immunoglobulin administered to pregnant women to prevent Rh-factor incompatibility injury to the developing child. Unlike postnatal exposure from TCVs in the recommended childhood vaccination schedule, prenatal exposures would not be overmatched in a study design that stratified the participants based on their birth year or HMO. Evidence from the background CDC report regarding the Price study showed a significant risk of regressive autism due to prenatal Thimerosal exposure levels, at exposure levels as low as 16 μg of Hg [33]. However, the risk of regressive autism due to prenatal Thimerosal exposure  reported in that paper was 1.86 and yielded a  value of 0.072 which was deemed as insignificant based on the authors’ “cut-off” value of . However,  values between 0.05 and 0.10 are “marginally significant” and should merit further study. In addition, upon further analysis, it was found that the 2009 background report [33] to the Price et al. [26] study showed that the prenatal Thimerosal exposure model was run in six different ways and that the most reliable methods (those that factored out the postnatal Thimerosal exposure effects) found highly statistically significant relative risks of up to 8.73 () for regressive ASD due to prenatal Thimerosal exposures from Thimerosal-containing influenza vaccines and Rho immunoglobulin products relative to no such prenatal Thimerosal exposures. Curiously, these more compelling results were not reported in the paper. Withholding these data from the publication and, instead, reporting a significantly lower value could appear to constitute scientific malfeasance on the part of the authors of this study.

8. Conclusion

As seen in this review, the studies upon which the CDC relies and over which it exerted some level of control report that there is no increased risk of autism from exposure to organic Hg in vaccines, and some of these studies even reported that exposure to Thimerosal appeared to decrease the risk of autism. These six studies are in sharp contrast to research conducted by independent researchers over the past 75+ years that have consistently found Thimerosal to be harmful. As mentioned in the Introduction section, many studies conducted by independent investigators have found Thimerosal to be associated with neurodevelopmental disorders. Several studies, for example, including three of the six studies covered in this review, have found Thimerosal to be a risk factor for tics [101724253435]. In addition, Thimerosal has been found to be a risk factor in speech delay, language delay, attention deficit disorder, and autism [10111517242534].

Considering that there are many studies conducted by independent researchers which show a relationship between Thimerosal and neurodevelopmental disorders, the results of the six studies examined in this review, particularly those showing the protective effects of Thimerosal, should bring into question the validity of the methodology used in the studies. A list of the most common methodological issues with these six studies is shown in Table 1. Importantly, other than the Hviid et al. [23] study, five of the publications examined in this review were directly commissioned by the CDC, raising the possible issue of conflict of interests or research bias, since vaccine promotion is a central mission of the CDC. Conceivably, if serious neurological disorders are found to be related to Thimerosal in vaccines, such findings could possibly be viewed as damaging to the vaccine program.

Table 1: Methodological issues most common in each of the six reviewed studies.

Conflict of Interests

All of the investigators on the present study have been involved in vaccine/biologic litigation.


Funding was provided by the nonprofit Institute of Chronic Illnesses, Inc. and CoMeD, Inc.


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