AUTISM PREVENTION FATHER BABIES 24-34 PATERNAL AGE IS KEY IN NON-FAMILIAL AUTISMVaccines

"It is very possible that PATERNAL AGE is the major predictor of(non-familial) autism." Harry Fisch, M.D., author "The Male Biological Clock". Sperm DNA mutates and autism, schizophrenia bipolar etc. results. What is the connection with autoimmune disorders? Having Type 1 diabetes, SLE,etc. in the family, also if mother had older father. NW Cryobank will not accept a sperm donor past 35th BD to minimize genetic abnormalities.VACCINATIONS also cause autism.

Monday, April 26, 2010

Does Increased Parental Age Mean Increased Risk?

Home > Life Sciences > Neuroscience > The Science of Motherhood Autism: Does Increased Parental Age Mean Increased Risk?
By Kimberly Crandell | April 26th 2010 12:26 PM | Print | E-mail | Track Comments


•Autism: Does Increased Parental Age Mean Increased Risk?

The possibility that autism is more common in offspring of older parents has generated considerable interest. To investigate the theory, a study using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network, was developed to examine the relation between parental age at delivery and the prevalence of autism spectrum disorder (ASD). Confirmation of such an association has important public health implications in light of increasing trends in recent decades for couples to delay having children.

The study used date from 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder. In evaluating the association between parental age and autism risk, it was important to account for other variables related to both parental age and. Birth order is a potentially confounding factor because it is positively associated with parental age and has been reported in some studies to be associated with autism risk, with at least 3 studies reporting firstborn children to be at increased risk of autism. The goal of this study was to determine, in a large, population-based cohort of US children, whether advancing maternal and paternal age each independently increase a child's risk of developing autism after controlling for the other parent's age, birth order, and other risk factors.

Results
In unadjusted analyses, both mean maternal age and mean paternal age were significantly higher for ASD cases than for the birth cohort as a whole. With parental age 25–29 years as the reference group, the odds of developing ASD was significantly reduced for parental age <20 years and increased for maternal age 35 and paternal age 40 years. Those age cutoffs (maternal age 35, paternal age 40 years) were used to classify each parent's age as "older" versus "younger." Other significant predictors of ASD in unadjusted analyses included low birth order, male gender, advanced maternal education, and preterm birth.

Multivariable analysis of parental ages modeled as categorical variables
After the data was adjusted for the other parent's age and other covariates, the increases in ASD risk associated with maternal age 35 years and paternal age 40 years (relative to age 25–29 years) were slightly reduced compared with the unadjusted analysis. In contrast, the results for birth order suggest that the decline in ASD risk associated with increasing birth order is somewhat stronger in the adjusted analysis than in the unadjusted analysis. In addition, the apparent increase in ASD risk associated with higher levels of maternal education in the unadjusted analysis is no longer evident in the adjusted model, suggesting that the apparent maternal education effect is due to its association with parental age.

Parental ages modeled as continuous variables
In unadjusted analyses, the risk of developing ASD increased significantly with each 10-year increase in both maternal age and paternal age. After adjustment for age of the other parent and other covariates, each 10-year increase in maternal age was associated with a 20% increase in ASD risk while each 10-year increase in paternal age was associated with a 30% increase in ASD risk.

Combined effects of parental age and birth order
The risk of ASD within each of 3 parental age categories (both parents "younger," 1 parent "older," and both parents "older") was highest among firstborn children and declined with increasing birth order . Considering the combined effects of parental age and birth order, (excluding from the analysis births to mothers aged <20 years), the lowest risk group to be third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years. The risk of ASD increased with both declining birth order and increasing number of older parents. The highest risk group included firstborn offspring of mothers aged 35 years and fathers aged 40 years, with a risk 3 times that of the reference group.

The overall results of this study provide the most compelling evidence to date that ASD risk increases with both maternal and paternal age and decreases with birth order.

Source: American Journal of Epidemiology, Advanced Parental Age and the Risk of Autism Spectrum Disorder

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Saturday, April 17, 2010






The FDA Shuts Down Common Infant Vaccine After Startling Discovery Posted by Dr. Mercola | April 17 2010 | 66,430 views Email this to a friend Share this article Next Article

“U.S. federal health authorities recommended … that doctors suspend using Rotarix, one of two vaccines licensed in the U.S. against rotavirus, saying the vaccine is contaminated with material from a pig virus,” CNN reports.

The Rotarix vaccine, which is made by GlaxoSmithKline and was approved by the FDA in 2008, has already been given to about 1 million U.S. children along with 30 million worldwide. The vaccine was found to contain DNA from porcine circovirus 1.

“The FDA learned about the contamination after an academic research team using a novel technique to look for viruses in a range of vaccines found the material in GlaxoSmithKline's product and told the company,” FDA Commissioner Dr. Margaret Hamburg told CNN.
Sources:
CNN March 22, 2010



Dr. Mercola's Comments:


One million U.S. children, and about 30 million worldwide, have already received GlaxoSmithKline’s Rotarix vaccine. Now a research team has discovered it is contaminated with “a substantial amount” of DNA from a pig virus.

What is pig virus DNA doing in a vaccine intended to prevent rotavirus disease, which causes severe diarrhea and dehydration?

It’s anybody’s guess, although CNN reported that GlaxoSmitthKline detected the substance in the cell bank and the seed used to make the vaccine, “suggesting its presence from the early stages of vaccine development.”

It is actually common for vaccines to contain various animal matter, including foreign animal tissues containing genetic material (DNA/RNA), but even FDA Commissioner Dr. Margaret Hamburg told CNN:

"It [Pig virus DNA] should not be in this vaccine product and we want to understand how it got there.

It's not an easy call and we spent many long hours debating the pros and cons but, because we have an alternative product and because the background rates of this disease are not so severe in this country, we felt that the judicious thing to do was to take a pause, to really ask the critical questions about what this material was doing in the vaccine, how it got there."

Disturbing Findings in Rotarix and Two Other Common Childhood Vaccines
Dr. Eric Delwart is the researcher who, along with colleagues, made the discovery of contamination in Rotarix. Their intent was reportedly to “show that live attenuated vaccine only contained the expected viral genomes and no other,” but what they found told a different story.

Using new technology to test eight infectious attenuated viral vaccines, the results showed three of the vaccines contained “unexpected viral sequences”:

1.A measles vaccine was found to contain low levels of the retrovirus avian leukosis virus

2.Rotateq, Merck’s rotavirus vaccine, was found to contain a virus similar to simian (monkey) retrovirus

3.Rotarix (GlaxoSmithKine’s rotavirus vaccine) was found to contain “significant levels” of porcine cirovirus 1

So in their tests, nearly 40 percent of the vaccines they tested contained viral contaminants. The implications of these findings on the alleged safety of the vaccine supply remains to be seen, but clearly there is contamination occurring that was a complete surprise to researchers, health officials and vaccine manufacturers alike.

As Barbara Loe Fisher, founder of the National Vaccine Information Center (NVIC), said in her commentary on the Rotarix contamination issue:

“There are lots of questions about how the manufacturer of Rotarix vaccine and the FDA both missed the pig virus DNA contaminating the original seed stock and all doses of Rotarix vaccine given to more than one million American children in the past few years.

Is there state-of-the-art technology that is being used by private laboratories but not by drug companies and the FDA?

Why did the independent team of scientists, who found the contamination, notify the vaccine manufacturer first rather than also immediately reporting their finding directly to the FDA?

What about the significance of finding bird viral DNA in measles vaccine and the monkey viral DNA in RotaTeq vaccine?”

There are clearly a lot of unanswered questions right now. At the very least, it certainly makes you wonder what other “unknown” contaminants are lurking in vaccines. At worst, we could be injecting children with substances that could potentially cause serious health problems down the road.
Animal Ingredients Common in Vaccines
You should know that it is very common for vaccine manufacturers to use cells from animals and birds in their manufacturing process.

To put this in perspective, Barbara Loe Fisher has explained what animal material is par for the course in manufacturing the Rotarix vaccine for your children:

“Rotarix is a genetically engineered vaccine that GSK created by isolating human rotavirus strain infecting a child in Cincinnati and using African Green monkey kidney cells to produce the original viral seed stock from which all Rotarix vaccine has been made.

In the FDA licensing process, Rotarix had to meet certain FDA standards, that included demonstrating the vaccine was not contaminated with, for example TSE (Transmissable Spongiform Encephalopathy or “mad cow” disease, a brain wasting disease) or with cow viruses because bovine (cow) serum was used to prepare the original viral seed stock.

Porcine trypsin, an enzyme in the pancreatic juice of a pig, was also used to make the viral seed stock.”

So the fact that Rotarix contains animal material is not a surprise … it’s the type of animal material, an unexpected variety, that has even the FDA raising their eyebrows.

Why it’s Dangerous to Have Various Animal DNA in Vaccines …
Both the FDA and GlaxoSmithKline spokespeople continue to state that no safety risk has been uncovered from the contamination, at least not yet.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, said “a substantial amount” of the DNA was found in the vaccine. But, he stressed, “there is no evidence that it causes any disease. … There is no evidence that it ever does anything.”

Dr. Paul Offit added, “The PCV1 virus they found is an orphan virus, i.e., it is not associated with disease”.

Of course there are no studies provided or have ever been done to show this, it doesn’t stop them from making these statements without any facts to back up their safety assurance, despite the fact that SV40 from monkeys has been associated with cancer in multiple studies.

History has shown that it can indeed be very dangerous when an animal virus unintentionally enters the vaccine supply.

During the 1950s and 1960s, the polio vaccine, which is still given in the United States, typically four times during a child's first 16 months of life, was widely contaminated with the monkey virus, SV40, which had gotten into the vaccine during the manufacturing process (monkey kidney cells, where SV40 thrived, were used to develop polio vaccines).

In lab tests, the virus was found to cause several different types of cancer, including brain cancer, and now SV40 is showing up in a variety of human cancers such as lung, brain, bone and lymphatic.

According to the authors of The Virus and the Vaccine: The True Story of a Cancer-Causing Monkey Virus, Contaminated Polio Vaccine, and the Millions of Americans Exposed, leading scientists and government officials turned their heads to repeated studies showing that SV40 was in the vaccine, and even today some well-known agencies are still dismissing study results.

The virus is even showing up in children too young to have received the contaminated vaccine, and some experts are now suggesting the contaminated virus may have been in the polio vaccine up until as late as 1999.

It is because of risks like this that Barbara Loe Fisher said:

“With mounting evidence that cross-species transfer of viruses can occur, the United States should no longer be using animal tissues to produce vaccines.”

This is also the same reason why Donald Miller, a cardiac surgeon and professor of surgery at the University of Washington, suggests in his more User-Friendly Vaccination Schedule that if you choose to get your child vaccinated against polio, you request only an inactivated (dead) virus vaccine that is cultured in human cells, not monkey kidney cells.

The United States no longer uses the live oral polio vaccine, so parents don't really have to ask for the injected version. However, if you live internationally, this is still an issue.

Are the Benefits of Rotarix Worth the Risks?
Even without a potential contamination scare, there are serious risks to every vaccine. So before vaccinating you really need to be certain that the benefits will outweigh those risks.

In the case of Rotarix, along with RotaTeq (a similar vaccine made by Merck), the benefits are very questionable, especially if you live in the United States or another developed country.

Rotavirus is very contagious and does cause more than 500,000 deaths in young children each year, but this is mostly in developing countries. In the United States, rotavirus is responsible for only “several dozen” deaths a year, according to Hamburg.

Typically, when a child in the United States contracts rotavirus, and most do, only rest and fluids are required to recover. This infection also provides natural immunity that will protect your child for life.

As NVIC writes

“The CDC estimates that, by age 3, almost every US child has had a case of rotavirus. Once a child has been infected with a strain of rotavirus, he or she develops antibodies and is either immune for life or has a milder case if infected with that same strain in the future.

Most healthy children, who are infected with several strains of rotavirus in the first few years of life, develop lifelong natural immunity to rotavirus infection.”

The rotavirus vaccine, meanwhile, has shown little benefit for rotavirus rates in the United States. According to NVIC:

“Today, even though almost all US infants receive vaccines for rotavirus, and despite efforts to improve the management of childhood rotavirus-associated diarrhea, hospitalizations of children in the U.S. with the disease have not significantly declined in the past two decades.”

Along with showing little benefit for a disease that is typically entirely treatable with fluids and rest, a recent drug review by the FDA found that Rotarix is associated with a significant increase in pneumonia-related deaths in children, compared to a placebo.

So with this particular vaccine, children are taking on serious risks with what appears to be very little benefit -- and that was before the contamination was uncovered.

The moral of the story?

Whatever you do, please do your homework before subjecting your children to any vaccine. A great way to get started is to simply use the Search Feature at the top of each of my Web pages and search my site as it contains a litany of research on vaccine safety, and the lack thereof.



Related Links:
Pulled Rotavirus Vaccine Proved Dangerous

Vaccine Doctor Given at Least $30 Million Dollars to Push Vaccines

Overlooked Contaminant Found in Donated Blood…

Tuesday, April 13, 2010

A Newly published Study

Parental and Grandparental Ages in the Autistic
Spectrum Disorders: A Birth Cohort Study
Jean Golding*, Colin Steer, Marcus Pembrey
Centre for Child and Adolescent Health, Department of Community Based Medicine, University of Bristol, Bristol, United Kingdom
Abstract
Background: A number of studies have assessed ages of parents of children with autistic spectrum disorders (ASD), and
reported both maternal and paternal age effects. Here we assess relationships with grandparental ages.
Methods and Findings: We compared the parental and grandparental ages of children in the population-based Avon
Longitudinal Study of Parents and Children (ALSPAC), according to their scores in regard to 4 autistic trait measures and
whether they had been given a diagnosis of ASD. Mean maternal and paternal ages of ASD cases were raised, but this
appears to be secondary to a maternal grandmother age effect (P = 0.006): OR = 1.66[95%CI 1.16, 2.37] for each 10-year
increase in the grandmother’s age at the birth of the mother. Trait measures also revealed an association between the
maternal grandmother’s age and the major autistic trait–the Coherence Scale (regression coefficient b = 0.142,
[95%CI = 0.057, 0.228]P = 0.001). After allowing for confounders the effect size increased to b = 0.217[95%CI 0.125,
0.308](P,0.001) for each 10 year increase in age.
Conclusions: Although the relationship between maternal grandmother’s age and ASD and a major autistic trait was
unexpected, there is some biological plausibility, for the maternal side at least, given that the timing of female meiosis I
permits direct effects on the grandchild’s genome during the grandmother’s pregnancy. An alternative explanation is the
meiotic mismatch methylation (3 M) hypothesis, presented here for the first time. Nevertheless the findings should be
treated as hypothesis generating pending corroborative results from other studies.
Citation: Golding J, Steer C, Pembrey M (2010) Parental and Grandparental Ages in the Autistic Spectrum Disorders: A Birth Cohort Study. PLoS ONE 5(4): e9939.
doi:10.1371/journal.pone.0009939
Editor: Chenxi Wang, University of Louisville, United States of America
Received November 12, 2009; Accepted February 24, 2010; Published April 1, 2010
Copyright: 2010 Golding et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The UK Medical Research Council (MRC), the Wellcome Trust and the University of Bristol currently provide core support for ALSPAC. The statistical
analyses for this paper were specifically funded by the MRC. The funders had no role in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: jean.golding@bristol.ac.uk
Introduction
There is evidence from many parts of the developed world that
the prevalence of diagnosed autistic spectrum disorder (ASD) has
been rising dramatically. Although evidence from twin studies
suggests a strong level of heritability, it is clear that there must also
be other factors at play. Parental ages have received some
attention - there have been a few case control studies comparing
ages of mothers of children with autistic spectrum disorder (ASD)
with controls and showing that ASD mothers tended to be older
than controls, but these studies either had selected non-population
based cases, or had inadequate controls or numbers too small for
adequate conclusions. In recent years, however, there have been a
number of large population based studies of cases of ASD
compared either with all births born over the same period or with
a set of controls randomly selected from the population at risk.
Their conclusions have varied. For example, there have been three
studies from Scandinavia, taking advantage of their birth registries
and their facility to link these with case registries. That from
Sweden, compared 408 cases with 2040 controls and reported no
association with advanced maternal age [1]; the two studies from
Denmark covering births from 1984–98 [2] and 1973–98 [3]
overlapped considerably, yet they come to different conclusions in
regard to parental age. One [2] states that maternal age was
significantly associated with autism but that this was secondary to a
paternal age effect, whereas the other reports that neither were
significant on adjusting for one another [3]. The latter study fell
into the trap of failing to take account of collinearity - thus if you
have two factors closely correlated such as the ages of each parent,
then taking account of both simultaneously will automatically
result in neither showing an association with the outcome under
consideration. In Western Australia, this problem was circumvented
by using a step-wise procedure and offering both maternal
and paternal ages [4]. Although both factors were univariably
highly associated with ASD (P,0.001), it was only maternal age
that entered the equation with an almost 3-fold increase in risk to
children of mothers aged 35+ compared with those ,25.
Conversely a study of Israeli conscripts found increased paternal
but not maternal ages [5], but two major studies of births in the
USA in 1994 showed independent relationships with both
maternal and paternal ages [6,7].
Thus there is a lack of clarity as to whether it is the age of the
mother, or of the father, or both that are related to ASD. In
reviewing the literature two publications [8,9] concluded that both
older maternal and older paternal ages played a role. Because of
the lack of agreement, we decided to address the topic more
PLoS ONE | www.plosone.org 1 April 2010 | Volume 5 | Issue 4 | e9939
broadly. We take advantage of a population based study to assess
the parental ages at the birth of the study children with ASD,
compared with those of the rest of the population, and also assess
whether ages of the preceding generation may be important. We
consider not only the children who have been diagnosed, but also
the various traits that contribute to the autistic spectrum disorders.
Materials and Methods
The Avon Longitudinal Study of Parents and Children
(ALSPAC) started in September 1990 and aimed to enrol all
pregnant women resident in the geographic area of Avon, in southwest
England, who had an expected date of delivery in the period
April 1st 1991 to December 31st 1992 inclusive. The aim of the study
was to assess the contribution of the environment (broadly defined
to include both the physical and psychosocial influences) on the
health, development and wellbeing of children from the earliest ages
[10]. The study also aims to look at the way in which genetic
variation influences a variety of outcomes and how these influences
may be modified by the environment. In all, 14075 children were
born to 13881 mothers, an estimated 80%of the eligible population.
A total of 13971 children survived to age 7 years. Ethical approval
for the study was obtained from the ALSPAC Law and Ethics
Committee and the Local Research Ethics Committees.
A dual approach was made to identify the children from the
cohort with ASD. Both the health service records, where a
multidisciplinary team had reached this diagnosis, and the
education system, where ASD had been given as a reason for
special educational needs, were used [11]. A total of 86 children
were identified in this way.
In parallel we have looked at traits associated with ASD in the
ALSPAC study, and shown that 4 traits are particularly predictive
of ASD [12]: the coherence scale of the Children’s Communication
Checklist (CCC) at about 9 y [13]; the Social and
Communication Disorders Checklist (SCDC) at about 8 y [14];
the sociability score from the EAS temperament scale at 38 m
[15], and a scale of repetitive behaviour at 69 m derived for the
ALSPAC Study. For each scale the higher the results, the more
autistic the behaviour. All four traits were highly associated with
the ASD diagnosis explaining individually between 10% (sociability)
and 46% (coherence) of the log-likelihood.
Here we look at the ages of the parents and the grandparents at
the birth of the study child and study parents, respectively,
comparing children with and without ASD and the worst 10% of
scores for the autistic traits. We used stepwise logistic regression for
these dichotomous outcomes. We also analysed the traits as
continuous variables using multiple regression.
Results
Unadjusted associations with autistic measures
Figure 1 demonstrates the variation in the rate of ASD
according to the maternal and paternal ages and shows that there
is a lower prevalence of children with an ASD if the parents are
young (,25), and increased rates at ages 30–34. The rates of ASD
when a parent is 35 or more are similar to the rates at ages 25–29
in this study.
However for the maternal grandparents the rates of ASD in
their grandchildren are highest if they were aged 35 or more at the
time of birth of the study mother (Figure 1). There is also evidence
among the paternal grandparents of an increase in risk when the
parents were aged 30 or more.
Comparisons of the mean ages show similar patterns–the mean
ages of the parents and grandparents of the children with ASD
were higher than found for those without ASD (Table 1). The
greatest differences were demonstrated for the grandmothers, with
mean differences of 1.90 and 1.97 years for the maternal and
paternal grandmothers respectively. Linear regression demonstrates
the increase in risk of ASD with each 10 year increase in
age, and shows that similar effect sizes are found for ages of
mothers and grandmothers (Table 2).
In Tables 3a and b, relationships with the ages are shown for the
4 autistic traits considered. Maternal age was associated with the
SCDC trait, such that the younger the mother the more autistic
the trait. Coherence showed a similar but less marked younger
mother pattern. There were no significant associations with
paternal age. There were, however, significant trends for older
maternal grandmothers to be associated with worse levels on the
Coherence Scale whether analysed according to the worst decile of
the scale (P =0.025, Table 3), or using the continuous scale
(P= 0.007, Table 4). There were no other traits showing
statistically significant associations with grandparental age.
Correlations between ages
There is, however, a strong correlation between ages of spouses.
Table 5 shows that there is also a strong correlation between the
parent’s age at the birth of the study child and the age of each
grandparent at the birth of the study parent. Although the
correlations between the ages of the maternal and the paternal
grandparents are low (0.05–0.08), those between the parents and
grandparents are higher but still modest (r = 0.17 to 0.26). The
correlation between the ages of spouses is higher for grandparents
than for parents.
Adjusted associations
ASD. To assess which of the highly correlated ages were most
important in regard to ASD, forward step-wise multiple regression
was used; on offering all the 6 age variables only one entered the
model–the maternal grandmother’s age: OR 1.66, [95% CI 1.16,
2.37] per 10 year increase in age (P= 0.006). In the presence of
this factor the mother’s age showed an odds ratio (OR) of 1.39
(95% CI 0.86, 2.24; P =0.177). The paternal grandmother’s age in
the presence of the maternal grandmother’s age, however, did
exhibit an effect that bordered on statistical significance (OR 1.54,
95%CI 0.97, 2.45; P= 0.069).
In order to ensure that the analysis using the ages as continuous
variables were not hiding important non-linear effects, we used the
ages as 4 categorical variables as shown in Figure 1, and used
stepwise logistic regression to determine which factors would enter.
Again it was only the maternal grandmother’s age that entered the
model (P= 0.004); once again, however, the paternal grandmother’s
age was of borderline significance in the presence of the
maternal grandmother’s age (P= 0.066) and the mother’s age
given that of her own mother was not statistically significant
(P= 0.169). Numbers were too small for detailed multivariable
analysis, but the only unadjusted socio-demographic or psychosocial
factor that was significantly associated with ASD was paternal
social class. Taking this into account the maternal grandmother
effect size did not change substantially (OR =1.69, 95%CI 1.15,
2.49, P= 0.007); n= 9957.
Analyses were also repeated taking into account the nonindependence
of multiple births. Both maternal and paternal
grandmother effects were strengthened and exerted independent
effects–OR = 2.04 [1.26, 3.29] and 1.06 [1.01, 1.11] respectively.
But in all other respects, the conclusions were not affected by these
adjustments.
Autistic traits. In regard to the coherence trait, only the age
of the maternal grandmother entered the logistic regression,
Grandparental Age and ASD
PLoS ONE | www.plosone.org 2 April 2010 | Volume 5 | Issue 4 | e9939
Grandparental Age and ASD
PLoS ONE | www.plosone.org 3 April 2010 | Volume 5 | Issue 4 | e9939
indicating that the child was 1.17 times more likely to be in the
worst decile of this trait for each 10 year increase in grandmother’s
age [95% CI 1.02, 1.34], P= 0.025. When the scale was used
linearly, both the grandmother’s and the mother’s ages entered–
the grandmother showing an adverse effect with increasing age
(b = 0.14, 95%CI 0.06, 0.23, P= 0.001), whereas maternal age
independently showed the reverse association (b =20.14, 95% CI
20.25, 20.03, P = 0.011). The only other trait that showed any
independent association with an age measure was maternal age
which entered the SCDC model with OR= 0.80 [95% CI 0.68,
0.93] for the worse decile and b=20.30 [95%CI 20.48, 20.13]
for linear trend (P= 0.005 and 0.001 respectively): i.e. the SCDC
trait score increased as the mother’s age decreased.
Analysis to assess whether the relationship of the maternal
grandmother’s age with the ‘Coherence’ score was an artefact first
investigated over 100 environmental, behavioural or psychological
measures that might be related to this trait. On assessment of the
unadjusted associations we selected 35 which were highly
significant (P,0.001). Each of these were then examined to
determine their effect on the regression coefficient for the ages.
Only maternal personality at 18 w gestation (29.8%) and parity
(22.1%) attenuated the age effect. In all, 7 variables had an effect
between 10 and 20% (maternal social class, paternal education,
paternal grandmother’s education, repetitive behaviour at 30 m,
maternal depression scale at 32 weeks gestation and 8 months
postnatally and a Family Adversity Scale covering the first 2 years
of the study child’s life). There remained 6 factors with an effect
.20%. (maternal education level, housing tenure, child’s passive
smoke exposure at 15 m, whether the TV was on in the afternoons
at 18 m, and the Family Adversity Level in pregnancy and in the
3rd–4th year of the child’s life). Maternal age was also kept in the
analysis. The regression coefficients for maternal age and for
maternal grandmother’s ages on inclusion of the 6 factors were
b=20.046 [95% CI 20.173, + 0.080] (P =0.474) and b =0.217,
[95% CI 0.125, 0.308] (P,0.001) respectively per 10 year increase
in age (n= 5989). Further analysis taking account of the child’s IQ
resulted in b= 0.207 [95% 0.115, 0.299] (P,0.005) per 10 year
increase in maternal grandmother’s age (n= 4770).
Adjustments for multiple births did not alter the conclusions.
Missing data. As Table 1 shows, varying amounts of missing
data existed for different ages varying from zero for maternal age
(data obtained from registration details) to 45% for paternal
grandfather age (data obtained from a partner questionnaire
administered during pregnancy). Complete data were available for
5851 (42%) children. Analyses using this sample suggested a
similar dominant effect for maternal grandmother age as reported
in Table 2 and in Adjusted associations above. Athough this age effect
was somewhat higher for the restricted sample OR= 2.17 [95%
1.32, 3.55], this effect was not statistically different from the result
of OR=1.65 obtained for 11075 children (interaction p =0.127).
This result may imply the transition from observed to the total
sample of 13971 children will also have a minimal impact on the
associations reported.
Confounding. The associations of outcomes and predictors
with socio-demographic variables are shown in Table 6. While
strong associations existed, in general, there was little evidence of
confounding. For instance, with gender, associations were only
present for outcomes but not for predictors. For others, such as
social class, education and housing, the direction of associations
between outcomes and predictors tended to occur in opposite
directions. This may explain the result above whereby adjustment
tended to strengthen the associations.
Discussion
There have been a number of population studies showing that
children with ASD are more likely to be born to older parents. In
this study, for the first time to our knowledge, we have assessed
possible relationships with the ages of the parents’ own parents at
the time of their birth. We had no prior hypotheses as to whether
we would find relationships through the male or female line, but
found that the ages of the grandmothers were higher than
expected, and that the relationship with the maternal grandmother
was statistically significant (P= 0.006).
There is increasing recognition that trying to find a biological
basis for syndromes such as ASD is probably best served by study
Figure 1. Rates per 1000 of a child having ASD are shown according to ages of parents at child’s birth and of grandparents at
parents’ birth with 95% CIs.
doi:10.1371/journal.pone.0009939.g001
Table 1. Comparison of mean ages of parentsa and
grandparentsb of children with and without ASD.
ASD Non- ASD
Mean
difference
Age of n
Mean
(SD) n
Mean
(SD) [95% CI]
Mother 86 29.24
(4.97)
13885 27.99
(4.96)
1.26 [0.20, 2.31]c
Father 71 31.55
(5.30)
11599 30.71
(5.74)
0.84 [20.50,
2.17]
Maternal
grandmother
76 28.68
(6.20)
11001 26.79
(5.85)
1.90 [0.58, 3.22]d
Maternal
grandfather
73 31.04
(6.01)
10164 29.88
(6.72)
1.16 [20.39,
2.71]
Paternal
grandmother
51 29.27
(6.43)
7977 27.30
(5.95)
1.97 [0.33, 3.61]e
Paternal
grandfather
50 31.86
(7.09)
7594 30.40
(6.84)
1.46 [20.44,
3.37]
aage of parent at birth of study child.
bage of grandparent at birth of the parent.
cP = 0.019.
dP = 0.005.
eP = 0.018.
doi:10.1371/journal.pone.0009939.t001
Table 2. Increase in risk [95% confidence interval] of child
having ASD for each 10 year increase in age of parents and
grandparents adjusted for gender.
Age of OR [95% CI] P
Mother 1.60 [1.05, 2.44] 0.029
Father 1.24 [0.84, 1.82] 0.278
Maternal grandmother 1.66 [1.16, 2.37] 0.006
Maternal grandfather 1.27 [0.92, 1.75] 0.140
Paternal grandmother 1.65 [1.07, 2.54] 0.023
Paternal grandfather 1.29 [0.89, 1.87] 0.176
doi:10.1371/journal.pone.0009939.t002
Grandparental Age and ASD
PLoS ONE | www.plosone.org 4 April 2010 | Volume 5 | Issue 4 | e9939
of the component traits [16,17]. Elsewhere we have investigated
within ALSPAC the associations between ASD and 90 different
trait scales. Of these, 4 were identified as independently associated
with ASD, thus providing a compromise between parsimony and
explanatory power [12]; these were coherence, social communication,
sociability and repetitive behaviour; together they accounted
for 54% of the variance. Of the 4 traits the coherence scale
showed the strongest relationship with ASD. Therefore in this
study, as well as looking at study subjects which have an ASD
diagnosis, we have assessed relationships with these 4 traits. We
showed that the coherence trait, whether treated as a continuous
scale or dichotomously studying the worst decile of the
distribution, was significantly associated with the maternal
grandmother’s age.
In regard to whether the grandmother’s age effects might be
explained by older women being more likely to have daughters (i.e.
study mothers) with autistic traits, we examined the information
that had been collected from the study parents during pregnancy
and later. For ASD there was no hint of any associations with
maternal history of child guidance or speech therapy or of current
unusual personality traits (data not shown). The parents had
similar social networks and education levels to the rest of the
population, but there were positive associations with paternal
social class such that the children of fathers in non-manual as
opposed to manual occupations were at increased risk of ASD
[11]. Taking this into account the maternal grandmother effect
remained strongly associated.
Although analyses of data on the ASD cases suffer from lack of
statistical power, this was not true of the trait measures. The
Coherence trait which has been shown to be closely related to a
diagnosis of ASD in our data, had sufficient power for a number of
factors to be taken into account. Unadjusted analyses concerning
over 100 potential confounders were examined and 6 showing a
change of at least 20% in the effect size were selected for
multivariable analysis. The result was an increase in the regression
coefficient from 0.142 [95% CI 0.057, 0.228] to 0.217 [95% CI
0.125, 0.308] per 10 year increase in maternal grandmother’s age.
In a further analysis we took the child’s IQ into account in order to
ensure that it was the Coherence trait we were assessing rather
than some effect of the child’s intellectual ability, but again this
made little difference to the relationship with maternal grandmother’s
age.
This maternal grandmother’s age effect, found for both ASD
and for one of the major autistic traits, was unexpected and will
need replication, but it is biologically plausible because of the
timing of meiosis in females. As Figure 2 illustrates, the paired (and
recombining) grandparental chromosomes that will be transmitted
from the mother to her offspring are already there in the fetal
Table 3. Increase in risk [95% confidence interval] of child being in the worst decile of each autistic trait for each 10 year increase
in age of parents and grandparents adjusted for gender.
UNADJUSTED OR [95% CI]
Age of Coherence SCDCa RBb Sociability
Motherc 0.92 [0.79, 1.09] (P = 0.337) 0.80 [0.68, 0.93] (P = 0.005) 0.94 [0.79, 1.13] (P = 0.520) 0.96 [0.84, 1.09] (P = 0.529)
Fatherc 1.13 [0.98, 1.29] (P = 0.088) 0.91 [0.79, 1.05] (P = 0.197) 0.95 [0.82, 1.11] (P = 0.557) 0.99 [0.89, 1.12] (P = 0.928)
Maternal grandmotherd 1.17 [1.02, 1.34] (P = 0.025) 0.99 [0.86, 1.13] (P = 0.839) 0.99 [0.85, 1.16] (P = 0.921) 0.95 [0.84, 1.06] (P = 0.341)
Maternal grandfatherd 1.13 [1.00, 1.28] (P = 0.052) 0.97 [0.86, 1.10] (P = 0.663) 1.03 [0.89, 1.19] (P = 0.684) 1.00 [0.90, 1.11] (P = 0.936)
Paternal grandmotherd 1.00 [0.86, 1.17] (P = 0.980) 1.15 [0.98, 1.34] (P = 0.084) 1.04 [0.87, 1.24] (P = 0.691) 1.11 [0.97, 1.26] (P = 0.125)
Paternal grandfatherd 0.98 [0.85, 1.12] (P = 0.751) 1.07 [0.94, 1.23] (P = 0.316) 1.09 [0.94, 1.28] (P = 0.245) 1.07 [0.95, 1.20] (P = 0.273)
aSocial and Communication Disorders Checklist.
bRepetitive behaviour score.
cage at birth of study child.
dage of grandparent at birth of the parent.
doi:10.1371/journal.pone.0009939.t003
Table 4. Linear regression of parental and grandparental ages on autistic traits; results per 10 years increase in age, high scores
indicate more autistic like traits adjusted for gender.
UNADJUSTED REGRESSION COEFFICIENT [95% CI]
Age of Coherence SCDCa RBb Sociability
Motherc 20.13 [20.23, 20.03] (P = 0.009) 20.30 [20.48, 20.13] (P = 0.001) 20.01 [20.03, +0.01] (P = 0.509) +0.03 [20.10. +0.16] (P = 0.676)
Fatherc +0.02 [20.06, +0.11] (P = 0.594) 20.12 [20.27, +0.03] (P = 0.110) +0.00 [20.02, +0.02] (P = 0.794) 20.02 [20.13, +0.10] (P = 0.779)
Maternal grandmotherd +0.12 [+0.03, +0.20] (P = 0.007) 20.11 [20.25, +0.04] (P = 0.152) +0.00 [20.01, +0.02] (P = 0.645) 20.01 [20.13, +0.10] (P = 0.799)
Maternal grandfatherd +0.07 [20.01, +0.14] (P = 0.084) 20.08 [20.21, +0.05] (P = 0.233) +0.01 [20.01, +0.02] (P = 0.410) +0.00 [20.10, +0.10] (P = 0.994)
Paternal grandmotherd 20.01 [20.10, +0.09] (P = 0.914) +0.09 [20.08, +0.25] (P = 0.301) +0.00 [20.02, +0.02] (P = 0.919) +0.09 [20.03, +0.22] (P = 0.150)
Paternal grandfatherd 20.05 [20.14, +0.03] (P = 0.209) +0.03 [20.12, +0.18] (P = 0.684) +0.01 [20.01, +0.03] (P = 0.290) +0.04 [20.07, +0.15] (P = 0.469)
aSocial and Communication Disorders Checklist.
bRepetitive behaviour score.
cage at birth of study child.
dage of grandparent at birth of the parent.
doi:10.1371/journal.pone.0009939.t004
Grandparental Age and ASD
PLoS ONE | www.plosone.org 5 April 2010 | Volume 5 | Issue 4 | e9939
ovary from the second trimester of the grandmother’s pregnancy.
This permits a direct grand-maternal effect on the germ line that
will be passed to the grandchild.
Although in this study maternal and paternal ages were raised,
our analysis indicates that the primary association with ASD risk is
the maternal grandmother’s age. If this is confirmed in other
studies, it suggests three broad possibilities–
a) Women with older mothers are more likely to push for a
diagnosis for their child. Although there is no literature on
this it is known that older mothers tend to recognise signs of
ASD earlier [18], and it is likely that older grandmothers
would do the same. However this does not explain the
association between maternal grandmother’s age and the
Coherence trait, since the scale involved was completed by a
large population of mothers, and did not depend on any
diagnosis.
b) There is something about early stages of meiosis I in the fetal
ovaries that is particularly sensitive to maternal age effects,
with the (genomic) malfunction being played out in the
grandchild.
c) An inherited risk factor is amplified in some way by passage
across at least one generation, i.e. the maternal age effect
increases the ASD risk in the daughter to a lesser degree than
in the grandchild. This could happen in two ways:
enrichment for those germ cells that happen to carry an
increased ASD risk or some progressive change to the
genome. Candidates for the former include an age-related
loss of selection against oogonia or oocytes with de novo genetic
damage or indeed a proliferative advantage of cells with an
ASD risk genotype. Candidates for progressive change to the
genome include a dynamic triplet repeat mutation, as in
fragile X, but where older maternal age is associated with de
novo premutations, or some epigenetic spreading of the
genetic malfunction during transmission to the next generation,
e.g. at meiosis.
The last two scenarios imply a transmitted change in the
genome or other heritable material. Twin [19] and sibling risk
studies [2] show that ASD is highly heritable with monozygotic
twins having 92% concordance compared to 10% in dizygotic
twins. It is usually assumed that this heritability is genetic, although
Table 5. Correlations between parental and grandparental ages–all study families.
Age of M F MGM MGF PGM PGF
Mother (M) 1.000
Father (F) 0.661 1.000
Maternal grandmother (MGM) 0.255 0.195 1.000
Maternal grandfather (MGF) 0.230 0.205 0.809 1.000
Paternal grandmother (PGM) 0.190 0.189 0.076 0.058 1.000
Paternal grandfather (PGF) 0.172 0.177 0.068 0.050 0.790 1.000
[ages are those of parents at the birth of the study child, and of grandparents at the birth of the study parent].
All correlations were statistically significant p,0.001.
doi:10.1371/journal.pone.0009939.t005
Table 6. Association of ASD, traits and age variables with socio-demographic variables.
Gender Birth order Social class Education Housing
ASD 0.152 (1.403)*** 1.525 (1.280) 0.803 (1.104)* 0.984 (1.094) 0.898 (1.196)
Traits
Coherence 20.461 (0.046)*** 0.164 (0.048)*** 0.055 (0.020)** 20.129 (0.020)*** 0.122 (0.039)**
SCDC 20.856 (0.082)*** 20.161 (0.084) 0.089 (0.034)** 20.119 (0.034)*** 0.287 (0.067)***
RB 20.055 (0.010)*** 0.002 (0.010) 20.000 (0.004) 20.006 (0.004) 0.033 (0.008)***
Sociability 20.331 (0.062)*** 0.688 (0.063)*** 0.070 (0.026)** 20.191 (0.025)*** 20.011 (0.049)
Ages
M 20.155 (0.087) 2.656 (0.086)*** 21.061 (0.034)*** 1.050 (0.033)*** 22.068 (0.061)***
F 20.245 (0.108)* 2.409 (0.108)*** 20.954 (0.043)*** 0.877 (0.043)*** 21.689 (0.081)***
MGM 20.078 (0.113) 0.201 (0.116) 20.503 (0.047)*** 0.685 (0.045)*** 20.888 (0.086)***
MGF 20.010 (0.135) 0.271 (0.139) 20.529 (0.056)*** 0.744 (0.054)*** 20.729 (0.105)***
PGM 20.165 (0.136) 0.453 (0.137)*** 20.536 (0.056)*** 0.553 (0.055)*** 20.796 (0.105)***
PGF 20.357 (0.159)* 0.545 (0.161)*** 20.524 (0.066)*** 0.562 (0.065)*** 20.782 (0.125)***
Gender effect is for females. Birth order coded as 0 (no older siblings) and 1 (one or more older siblings). Paternal social class coded as I, II, III non-manual, III manual and
IV+V combined. Maternal educational qualifications coded as none or CSE, vocational, O level, A level or degree. Housing coded as mortgaged/owned, local authority
housing and other. Traits are coded so that low scores reflect a more favourable response. Traits are labelled as in Table 3. Age variables are labelled as given in Table 4.
Reported effect sizes relate to a linear trend. Effect sizes are ORs for ASD and regression coefficients for other outcomes. Standard errors (or exp(SE) for ASD) are given in
parentheses.
doi:10.1371/journal.pone.0009939.t006
Grandparental Age and ASD
PLoS ONE | www.plosone.org 6 April 2010 | Volume 5 | Issue 4 | e9939
transmission of molecular information other than through DNA
sequence (e.g. microRNAs) cannot be ruled out [20]. Recently,
specific genetic risk factors for ASD have been reported, but they
are very heterogeneous. To date one common single nucleotide
polymorphism (SNP) variant associated with ASD risk has been
reported [21], but there have been several studies showing an
excess of rare microdeletions and in some cases microduplications
in ASD compared with controls [22–25]. These so-called copy
number variants (CNVs) may be inherited from a parent or arise
de novo, i.e. new mutations. Some studies [24] deliberately excluded
inherited CNVs in an attempt to enrich for causal variants, whilst
a recent study of smaller deletions and duplications involving the
coding regions (exons) of genes demonstrates that possible
susceptibility CNVs are often inherited [25]. However when
inherited in multiplex families (i.e. with several affected family
members) there is imperfect segregation with ASD with affected
siblings often not inheriting the exonic deletion [25]. This result is
less easy to explain in a multiplex family than some asymptomatic
family members carrying the exonic deletion, if indeed the
inherited deletion is contributing to the familial ASD.
There are few published data on the possible mediators of
(grand)maternal age effects that help distinguish between scenarios
b and c above. A recent study of reproductive and epigenetic
outcomes with aging mouse oocytes found morphological
abnormalities (increased trophoblast giant cells) in the resulting
placentae [26], which raises the possibility of impaired transpla-
Figure 2. Three generations of genotypes are illustrated (A): that involving the grandmother’s pregnancy, her female fetus and the
fetal ovary that contains the emerging genotype of the grandchild. The grandmother has two normal, wild type genes (++). The fetus has a
deletion of the gene inherited from grandfather (n) which confers some susceptibility to autistic spectrum disorder. The hypothesised mispairing of
the grandparental chromosomes at the site of the gene deletion (n) in the fetal oocytes is shown (B). The chromosome containing the wild type
gene loops out at meiotic pairing and this gene becomes liable to be silenced by DNA methylation. This results in no grandchild receiving a
functional gene.
doi:10.1371/journal.pone.0009939.g002
Grandparental Age and ASD
PLoS ONE | www.plosone.org 7 April 2010 | Volume 5 | Issue 4 | e9939
cental transfer of nutrients or metabolic signals to the germ line in
the fetal ovaries. Despite early work suggesting a reduction in
DNA methyltransferases with age, the authors found no
impairment of DNA methylation at imprinted genes and more
widely across the genome.
Given the ongoing generation of de novo CNVs, deterioration
with maternal age in the ‘surveillance’ mechanisms for eliminating
cells with genetic imbalance is a possibility. Less selection against
oogonia with a high CNV load in the fetal ovaries would increase
the ASD risk. Recent work in relation to Down syndrome indicates
that ovarian trisomy 21 mosaicism is common and the maternal
age effect is likely to be, in part, a change in oocyte selection [27].
DNA fragmentation is increased in oocytes from older mice [28]
as is mitochondrial dysfunction [29] which in turn may
compromise the cell quality surveillance role of mitochondria
through apoptosis [30]. However, human research on the
development of oocytes and influences on female meiosis is
necessarily limited, so family based genetic and epigenetic studies
might prove more productive.
One possibility, prompted by our data suggesting a maternal
grandmother age effect in ASD, would be to test what we have
called the meiotic mismatch methylation (3 M) hypothesis (Fig. 2b).
Mispairing of a chromosome bearing an ASD risk deletion with
the normal homologous chromosome during early meiosis I (in the
ovaries of the mother as a fetus) might lead to methylation and
silencing of the normal gene. If this were the case then all the
mother’s children would inherit a risk allele, either the deletion or
a gene silenced by DNA methylation. All other ASD risk factors
being equal, such a meiotic mismatch methylation (beginning
during the grandmother’s pregnancy) would lead to a higher risk
of ASD in the grandchildren than in the mother. It is known that
meiotic mismatches are accommodated in various ways and the
looping out illustrated in Fig. 2b has been known as one such
mechanism for a long time [31].
Beyond the inherited ASD risk deletion (or duplication) itself,
are there any distinctive features of genomic regions harbouring
CNVs that might predispose to meiotic mismatch and DNA
methylation? Such genomic regions tend to contain repeated DNA
sequences (that are implicated in the generation of the CNV in the
first place [32]), and such sequences can lead to other forms of
mismatch at meiosis such as non-allelic-homologous-pairing. The
key question is whether these perturbations of meiotic pairing
trigger spread of DNA methylation to silence the otherwise
functional normal gene (wild type allele). DNA methylation is
believed to have first evolved as a genome defence system to
silence transposons and the like and such sequences are
preferentially methylated [33], so the same genomic architecture
that predisposes to CNVs might also attract DNA methylation.
The 3 M hypothesis is testable in family studies such as reported
by Bucan et al [25] where a specific ASD risk CNV is segregating.
It would predict that those affected members not carrying the CNV
would have DNA methylation silencing of the wild type allele.
Acknowledgments
We are extremely grateful to all the families who took part in this study, the
midwives for their help in recruiting them, and the whole ALSPAC team,
which includes interviewers, computer and laboratory technicians, clerical
workers, research scientists, volunteers, managers, receptionists and nurses.
This publication is the work of the authors who will serve as guarantors for
the contents of this paper.
Author Contributions
Conceived and designed the experiments: JG CDS MP. Performed the
experiments: JG MP. Analyzed the data: CDS. Wrote the paper: JG CDS
MP.
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PLoS ONE

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Saturday, April 10, 2010

Why Medical Authorities Went to Such Extremes to Silence Dr. Andrew Wakefield





Why Medical Authorities Went to Such Extremes to Silence Dr. Andrew Wakefield Posted by Dr. Mercola | April 10 2010 | 42,970 views Email this to a friend Share this article Next Article

In this interview, Dr. Andrew Wakefield shares his personal and professional insights into a number of topics, from the gut-brain connection so often seen in autistic children, to the safety of a number of childhood vaccines.

But most importantly, he sets the record straight on the harsh criticism he’s endured as the author of one of the most controversial vaccine-causing-autism studies ever done.

In addition to his hotly contested MMR study, published in the journal Lancet in 1998, he has published about 130-140 peer-reviewed papers looking at the mechanism and cause of inflammatory bowel disease, and has extensively investigated the brain-bowel connection in the context of children with developmental disorders such as autism.
Sources:
Andrew Wakefield Interview (Full Transcript)



Dr. Mercola's Comments:


As a gastrointestinal surgeon, Dr. Wakefield has investigated the connection between developmental disorders and bowel disease, and early exposure to vaccines. For example, in the beginning of our interview, he discusses the curious link between an unusual exposure to the measles virus and subsequent development of Crohn’s disease, and in many cases, autism.

One of the routes of this type of exposure is clearly vaccination.

One of the primary reasons for this interview was to discuss Dr. Wakefield’s recent media exposure, and allow him the opportunity to finally set the public record straight.

As you probably know, the scientific peer-review process is designed to ferret out the truth. But in some cases, such as the case of Dr. Wakefield, this process can become perverted by conflicts of interest.

There are tens, if not hundreds of billions of dollars involved in the vaccine industry, and as a consequence there’s major pressure to suppress negative findings, such as the findings Dr. Wakefield uncovered.

In the last few months, he has been severely criticized in the media. Like every story there are always two sides and up until now he has not shared his due to advice he had received from his attorneys. That advice has now changed, and I wanted to provide him with the opportunity to tell his side of the story. In this interview, Dr. Wakefield opens up publicly for the first time.

If you have any interest in the vaccine controversy, I can strongly assure you that watching this fascinating video will be very rewarding.

Study Lands Dr. Wakefield in Hot Water
The story begins with the publication of a case series in the prestigious medical journal The Lancet, in February 1998.

A case series essentially tells the clinical story of a group of patients with a constellation of signs and symptoms that link them together. In this case, it was a group of autistic children with gastric problems, which led to the discovery of a novel bowel disease.

But rather than celebrating the discovery of a tangible, treatable problem that can help these children and others suffering with similar health issues, it became a hotly debated controversy in which Dr. Wakefield’s reputation was smeared.

Why?

Because part of the patients’ story included regression after a vaccine.

“… If those children had regressed after natural chickenpox, you and I would not be sitting here now. But they didn’t. They regressed after a vaccine,” says Wakefield.

The vaccine in question was the MMR vaccine.

Since then, Dr. Wakefield’s study -- which suggests there may be a link between the MMR vaccine, bowel disease, and autism -- has remained one of the most controversial studies on the topic of vaccine safety.

He knew he was about to enter treacherous waters when it was published, and he knew he needed to be prepared for the inevitable backlash from the vaccine industry. Says Dr. Wakefield:

“… I decided that I was going to review all of the safety studies about measles and measles-containing vaccines because if I was going to challenge the status quo and say things that might have an adverse effect on vaccine uptake, I had to know what I was talking about.

So I read all the papers, and I was absolutely appalled with the quality of the safety studies of the single [measles, mumps, and rubella vaccines], and the combined MMR vaccine in particular.”

His research led him to write a 250-page report, concluding that he could not support the use of the combined three-in-one MMR vaccine.

It simply was not safe.

This recommendation was made public during a press conference in February of 1998, at which time single vaccines were still available in the UK. But in order to protect MMR vaccine policy, in September of that same year, the British government withdrew the importation license for the single measles vaccine, leaving parents without any choice – they either had to vaccinate their children with the triple MMR vaccine, or not vaccinate.

The result?

A decline in vaccination, and an increase in measles outbreaks… But rather than acknowledging the lack of safe options, Dr. Wakefield was singled out as an “anti-vaccine advocate” whose recommendations caused a decline in children being vaccinated, and hence responsible for the increase in measles.

Says Wakefield:

“… it’s my opinion that it is entirely their responsibility that there has been a declining vaccine uptake in the UK, because they removed the option of the single vaccines and there have been outbreaks of infectious disease as a consequence.”

But that’s just the background of the story. Dr. Wakefield’s real media troubles had just barely begun.

Why are So Many Important Safety Studies Being Ignored?
As with most stories, a series of events took place, which recently catapulted Dr. Wakefield back into the media spotlight.

In the years after his initial controversial finding, linking the MMR vaccine to Crohn’s disease and autism, he published another 19 papers on the vaccine-induced disorder.

All were peer reviewed. However, strangely enough, none of these 19 papers are ever discussed in the media. The only study that keeps seeing the light of day is the original study from 1998, along with the original questions about conflicts of interest, which he explains in great detail in this interview.

This is very interesting indeed, because not only has he continued his own studies, but since then, a large number of replication studies have been performed around the world, by other researchers, that confirm his initial findings.

Says Wakefield:

“… it’s been replicated in Canada, in the U.S., in Venezuela, in Italy… [but] they never get mentioned. All you ever hear is that no one else has ever been able to replicate the findings.

I’m afraid that is false.”

For those of you who have swallowed this type of reporting hook line and sinker, here is a list of 28 studies from around the world that support Dr. Wakefield’s controversial findings:

1.The Journal of Pediatrics November 1999; 135(5):559-63
2.The Journal of Pediatrics 2000; 138(3): 366-372
3.Journal of Clinical Immunology November 2003; 23(6): 504-517
4.Journal of Neuroimmunology 2005
5.Brain, Behavior and Immunity 1993; 7: 97-103
6.Pediatric Neurology 2003; 28(4): 1-3
7.Neuropsychobiology 2005; 51:77-85
8.The Journal of Pediatrics May 2005;146(5):605-10
9.Autism Insights 2009; 1: 1-11
10.Canadian Journal of Gastroenterology February 2009; 23(2): 95-98
11.Annals of Clinical Psychiatry 2009:21(3): 148-161
12.Journal of Child Neurology June 29, 2009; 000:1-6
13.Journal of Autism and Developmental Disorders March 2009;39(3):405-13
14.Medical Hypotheses August 1998;51:133-144.
15.Journal of Child Neurology July 2000; ;15(7):429-35
16.Lancet. 1972;2:883–884.
17.Journal of Autism and Childhood Schizophrenia January-March 1971;1:48-62
18.Journal of Pediatrics March 2001;138:366-372.
19.Molecular Psychiatry 2002;7:375-382.
20.American Journal of Gastroenterolgy April 2004;598-605.
21.Journal of Clinical Immunology November 2003;23:504-517.
22.Neuroimmunology April 2006;173(1-2):126-34.
23.Prog. Neuropsychopharmacol Biol. Psychiatry December 30 2006;30:1472-1477.
24.Clinical Infectious Diseases September 1 2002;35(Suppl 1):S6-S16
25.Applied and Environmental Microbiology, 2004;70(11):6459-6465
26.Journal of Medical Microbiology October 2005;54:987-991
27.Archivos venezolanos de puericultura y pediatría 2006; Vol 69 (1): 19-25.
28.Gastroenterology. 2005:128 (Suppl 2);Abstract-303
The Real Dangers of Indemnifying Vaccine Manufacturers Against Lawsuits
Says Wakefield:

“In the background, things were going on behind the scenes that we didn’t know about… The Department of Health had contacted my medical school, the dean in particular, and had tried to close this research down... expressing concerns that it was unethical that all these children had autism. It wasn’t fair on them to go through these procedures.

Were they justified?

Well, here you had the world’s leading pediatric gastroenterologist and his colleagues saying, “Yes, they are justified, and here are the findings. We’re happy to show you the findings at any stage, in any venue that you like.”

But nonetheless, there was a concerted effort behind the scenes to stop the work.

And it was particularly the concern of the Department of Heath that there was pending litigation where I had agreed to act as an expert in the litigation… not trying to prove that it was right or wrong, but doing my best as an expert to determine whether there is a case in law against the vaccine manufacturers.”

This was around 1996-97. Wakefield says he “felt there was a professional and moral obligation” to get involved in the potential litigation, “because these children, when their parents die or become infirmed, they are on the street, no one cares, and no one is going to look after them.”

However, litigation was never to become reality for any of the vaccine manufacturers.

“What had happened when the MMR was introduced in the UK is that somehow the Department of Health or the government had done a deal with the manufacturers of one of the vaccines, SmithKline Beecham, to indemnify them against litigation,” says Wakefield.

“Now, why would they do that? What was the purpose of that?

Well, it turns out that the vaccine that they had at the time contained a strain of the mumps virus, Urabe AM9, which was dangerous. It caused meningitis.

… It was introduced into Canada and very quickly they found that it caused meningitis.

Rapidly after that, it was withdrawn in Canada, [but] it was still introduced in the UK, and it’s my opinion that SmithKline Beecham did not want to introduce it because they knew of these problems. They had a potential liability, a real liability.

And the government therefore, in order to give the contract to the home team, to a British company, indemnified them.”

As could be expected, the MMR vaccine containing the Urabe AM9 strain had to be withdrawn four years later because it was causing meningitis…

However, this dangerous vaccine was not taken off the market.

Instead, it was sent to Third World countries, including Brazil, where it ended up causing an epidemic outbreak of -- you guessed it – meningitis.

Dr. Wakefield feels it’s high time to expose this kind of cruel pandering of dangerous wares, without any risk, and I couldn’t agree more.

You are paying the price for corporate greed in every sense of the word. In fact, parents everywhere are paying money to put their children’s health at significant risk, without any recourse or assistance when something goes wrong –which it does more frequently than any of our health officials want to admit.

More Dirty Games…
Dr. Wakefield’s story is a cautionary tale of just how easy it can be to ruin someone’s hard-earned reputation, and just how difficult it can be to prove one's innocence – or rather, correctness -- even when you’re sitting with proof in hand.

“In 2004, I suddenly got this contact from a freelance journalist Brian Deer working on behalf of the Sunday Times making a whole series of allegations against me and my colleagues,” Dr. Wakefield says.

“In his opinion, these children did not need investigation. In his opinion, these children did not need a colonoscopy or a lumbar puncture or these other investigations that my clinical colleagues had deemed they most certainly did need.”

This is a journalist with no formal medical training whatsoever. It was just his opinion. But as a crafty wordsmith, he wove together a compelling tale of how Dr. Wakefield and his posse had rounded up autistic children for the purpose of creating a legal case against the vaccine manufacturers to bring about the downfall of the vaccine, in order to then launch his own vaccine onto the market.

It was a great story.

Too bad it wasn’t true.

Just for starters, had he done his homework, he would have realized the whole thing was impossible since the manufacturers were by then indemnified and couldn’t be sued anymore.

“He made so many factual errors, but he nonetheless managed to persuade the General Medical Council (GMC) to initiate a process of investigation against us. And by that stage, this had become such a political hot potato, the Minister of Health, and a number of people from the department... construed this case against us.

… So they determined that the world’s leading pediatric gastroenterologist was not fit to determine whether these children needed a colonoscopy or not for clinical indications.”

The world’s leading pediatric gastroenterologist he’s referring to here is not himself, but rather Professor John Walker-Smith, to whom Dr. Wakefield would refer parents of autistic children with highly complex medical histories.

“… So some doctors contacted me. Some parents put me in contact with their doctors, and I spoke to them. I communicated with them, and the referrals were made accordingly or not.

At the GMC, I was found guilty of causing children to have, for example, spinal taps because of this communication.

Now, that’s got to be a completely new charge -- causing children to have these tests. I didn’t do the test. I wasn’t there when the tests were done. I didn’t prescribe the tests. But I caused the children to have them because the parents called me and I suggested getting a referral to Walker-Smith.

That is how complex, and how bizarre and tortuous this process has become.”

There are many more complexities involved in this story and the latest rounds of media attention that has befallen Dr. Wakefield, which is why I strongly I urge you to listen to the entire interview above.

You can also read through the transcript in its entirety by clicking the Source link beneath the video.

Final Thoughts
This story, like so many other stories of great doctors and researchers who chase the truth and want nothing more than to protect those who cannot protect themselves from dangerous medicine, is a call to open your eyes, and to look deeper – to not simply believe the bits and pieces the media offers up as fact. Usually, there’s a lot more to the story.

And what you choose to believe – without sufficient amount of facts – can have serious ramifications on your health, and the health of your family.

Remember, you make serious, at times life-and-death, decisions based on what and who you believe…

So when it comes to vaccinating your child, how much do you really know about the vaccine in question? Who do you believe, and why?

Do you place your trust in the hands of those who have the most to gain and nothing to lose?

Or in the hands of those who have little, or nothing, to gain by your choice?

It’s up to you.

In the case of the MMR vaccine as a potential causative factor in autism and Crohn’s disease, this interview is filled with back-story and behind the scenes information about how the research has been, and continues to be, suppressed.

So listen to the interview, and continue doing your own research. Twenty-eight additional studies are listed above for your own investigation.

As always -- Make your decision an educated decision.



Related Links:
STOP! Read This Before Vaccinating for Anything

Vaccine Failure -- Over 1000 Got Mumps in NY in Last Six Months

The Vaccines That Worry Parents Most

Labels:

Thursday, April 08, 2010

Dr. Andrew Wakefield shares his personal and professional insights into a number of topics,









Silenced Whistle-Blower Finally Reveals the Forbidden Truth Posted by Dr. Mercola | April 10 2010 | 4,016 views Email this to a friend Share this article Next ArticleIn this interview, Dr. Andrew Wakefield shares his personal and professional insights into a number of topics, from the gut-brain connection so often seen in autistic children, to the safety of a number of childhood vaccines.

But most importantly, he sets the record straight on the harsh criticism he’s endured as the author of one of the most controversial vaccine-causing-autism studies ever done.

In addition to his hotly contested MMR study, published in the journal Lancet in 1998, he has published about 130-140 peer-reviewed papers looking at the mechanism and cause of inflammatory bowel disease, and has extensively investigated the brain-bowel connection in the context of children with developmental disorders such as autism.
Sources:
Andrew Wakefield Interview (Full Transcript)



Dr. Mercola's Comments:


As a gastrointestinal surgeon, Dr. Wakefield has investigated the connection between developmental disorders and bowel disease, and early exposure to vaccines. For example, in the beginning of our interview, he discusses the curious link between an exposure to the measles virus and subsequent development of Crohn’s disease, and in many cases, autism.

One of the routes of this type of exposure is clearly vaccination.

One of the primary reasons for this interview was to discuss Dr. Wakefield’s recent media exposure, and allow him the opportunity to finally set the public record straight.

As you probably know, the scientific peer-review process is designed to ferret out the truth. But in some cases, such as the case of Dr. Wakefield, this process can become perverted by conflicts of interest.

There are tens, if not hundreds of billions of dollars involved in the vaccine industry, and as a consequence there’s major pressure to suppress negative findings, such as the findings Dr. Wakefield uncovered.

In the last few months, he has been severely criticized in the media. Like every story there are always two sides and up until now he has not shared his due to advice he had received from his attorneys. That advice has now changed, and I wanted to provide him with the opportunity to tell his side of the story. In this interview, Dr. Wakefield opens up publicly for the first time.

If you have any interest in the vaccine controversy, I can strongly assure you that watching this fascinating video will be very rewarding.

Study Lands Dr. Wakefield in Hot Water
The story begins with the publication of a case series in the prestigious medical journal The Lancet, in February 1998.

A case series essentially tells the clinical story of a group of patients with a constellation of signs and symptoms that link them together. In this case, it was a group of autistic children with gastric problems, which led to the discovery of a novel bowel disease.

But rather than celebrating the discovery of a tangible, treatable problem that can help these children and others suffering with similar health issues, it became a hotly debated controversy in which Dr. Wakefield’s reputation was smeared.

Why?

Because part of the patients’ story included regression after a vaccine.

“… If those children had regressed after natural chickenpox, you and I would not be sitting here now. But they didn’t. They regressed after a vaccine,” says Wakefield.

The vaccine in question was the MMR vaccine.

Since then, Dr. Wakefield’s study -- which suggests there may be a link between the MMR vaccine, bowel disease, and autism -- has remained one of the most controversial studies on the topic of vaccine safety.

He knew he was about to enter treacherous waters when it was published, and he knew he needed to be prepared for the inevitable backlash from the vaccine industry. Says Dr. Wakefield:

“… I decided that I was going to review all of the safety studies about measles and measles-containing vaccines because if I was going to challenge the status quo and say things that might have an adverse effect on vaccine uptake, I had to know what I was talking about.

So I read all the papers, and I was absolutely appalled with the quality of the safety studies of the single [measles, mumps, and rubella vaccines], and the combined MMR vaccine in particular.”

His research led him to write a 250-page report, concluding that he could not support the use of the combined three-in-one MMR vaccine.

It simply was not safe.

This recommendation was made public during a press conference in February of 1998, at which time single vaccines were still available in the UK. But for reasons still unknown, in September of that same year, the British government withdrew the license for the single measles vaccine, leaving parents without any choice – they either had to vaccinate their children with the triple MMR vaccine, or not vaccinate.

The result?

A decline in vaccination, and an increase in measles outbreaks… But rather than acknowledging the lack of safe options, Dr. Wakefield was singled out as an “anti-vaccine advocate” whose recommendations caused a decline in children being vaccinated, and hence responsible for the increase in measles.

Says Wakefield:

“… it’s my opinion that it is entirely their responsibility that there has been a declining vaccine uptake in the UK, because they removed the option of the single vaccines and there have been outbreaks of infectious disease as a consequence.”

But that’s just the background of the story. Dr. Wakefield’s real media troubles had just barely begun.

Why are So Many Important Safety Studies Being Ignored?
As with most stories, a series of events took place, which recently catapulted Dr. Wakefield back into the media spotlight.

In the years after his initial controversial finding, linking the MMR vaccine to Crohn’s disease and autism, he published another 19 papers on the vaccine-induced disorder.

All were peer reviewed. However, strangely enough, none of these 19 papers are ever discussed in the media. The only study that keeps seeing the light of day is the original study from 1998, along with the original questions about conflicts of interest, which he explains in great detail in this interview.

This is very interesting indeed, because not only has he continued his own studies, but since then, a large number of replication studies have been performed around the world, by other researchers, that confirm his initial findings.

Says Wakefield:

“… it’s been replicated in Canada, in the U.S., in Venezuela, in Italy… [but] they never get mentioned. All you ever hear is that no one else has ever been able to replicate the findings.

I’m afraid that is false.”

For those of you who have swallowed this type of reporting hook line and sinker, here is a list of 14 studies from around the world that support Dr. Wakefield’s controversial findings:

1.The Journal of Pediatrics November 1999
2.The Journal of Pediatrics 2000; 138(3): 366-372
3.Journal of Clinical Immunology November 2003; 23(6): 504-517
4.Journal of Neuroimmunology 2005
5.Brain, Behavior and Immunity 1993; 7: 97-103
6.Pediatric Neurology 2003; 28(4): 1-3
7.Neuropsychobiology 2005; 51:77-85
8.The Journal of Pediatrics May 2005
9.Autism Insights 2009; 1: 1-11
10.One Year Follow-Up Study
11.Canadian Journal of Gastroenterology February 2009; 23(2): 95-98
12.Annals of Clinical Psychiatry 2009:21(3): 148-161
13.Journal of Child Neurology June 29, 2009
14.Journal of Autism and Developmental Disorders 200
The Real Dangers of Indemnifying Vaccine Manufacturers Against Lawsuits
Says Wakefield:

“In the background, things were going on behind the scenes that we didn’t know about… The Department of Health had contacted my medical school, the dean in particular, and had tried to close this research down... expressing concerns that it was unethical that all these children had autism. It wasn’t fair on them to go through these procedures.

Were they justified?

Well, here you had the world’s leading pediatric gastroenterologist and his colleagues saying, “Yes, they are justified, and here are the findings. We’re happy to show you the findings at any stage, in any venue that you like.”

But nonetheless, there was a concerted effort behind the scenes to stop the work.

And it was particularly the concern of the Department of Heath that there was pending litigation where I had agreed to act as an expert in the litigation… not trying to prove that it was right or wrong, but doing my best as an expert to determine whether there is a case in law against the vaccine manufacturers.”

This was around 1996-97. Wakefield says he “felt there was a professional and moral obligation” to get involved in the potential litigation, “because these children, when their parents die or become infirmed, they are on the street, no one cares, and no one is going to look after them.”

However, litigation was never to become reality for any of the vaccine manufacturers.

“What had happened when the MMR was introduced in the UK is that somehow the Department of Health or the government had done a deal with the manufacturers of one of the vaccines, SmithKline Beecham, to indemnify them against litigation,” says Wakefield.

“Now, why would they do that? What was the purpose of that?

Well, it turns out that the vaccine that they had at the time contained a strain of the mumps virus, Urabe AM9, which was dangerous. It caused meningitis.

… It was introduced into Canada and very quickly they found that it caused meningitis.

Rapidly after that, it was withdrawn in Canada, [but] it was still introduced in the UK, and it’s my opinion that SmithKline Beecham did not want to introduce it because they knew of these problems. They had a potential liability, a real liability.

And the government therefore, in order to give the contract to the home team, to a British company, indemnified them.”

As could be expected, the MMR vaccine containing the Urabe AM9 strain had to be withdrawn four years later because it was causing meningitis…

However, this dangerous vaccine was not taken off the market.

Instead, it was sent to Third World countries, including Brazil, where it ended up causing an epidemic outbreak of -- you guessed it – meningitis.

Dr. Wakefield feels it’s high time to expose this kind of cruel pandering of dangerous wares, without any risk, and I couldn’t agree more.

You are paying the price for corporate greed in every sense of the word. In fact, parents everywhere are paying money to put their children’s health at significant risk, without any recourse or assistance when something goes wrong –which it does more frequently than any of our health officials want to admit.

More Dirty Games…
Dr. Wakefield’s story is a cautionary tale of just how easy it can be to ruin someone’s hard-earned reputation, and just how difficult it can be to prove one's innocence – or rather, correctness -- even when you’re sitting with proof in hand.

“In 2004, I suddenly got this contact from a freelance journalist Brian Deer working on behalf of the Sunday Times making a whole series of allegations against my colleagues and I,” Dr. Wakefield says.

“In his opinion, these children did not need investigation. In his opinion, these children did not need a colonoscopy or a lumbar puncture or these other investigations that my clinical colleagues had deemed they most certainly did need.”

This is a journalist with no formal medical training whatsoever. It was just his opinion. But as a crafty wordsmith, he wove together a compelling tale of how Dr. Wakefield and his posse had rounded up autistic children for the purpose of creating a legal case against the vaccine manufacturers to bring about the downfall of the vaccine, in order to then launch his own vaccine onto the market.

It was a great story.

Too bad it wasn’t true.

Just for starters, had he done his homework, he would have realized the whole thing was impossible since the manufacturers were by then indemnified and couldn’t be sued anymore.

“He made so many factual errors, but he nonetheless managed to persuade the General Medical Council (GMC) to initiate a process of investigation against us. And by that stage, this had become such a political hot potato, the Minister of Health, and a number of people from the department... construed this case against us.

… So they determined that the world’s leading pediatric gastroenterologist was not fit to determine whether these children needed a colonoscopy or not for clinical indications.”

The world’s leading pediatric gastroenterologist he’s referring to here is not himself, but rather Dr. John Walker-Smith, to whom Dr. Wakefield would refer parents of autistic children with highly complex medical histories.

“… So some doctors contacted me. Some parents put me in contact with their doctors, and I spoke to them. I communicated to them, and the referrals were made accordingly or not.

At the GMC, I was found guilty of causing children to have, for example, spinal taps because of this communication.

Now, that’s got to be a completely new charge -- causing children to have these tests. I didn’t do the test. I wasn’t there when the tests were done. I didn’t prescribe the tests. But I caused the children to have them because the parents called me and I suggested getting a referral to Walker-Smith.

That is how complex, and how bizarre and tortuous this process has become.”

There are many more complexities involved in this story and the latest rounds of media attention that has befallen Dr. Wakefield, which is why I strongly I urge you to listen to the entire interview above.

You can also read through the transcript in its entirety by clicking the Source link beneath the video.

Final Thoughts
This story, like so many other stories of great doctors and researchers who chase the truth and want nothing more than to protect those who cannot protect themselves from dangerous medicine, is a call to open your eyes, and to look deeper – to not simply believe the bits and pieces the media offers up as fact. Usually, there’s a lot more to the story.

And what you choose to believe – without sufficient amount of facts – can have serious ramifications on your health, and the health of your family.

Remember, you make serious, at times life-and-death, decisions based on what and who you believe…

So when it comes to vaccinating your child, how much do you really know about the vaccine in question? Who do you believe, and why?

Do you place your trust in the hands of those who have the most to gain and nothing to lose?

Or in the hands of those who have little, or nothing, to gain by your choice?

It’s up to you.

In the case of the MMR vaccine as a potential causative factor in autism and Crohn’s disease, this interview is filled with back-story and behind the scenes information about how the research has been, and continues to be, suppressed.

So listen to the interview, and continue doing your own research. Fourteen additional studies are listed above for your own investigation.

As always -- Make your decision an educated decision.



Related Links:
The Journal of Pediatrics November 1999

The Journal of Pediatrics 2000; 138(3): 366-372

Journal of Clinical Immunology November 2003; 23(6): 504-517

Journal of Neuroimmunology 2005

Brain, Behavior and Immunity 1993; 7: 97-103

Pediatric Neurology 2003; 28(4): 1-3

Neuropsychobiology 2005; 51:77-85

The Journal of Pediatrics May 2005

Autism Insights 2009; 1: 1-11

One Year Follow-Up Study

Canadian Journal of Gastroenterology February 2009; 23(2): 95-98

Annals of Clinical Psychiatry 2009:21(3): 148-161

Journal of Child Neurology June 29, 2009

Journal of Autism and Developmental Disorders 2008

Labels:

Wednesday, April 07, 2010

Do Men Have a Biological Clock Too?

Do Men Have a Biological Clock Too?

Labels:

Did 'Regular' Flu Shot Up Risks for H1N1 Flu?

Did 'Regular' Flu Shot Up Risks for H1N1 Flu?
Those who got seasonal vaccine were at higher risk, study found, but that shouldn't affect immunization next season

Labels:

Medical Board Drops All Original Charges and Allegations

Medical Board Drops All Original Charges and Allegations
Against World-Renowned Doctor After A Five-Year Fight Dr. Rashid Buttar

Labels:

Tuesday, April 06, 2010

[Age of Autism]
April 05, 2010
Statement from Dr. Andrew Wakefield Regarding GMC Hearing Sanctions
By Dr. Andrew Wakefield (See a .pdf here.)

On Wednesday April 7th, General Medical Council (GMC) lawyers will demand that I and likely two other doctors involved in the MMR-autism case should be erased from the UK’s medical register, removing our license to practice medicine. Doctors’ regulators have found the three of us - Professor John Walker-Smith, Professor Simon Murch and me - guilty of undertaking research on children with autism without approval from an ethics committee.
We can prove, with extensive documentary evidence, that this conclusion is false.

Let me make it absolutely clear that, at its heart, the GMC hearing has been about the protection of MMR vaccination policy. The case has been driven by an agenda to crush dissent that in my opinion serves the government and the pharmaceutical industry — not the welfare of children. It’s important to note that there has never been a complaint against any of the doctors by any parent involved in this case — only universal parental support and gratitude.

My colleagues, Professors Walker-Smith and Murch, are outstanding pediatricians and pediatric gastroenterologists. They have led the field of pediatric gastroenterology for decades, devoting their lives to caring for sick children. Our only “crime” in this matter has been to listen to the concerns of parents, act according to the demands of our professional training, and provide appropriate care to this neglected population of children. It is unthinkable that at the end of an unimpeachable career, Professor Walker-Smith would even consider unethical experimentation on children under his care.

In the course of our work, we discovered and treated a new intestinal disease syndrome in children with autism, alleviating suffering in affected children around the world. This should be cause for celebration. Instead, we have been vilified in the press, and demonized by a wasteful PR campaign by the Department of Health. The aim of this negative publicity was to discredit my criticism of vaccine safety research.

Sadly, my colleagues have suffered severe collateral damage in this effort to prevent valid scientific enquiry. They should be exonerated, and left alone with their reputations intact, in the certain knowledge that they have done only what is right.

The loss of my own medical license is, unfortunately, the cost of doing business. Although I do not take this loss lightly, the suffering - so much of it unnecessary - that I have seen among those affected by this devastating disease makes the professional consequences for me a small price to pay by comparison.

As long as a question mark remains over vaccine safety; as long as a safety-first vaccine policy is subordinate to profit and self-interest; as long as the benefits of vaccines are threatened by those who have compromised public confidence by denial of vaccine damage, and as long as these children need help; I will continue my work.

Dr Andrew Wakefield is an academic gastroenterologist, committed to understanding more about the role of intestinal inflammation and dysfunction in childhood developmental disorders. He is involved in a new initiative, focused specifically on issues of autism causation. His book Callous Disregard comes out in May 2010.

=====
In accordance with Title 17 U.S.C. Section 107, this material is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.

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