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

Parental Age and Autism Spectrum Disorders

2012-01-27T09:32:00.000-08:00

Parental Age and Autism Spectrum Disorders

The new guideline to doctors comes amid growing concerns about the number of women delaying childbearing.

2012-01-17T09:51:00.000-08:00

The new guideline to doctors comes amid growing concerns about the number of women delaying childbearing. In Canada, 11 per cent of first births now occur in women aged 35 and older, up from five per cent in 1987.

Photograph by: Thinkstock, canada.com

Men, and not just women, need to be aware of the "reproductive consequences" of postponing parenthood, new national guidelines on the risks of delayed child-bearing warn.

Though women especially should recognize that their "fecundity and fertility" starts to decline precipitously after 32, a man's semen quality and fertility also worsens with age, according to guidelines endorsed by the Society of Obstetricians and Gynaecologists of Canada.

In addition, babies born to fathers of "advanced paternal age" — defined as 40 and older at the time of conception — are at increased risk of genetic disorders, as well as schizophrenia, autism and some forms of cancer, according to the authors.

The new guideline to doctors comes amid growing concerns about the number of women delaying childbearing. In Canada, 11 per cent of first births now occur in women aged 35 and older, up from five per cent in 1987.

If the trend holds, society can expect to spend more on intensive care, special care nurseries and community services for children born to older parents who may have developmental, hearing, speech or language problems, the authors say.

Read more: http://www.canada.com/health/Postponing+parenthood+could+have+serious+consequences+warns+study/6007363/story.html#ixzz1jjrwcZMI

Mol Autism. 2010 Feb 22;1(1):2. Paternal age increases the risk for autism in an Iranian population sample.

2012-01-13T09:55:00.001-08:00

Mol Autism. 2010 Feb 22;1(1):2.
Paternal age increases the risk for autism in an Iranian population sample.
Sasanfar R, Haddad SA, Tolouei A, Ghadami M, Yu D, Santangelo SL.
SourceDepartment of Psychiatry, Harvard Medical School, Boston, MA, USA. ssantangelo@pngu.mgh.harvard.edu.

Abstract
BACKGROUND: Autism is a neurodevelopmental disorder which is known to have a strong genetic component and is most likely oligogenic. However, the necessary role of environmental factors has been well documented. Prior research suggests that parental characteristics, such as age and level of education, may be associated with a risk of autism. Parental age has been shown to be associated with many disorders, such as schizophrenia, childhood cancer and fetal death. However, results from studies of parental age and autism are inconsistent.

METHODS: In the present study, we investigated the association of autism with parental age in 179 autism cases and 1611 matched cohort children from Iran. Each case was matched with nine cohort controls on parental education, sex, order of birth, consanguineous marriage, urbanism and province of residence. The Cox regression model was used to carry out conditional logistic regression on the matched data.

RESULTS: There was a significant association between higher paternal age, but not maternal age, and an increasing risk of autism. An analysis of the combined effect of parental age and education also revealed that parents with higher education had an increased risk of having autistic children, with a dose-response effect of parental age.

CONCLUSIONS: This study, which is the first epidemiological study of autism in Iran, provides evidence of the association of paternal age and risk of autism.

PMID: 20678245 [PubMed] PMCID: PMC2907564Free PMC Article

Maternal and Paternal Age are Jointly Associated with Childhood Autism in Jamaica.

2012-01-13T09:53:00.001-08:00

Autism Dev Disord. 2012 Jan 10. [Epub ahead of print]
Maternal and Paternal Age are Jointly Associated with Childhood Autism in Jamaica.
Rahbar MH, Samms-Vaughan M, Loveland KA, Pearson DA, Bressler J, Chen Z, Ardjomand-Hessabi M, Shakespeare-Pellington S, Grove ML, Beecher C, Bloom K, Boerwinkle E.
SourceDivision of Epidemiology, Human Genetics, and Environmental Sciences (EHGES), School of Public Health, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, 77030, USA, Mohammad.H.Rahbar@uth.tmc.edu.

Abstract
Several studies have reported maternal and paternal age as risk factors for having a child with Autism Spectrum Disorder (ASD), yet the results remain inconsistent. We used data for 68 age- and sex-matched case-control pairs collected from Jamaica. Using Multivariate General Linear Models (MGLM) and controlling for parity, gestational age, and parental education, we found a significant (p < 0.0001) joint effect of parental ages on having children with ASD indicating an adjusted mean paternal age difference between cases and controls of [5.9 years; 95% CI (2.6, 9.1)] and a difference for maternal age of [6.5 years; 95% CI (4.0, 8.9)]. To avoid multicollinearity in logistic regression, we recommend joint modeling of parental ages as a vector of outcome variables using MGLM.

PMID: 22230961 [PubMed - as supplied by publisher]

Autism. 2011 Dec 16. [Epub ahead of print]

2011-12-20T08:36:00.001-08:00

Autism. 2011 Dec 16. [Epub ahead of print]

Advancing paternal age and simplex autism.

Puleo CM, Schmeidler J, Reichenberg A, Kolevzon A, Soorya LV, Buxbaum JD, Silverman JM.

Source

Temple University, Philadelphia, PA, USA.

Abstract

De novo events appear more common in female and simplex autism spectrum disorder (ASD) cases and may underlie greater ASD risk in older fathers' offspring. This study examined whether advancing paternal age predicts an increase in simplex (n = 90) versus multiplex ASD cases (n = 587) in 677 participants (340 families). Whether or not controlling for maternal age, results support a significant interaction of linear paternal age and sex of the child on simplex family type. Female ASD cases were significantly more likely to be simplex as paternal age increased, but the increase for males was not significant. Findings suggest that ASD arising from non-familial, de novo events may be far less prominent in males than in females, even if more prevalent in males, due to the substantially larger number of male cases attributable to other, more strongly male-biased risk factors.

Pre-, peri-, and neonatal risk factors for autism.

2011-11-17T08:29:00.001-08:00

Acta Obstet Gynecol Scand. 2011 Nov 15. doi: 10.1111/j.1600-0412.2011.01325.x. [Epub ahead of print]
Pre-, peri-, and neonatal risk factors for autism.
Guinchat V, Thorsen P, Laurent C, Cans C, Bodeau N, Cohen D.
SourceDepartment of child and adolescent psychiatry. Pitié-Salpêtrière Universitary Hospital, Paris, France Department of Obstetrics and Gynecology, Lillebaelt Hospital, Kolding, Denmark, Biotechnology and Biotherapy Unit, Research Centre-Brain and spinal cord Institute, Pierre and Marie Curie University /INSERM UMR_S 975/C.N.R.S. UMR 7225, Pitié-Salpêtrière Hospital, Paris, France, and Register for Disabled Children and the Isère county Perinatal Survey, Grenoble, France.

Abstract
Objective. To identify pre-, peri-, and neonatal risk factors for Pervasive Developmental disorders (PDD). Methods. We searched the Medline database through March 2011 for relevant case control and population based studies on pre-, peri-, and neonatal hazards related to Pervasive Developmental Disorders (PDD) including autism. We identified 85 studies for this review. Data were extracted systematically and organised according to risk factors related to family history, pregnancy, gestational age, delivery, birth milestones and the neonate's condition at birth. Results. During the prenatal period, risk factors for PDD were advanced maternal or paternal ages, being firstborn vs. third or later, maternal prenatal medication use, and mother's status as foreign born. During the perinatal and neonatal periods, the risk factors for PDD were preterm birth, breech presentation, planned cesarean section, low Apgar scores, hyperbilirubinemia, birth defect, and a birthweight small-for-gestational age. The influence of maternal preeclampsia, diabetes, vomiting, infections, and stress during pregnancy need to be studied more are insufficiently studied, to state. Discussion. Despite evidence for the association of some pre-, peri-, and neonatal risk factors associated with PDD, it remains unclear whether these risks are causal or play a secondary role in shaping clinical expression in individuals with genetic vulnerability. A plausible hypothsesis is that improvements in obstetrical and neonatal management have led to an increased rate of survivors with pre-existing brain damage. Given the variety of risk factors, we propose that future studies should investigate combinations of multiple factors, rather than focusing on a single factor.

© 2011 The Authors AOGS© 2011 Nordic Federation of Societies of Obstetrics and Gynecology.

The CDC Has Known All Along How Dangerous Vaccines Are - And Has Covered It Up...

2011-10-05T09:20:00.000-07:00

The CDC Has Known All Along How Dangerous Vaccines Are - And Has Covered It Up... (Part One)

Opinion by Consumer Advocate Tim Bolen

Tuesday, October 4th, 2011

De novo copy number variants associated with intellectual disability have a paternal origin and age bias.

2011-10-05T08:48:00.000-07:00

http://www.ncbi.nlm.nih.gov/pubmed/21969336

De novo copy number variants associated with intellectual disability have a paternal origin and age bias.
Hehir-Kwa JY, Rodríguez-Santiago B, Vissers LE, de Leeuw N, Pfundt R, Buitelaar JK, Pérez-Jurado LA, Veltman JA.
Source1Department of Human Genetics, Nijmegen Centre for Molecular Life Sciences and Institute for Genetic and Metabolic Disorders, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Abstract
BackgroundDe novo mutations and structural rearrangements are a common cause of intellectual disability (ID) and other disorders with reduced or null reproductive fitness. Insight into the genomic and environmental factors predisposing to the generation of these de novo events is therefore of significant clinical importance.MethodsThis study used information from single nucleotide polymorphism microarrays to determine the parent-of-origin of 118 rare de novo copy number variations (CNVs) detected in a cohort of 3443 patients with ID.ResultsThe large majority of these CNVs (76%, p=1.14×10(-8)) originated on the paternal allele. This paternal bias was independent of CNV length and CNV type. Interestingly, the paternal bias was less pronounced for CNVs flanked by segmental duplications (64%), suggesting that molecular mechanisms involved in the formation of rare de novo CNVs may be dependent on the parent-of-origin. In addition, a significantly increased paternal age was only observed for those CNVs which were not flanked by segmental duplications (p=0.02).ConclusionThis indicates that rare de novo CNVs are increasingly being generated with advanced paternal age by replication based mechanisms during spermatogenesis.

PMID:21969336[PubMed - as supplied by publisher]

The prevalence of spontaneous mutations increases with age in the male germline; consequently, older men have an increased risk of siring children with genetic disease due to de novo mutations.

2011-09-16T13:20:00.000-07:00

Mol Reprod Dev. 2011 Aug 5. doi: 10.1002/mrd.21374. [Epub ahead of print]
Age-related instability in spermatogenic cell nuclear and mitochondrial DNA obtained from Apex1 heterozygous mice.
Vogel KS, Perez M, Momand JR, Acevedo-Torres K, Hildreth K, Garcia RA, Torres-Ramos CA, Ayala-Torres S, Prihoda TJ, McMahan CA, Walter CA.
SourceDepartment of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas.

Abstract
The prevalence of spontaneous mutations increases with age in the male germline; consequently, older men have an increased risk of siring children with genetic disease due to de novo mutations. The lacI transgenic mouse can be used to study paternal age effects, and in this system, the prevalence of de novo mutations increases in the male germline at old ages. Mutagenesis is linked with DNA repair capacity, and base excision repair (BER), which can ameliorate spontaneous DNA damage, decreases in nuclear extracts of spermatogenic cells from old mice. Mice heterozygous for a null allele of the Apex1 gene, which encodes apurinic/apyrimidinic endonuclease I (APEN), an essential BER enzyme, display an accelerated increase in spontaneous germline mutagenesis early in life. Here, the consequences of lifelong reduction of APEN on genetic instability in the male germline were examined, for the first time, at middle and old ages. Mutant frequency increased earlier in spermatogenic cells from Apex1(+/-) mice (by 6 months of age). Nuclear DNA damage increased with age in the spermatogenic lineage for both wild-type and Apex1(+/-) mice. By old age, mutant frequencies were similar for wild-type and APEN-deficient mice. Mitochondrial genome repair also depends on APEN, and novel analysis of mitochondrial DNA (mtDNA) damage revealed an increase in the Apex1(+/-) spermatogenic cells by middle age. Thus, Apex1 heterozygosity results in accelerated damage to mtDNA and spontaneous mutagenesis, consistent with an essential role for APEN in maintaining nuclear and mtDNA integrity in spermatogenic cells throughout life. Mol. Reprod. Dev. Published 2011. This article is a U.S. Government work and is in the public domain in the USA.

Published 2011 Wiley-Liss, Inc. This article is a U.S. Government work and is in the public domain in the USA.

Father Time: Children with Older Dads at Greater Risk for Mental Illness

2011-08-29T21:35:00.001-07:00

Father Time: Children with Older Dads at Greater Risk for Mental Illness

Blaylock on autism and vaccines

2011-08-26T12:32:00.001-07:00

The present trend of increasing paternal age is accompanied by concerns for the development of complex multi-gene diseases, e.g. autism and schizophrenia,

2011-08-26T09:16:00.001-07:00

Biol Reprod. 2011 Aug 24. [Epub ahead of print]
Aging Results in Differential Regulation of DNA Repair Pathways in Pachytene Spermatocytes in the Brown Norway Rat.
Paul C, Nagano M, Robaire B.
Abstract
The present trend of increasing paternal age is accompanied by concerns for the development of complex multi-gene diseases, e.g. autism and schizophrenia, in progeny. Recent studies have established strong correlations between male age, increased oxidative stress, decreased sperm quality and structural aberrations of chromatin and DNA in spermatozoa. We tested the hypothesis that increasing age would result in altered gene expression relating to oxidative stress and DNA damage/repair in germ cells. To test this hypothesis, pachytene spermatocytes and round spermatids were isolated from Brown Norway (BN) rats at 4 (young) and 18 (aged) months of age. Microarray analysis was used to compare gene expression between the groups. The probe sets with significantly altered expression were linked to DNA damage/repair and oxidative stress in pachytene spermatocytes but not in round spermatids. Further analysis of pachytene spermatocytes demonstrated that genes involved in the base excision repair (BER) and nucleotide excision repair (NER) pathways were specifically altered. Quantitative RT-PCR confirmed that NER genes were upregulated (>1.5 fold) whereas BER genes were downregulated (>1.5 fold). At the protein level the members of the BER pathway were also altered by up to 2.3 fold; levels of NER proteins remained unchanged. Furthermore there was an increase in 8-oxo-2'-deoxyguanosine (8-oxodG) immunoreactivity in testes from aged males and in the number of spermatozoa positive for 8-oxodG. In conclusion, aging is associated with differential regulation of DNA repair pathways with a decrease in the BER pathway leading to deficient repair of 8-oxo-dG lesions in germ cells and spermatozoa.

GMO-DNA vaccines And Cytokine Storms

2011-06-22T21:20:00.000-07:00

GMO-DNA Vaccines And Cytokine Storms

By Richard Brown

A Positive Association found between Autism Prevalence and Childhood Vaccination uptake across the U.S. Population

2011-05-29T20:35:00.000-07:00

A Positive Association found between Autism Prevalence and Childhood Vaccination uptake across the U.S. Population
Journal of Toxicology and Environmental Health, Part A: Current Issues
Volume 74, Issue 14, 2011, Pages 903 - 916
Author: Gayle DeLonga
DOI: 10.1080/15287394.2011.573736
Peer Review Integrity
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Abstract
The reason for the rapid rise of autism in the United States that began in the 1990s is a mystery. Although individuals probably have a genetic predisposition to develop autism, researchers suspect that one or more environmental triggers are also needed. One of those triggers might be the battery of vaccinations that young children receive. Using regression analysis and controlling for family income and ethnicity, the relationship between the proportion of children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined. A positive and statistically significant relationship was found: The higher the proportion of children receiving recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.

Bribing Students to Take Vaccines

2011-05-10T21:12:00.001-07:00

83 Cases of Autism Associated with Childhood Vaccine Injury Compensated in Federal Vaccine Court

2011-05-10T17:43:00.000-07:00

83 Cases of Autism Associated with Childhood Vaccine Injury Compensated in Federal Vaccine Court

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Government program has been quietly paying awards to vaccine-injured children with autism for two decades but continues to deny vaccine-autism link. SafeMinds calls for immediate Congressional investigations.

WASHINGTON, May 10, 2011 /PRNewswire-USNewswire/ -- The following is being released by SafeMinds (www.SafeMinds.org):

For over 20 years, the federal government has publicly denied a vaccine-autism link, while at the same time its Vaccine Injury Compensation Program (VICP) has been awarding damages for vaccine injury to children with brain damage, seizures and autism. A new investigation, based on verifiable government data, breaks ground in the controversial vaccine-autism debate. The investigation found that a substantial number of children compensated for vaccine injury also have autism and that such cases have existed since 1989, the year after the VICP was formed.

SafeMinds' Executive Director, Lyn Redwood, RN, MSN comments, "This study dramatically shifts the debate on autism and vaccines. The question is no longer, Can vaccines cause autism? The answer is clear. Now, we have to ask, How many cases of autism have vaccines caused and how do we prevent new injuries from occurring?" The government has asserted that it "does not track" autism among the vaccine-injured. SafeMinds responds that not looking is the easiest way not to find something. SafeMinds is calling for immediate federal research into the mechanisms of injury in these children in an effort to protect other children from harm and Congressional action to reform the VICP.

The peer-reviewed study looked at cases of vaccine injury that have been monetarily compensated by the federal Vaccine Injury Compensation Program. It was published today in the Pace Environmental Law Review. The study investigated approximately 1300 cases of childhood brain injury as a result of vaccines in which the Special Masters ruled for the plaintiffs, looking for references to autism, symptoms of autism or disorders commonly associated with autism. It reports that twenty-one cases actually stated "autism or autism-like symptoms" in the court records. The researchers then identified and contacted 150 more compensated families to find out whether the children had autism. They were able to find an additional 62 cases (greater than 40% of their sample) for a total of 83 cases of autism. In 39 cases (47%) there was confirmation of autism beyond parental report.

The federal government has called autism a "national health emergency," conservatively affecting 1 in 110 children and costing the country billions of dollars each year. If a portion of autism cases are vaccine-induced and there is evidence that officials have been "looking the other way," this cannot be tolerated. The VICP's recent attempt to dismiss the over 5000 cases in the Omnibus Autism Proceedings is suspect in light of these new findings based on its own records.

SafeMinds calls on Congress to fully investigate the VICP, the only forum in which parents may bring claims of vaccine injury on behalf of their children.

SOURCE SafeMinds

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http://www.SafeMinds.org

[Recent progress of epidemiological research in search of the aetiology of autism].

2011-03-18T11:52:00.001-07:00

Nihon Shinkei Seishin Yakurigaku Zasshi. 2011 Feb;31(1):29-34.

[Recent progress of epidemiological research in search of the aetiology of autism].
[Article in Japanese]

Tsuchiya KJ, Matsumoto K, Takei N.

Research Center for Child Mental Development, Hamamatsu University School of Medicine, Handayama 1-20-1 Higashiku, Hamamatsu, 431-3192 Japan. tsuchiya@hama-med.ac.jp

Abstract
Autism and autism spectrum disorders (ASDs) are neurodevelopmental disorders characterised by the behavioral traits of impaired social cognition and communication, and repetitive and/or obsessive behaviour and interests. Studies point towards increased prevalence of autism/ASD. However, no treatment or prevention for the disorder has been established, since the aetiological pathway of this disorder remains largely unknown. Considering this lack of knowledge, epidemiological studies are expected to give clues for a better understanding of the disorder. As such, advanced paternal age at birth and low birthweight (or intrauterine growth retardation) have been reported to be candidate risk factors. These findings allow us to propose novel research strategies in search of the aetiology of autism/ASD. Following this trend, the authors initiated a research project, "the Hamamatsu Birth Cohort for Mothers and Children (HBC)", seeking risk factors for autism/ASD extensively. The HBC is expected to enroll 1,200 dyads of mother and child and to follow them until the child becomes 4 years of age.

PLoS One. 2011 Feb 17;6(2):e16715.

2011-03-08T08:40:00.000-08:00

PLoS One. 2011 Feb 17;6(2):e16715.

Autism and increased paternal age related changes in global levels of gene expression regulation.
Alter MD, Kharkar R, Ramsey KE, Craig DW, Melmed RD, Grebe TA, Bay RC, Ober-Reynolds S, Kirwan J, Jones JJ, Turner JB, Hen R, Stephan DA.

Center for Neurobiology and Behavior, Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.

Abstract
A causal role of mutations in multiple general transcription factors in neurodevelopmental disorders including autism suggested that alterations in global levels of gene expression regulation might also relate to disease risk in sporadic cases of autism. This premise can be tested by evaluating for changes in the overall distribution of gene expression levels. For instance, in mice, variability in hippocampal-dependent behaviors was associated with variability in the pattern of the overall distribution of gene expression levels, as assessed by variance in the distribution of gene expression levels in the hippocampus. We hypothesized that a similar change in variance might be found in children with autism. Gene expression microarrays covering greater than 47,000 unique RNA transcripts were done on RNA from peripheral blood lymphocytes (PBL) of children with autism (n = 82) and controls (n = 64). Variance in the distribution of gene expression levels from each microarray was compared between groups of children. Also tested was whether a risk factor for autism, increased paternal age, was associated with variance. A decrease in the variance in the distribution of gene expression levels in PBL was associated with the diagnosis of autism and a risk factor for autism, increased paternal age. Traditional approaches to microarray analysis of gene expression suggested a possible mechanism for decreased variance in gene expression. Gene expression pathways involved in transcriptional regulation were down-regulated in the blood of children with autism and children of older fathers. Thus, results from global and gene specific approaches to studying microarray data were complimentary and supported the hypothesis that alterations at the global level of gene expression regulation are related to autism and increased paternal age. Global regulation of transcription, thus, represents a possible point of convergence for multiple etiologies of autism and other neurodevelopmental disorders.

PMID: 21379579 [PubMed - in process]

Dr Andrew Wakefield answers critics in video interview, says BMJ has been hijacked by false journalism

2011-02-04T14:10:00.000-08:00

Dr Andrew Wakefield answers critics in video interview, says BMJ has been hijacked by false journalism
Friday, February 04, 2011
by Mike Adams, the Health Ranger
Editor of NaturalNews.com (See all articles...)

(NaturalNews) In a video interview with NaturalNews, Dr Andrew Wakefield, the doctor accused by the British Medical Journal of falsifying the data in a study questioning the safety of MMR vaccines, asserts that the BMJ has been "hijacked" by a politically-motivated journalist making utterly false allegations.

Dr Wakefield has been grilled in the mainstream media in a series of interviews which largely consist of uninformed journalists like Anderson Cooper and George Stephanopoulos hurling rapid-fire accusations without giving Dr Wakefield an opportunity to answer any of them. The mainstream media interviews have taken on the resemblance of theatrical productions rather than serious journalism.

In an effort to give Dr Wakefield a fair opportunity to answer his critics, we invited him for an interview on NaturalNews. He graciously accepted, and we filmed a series of three conversations which will be aired here on NaturalNews via our popular video website www.NaturalNews.TV

The first of these three is available right now at:
http://naturalnews.tv/v.asp?v=60825...

"An investigation will be forced upon them."
In this video interview, Dr Wakefield says that BMJ is factually incorrect in accusing Wakefield of falsifying the study data in his 1998 paper published in The Lancet.

"[The data] were faithfully reproduced in the Lancet paper, and they were made in the most scrupulous, meticulous way. Those are the facts. Brian Deer knew those facts. When he made his allegations to the BMJ, he knew those facts. Did he disclose them to the BMJ? More importantly, did the BMJ, as a peer reviewed scientific journal, did they check the facts? Because the facts were fully available to them in the book Callous Disregard."

Dr Wakefield also explains how this desperate move by the BMJ to attack Dr Wakefield has eroded the credibility of the publication:

"They have been hijacked by a freelance journalist who is not expert in any of these fields. They have handed over their journal to this man and allowed him to publish knowingly false allegations, and they have gone along with it. In my opinion, they [the BMJ] have blown their scientific credibility. In their desperation... their fundamental belief that vaccines must be safe, [they say] please don't tell me this terrible disease has been caused by the physician, don't tell me that. Tell me anything but that, and we will take any information, even information from Brian Deer, that will convince us it's safe, and we will publish that, because that conforms with our belief system. That makes us feel more comfortable. That makes us feel that we, as a profession, are not culpable in this extraordinary disorder."

In this interview, Dr Wakefield also discusses the motivation for the BMJ to grasp at any effort to discredit those who question the safety of vaccines:

"They are so keen to prove me wrong, to prove the parents wrong, and to exonerate the medical profession, their political friends, their pharmaceutical friends, whoever it is, that they have gone ahead in this reckless way and done this. And now, based upon the clear, unambiguous, historical factual records, then I can come out and talk to you like this and say this without any fear of retribution from the BMJ because they've got themselves into this mess. The facts are the facts."

He goes on to say about the BMJ, "An investigation will be forced upon them."

Why the mainstream media won't conduct an honest, intelligent interview with Dr Wakefield
What struck me in this experience of interviewing Dr Wakefield is that this man has deeply-held compassion for the lives of children, and he combines that with rare courage and a commitment to real scientific thinking that dares to ask unpopular questions in the search for the truth.

A true scientist is one who pursues the evidence without regard to the political climate. Facts are stubborn things, as John Adams famously said, and Dr Wakefield has been accused of falsifying them simply because the facts he discovered were not to the liking of those who run today's medical monopoly.

I see in Dr Wakefield the kind of thinker who has historically played a key role in scientific revolutions, when one era of outmoded "scientific thinking" was replaced with a new era of deeper human understanding.

Dr Wakefield was also very polite, thoughtful and kind in our interactions. Experiencing this myself, I find it astonishing that people like Anderson Cooper never had the journalistic honesty to give Dr Wakefield an opportunity to tell his story in a fair interview. Then again, we all probably know why the mainstream media isn't interested in the actual scientific facts here: All the major media outlets are funded in large part by the pharmaceutical interests!

Dr Wakefield speaks on this issue, saying:

"Will the mainstream media now take this real story, the real facts, and actually do their job as journalists and report the facts? Will they report the truth? I doubt it. Why? Because they're owned. Their salaries are paid, albeit indirectly, in large part by pharmaceutical revenues. And the first thing that will happen when they try and do a story which deconstructs these arguments, the BMJ's arguments, and actually reconstructs them in light of the truth, [is that] there will be a call from their advertisers, saying [no]. So what will the mainstream media do? Will it live up to its job, its duty to the people to report the truth, or will it show complete disinterest? Anderson Cooper has been presented with the same nine questions. What was your story based upon? Show us the facts. Did you do your homework? Now are you going to pay similar attention to these documented historical facts? We shall see."

Watch the full interview yourself at:
http://naturalnews.tv/v.asp?v=60825...

Remember, this is only the first in a series of three interviews with Dr Andrew Wakefield. We intend to publish the other two interviews next week here on NaturalNews. There is much more to this story than is being dumbed down in the conventional press -- this story may ultimately turn out to reveal the BMJ engaging in the most colossal mistake in the history of peer-reviewed "science" publications. The editors of BMJ must be sitting in a room right now, reviewing the facts of the case, with their jaws dropping to the floor as they realize they've been had by Brian Deer. There were duped -- exploited by an individual with a political agenda -- to engage in the printing of outright falsehoods in the name of the British Medical Journal.

As you will see in these three interviews, the BMJ has given us a milestone in the history of the end of the dark chapter of chemical-based medicine: This "scientific" publication has revealed, for the whole world to see, that the Emperor of Vaccines wears no clothes, and that those who defend the Emperor will stoop to any level to defend their fictions, even at the cost of revealing their own lack of scientific credibility.

To debate with the conclusions of a physician is one thing; to outright destroy the career and reputation of a man engaged in what can only be called "unpopular" but important scientific investigation is the action of a dogmatic, unscientific institution which can tolerate no real questions at all.

That's not science. It's dogma. And in its desperation to vilify Wakefield, the BMJ has proven to the whole world, once and for all, that the vaccine industry is so afraid of the weakness of its position that it must resort to publishing false accusations in the name of science in order to try to fend off real scientific skepticism.

In seeking to destroy Dr Wakefield, in other words, the British Medical Journal, we will shortly observe, has only succeeded in destroying its own credibility. This story continues in the weeks and months ahead...

Watch this video interview now at:
http://naturalnews.tv/v.asp?v=60825...

Learn more: http://www.naturalnews.com/031211_Andrew_Wakefield_BMJ.html#ixzz1D1xCk5Q8

Sherri Tenpenny, M.D. on Vaccines

2011-02-03T08:42:00.000-08:00

Vaccines Full Story

2011-02-02T08:52:00.000-08:00

http://naturalnews.tv/v.asp?v=BAE7F6323813CFAFB8338173FB11D429

Vaccines Full Story PDF

2011-02-01T08:11:00.000-08:00

http://www.naturalnews.com/SpecialReports/VaccinesFullStory/v1/VaccineReport-EN.pdf

Am J Epidemiol. 2009 Nov 1;170(9):1118-26. Epub 2009 Sep 25.

2011-01-26T10:59:00.001-08:00

Am J Epidemiol. 2009 Nov 1;170(9):1118-26. Epub 2009 Sep 25.

Risk of autism and increasing maternal and paternal age in a large north American population.
Grether JK, Anderson MC, Croen LA, Smith D, Windham GC.

Environmental Health Investigations Branch, California Department of Public Health, Richmond, California 94804, USA. judith.grether@cdph.ca.gov

Abstract
Previous studies are inconsistent regarding whether there are independent effects of maternal and paternal age on the risk of autism. Different biologic mechanisms are suggested by maternal and paternal age effects. The study population included all California singletons born in 1989-2002 (n = 7,550,026). Children with autism (n = 23,311) were identified through the California Department of Developmental Services and compared with the remainder of the study population, with parental ages and covariates obtained from birth certificates. Adjusted odds ratios and 95% confidence intervals were used to evaluate the risk of autism associated with increasing maternal and paternal age. In adjusted models that included age of the other parent and demographic covariates, a 10-year increase in maternal age was associated with a 38% increase in the odds ratio for autism (odds ratio = 1.38, 95% confidence interval: 1.32, 1.44), and a 10-year increase in paternal age was associated with a 22% increase (odds ratio = 1.22, 95% confidence interval: 1.18, 1.26). Maternal and paternal age effects were seen in subgroups defined by race/ethnicity and other covariates and were of greater magnitude among first-born compared with later-born children. Further studies are needed to help clarify the biologic mechanisms involved in the independent association of autism risk with increasing maternal and paternal age.

Blaylock: Big Pharma Vilified Researcher for Threatening Vaccine Program

2011-01-13T12:50:00.000-08:00

Blaylock: Big Pharma Vilified Researcher for Threatening Vaccine Program

Thursday, January 13, 2011 10:52 AM

By Russell L. Blaylock, M.D.

Read more: Blaylock: Big Pharma Vilified Researcher for Threatening Vaccine Program

Delayed fathering and risk of mental disorders in adult offspring.

2011-01-12T08:03:00.000-08:00

http://www.ncbi.nlm.nih.gov/pubmed/21220193

Early Hum Dev. 2011 Jan 8. [Epub ahead of print]

Delayed fathering and risk of mental disorders in adult offspring.
Krishnaswamy S, Subramaniam K, Ramachandran P, Indran T, Abdul Aziz J.

University of New England, Locked bag 4, NSW 2351, Australia.

Abstract
INTRODUCTION: Delayed parenting and child bearing at a very young age impose various risks to development of the offspring.

OBJECTIVE: This study aims to investigate the association between disparities in parental age and increased risk factor for common mental disorders in the progenies during adulthood.

METHODOLOGY: The Malaysian Mental Health Survey (MMHS) was analysed for this study. Respondents were asked to estimate the age of their parents at their birth. Presence of common mental disorders (CMD) was determined by referring to the diagnosis given by the Clinical Interview Schedule-Revised (CIS-R) instrument in the Programmed Questionnaire System (PROQSY) format. The association between parental age disparities and CMD was studied using logistic regression.

RESULT: Fifty three percent (n=1972) of the MMHS respondents (N=3666) knew the age of both parents and were included in the study. Three percent (n=53) had significant disparity in parental age, or a difference of 11years or more. Respondents born to parents with significant age disparity had a prevalence rate of 24% (95% CI=22.12-25.89) for CMD in comparison to 6% (95% CI=5.99-6.11) in their counterparts and 3.4 times higher risk for CMD, after adjusting for demographic factors, paternal age at birth and presence of family history of mental disorders. Amongst those born to older fathers aged 50 and above, the presence of disparity increased the rate for CMD to 42% (95% CI=39.82-44.18).

DISCUSSION: Disparity in parental age was significantly associated with increased risk for CMD. Various psychosocial factors contributing to age disparity in both the father and the mother could predispose to stress and mental health problems.

Copyright Â© 2010 Elsevier Ltd. All rights reserved.

keeping-anderson-cooper-honest-is-brian-deer-the-fraud

2011-01-10T13:43:00.000-08:00

http://www.ageofautism.com/2011/01/keeping-anderson-cooper-honest-is-brian-deer-the-fraud.html

January 06, 201 1CryShame Response to BMJ Report Andrew Wakefield

2011-01-06T18:25:00.000-08:00

January 06, 2011
CryShame Response to BMJ Report
From UK's CryShame:

PARENTS OF AUTISTIC CHILDREN SPEAK OUT AGAINST BMJ CLAIMS THAT WAKEFIELD 'S RESEARCH WAS FRAUDULENT HERE WE GO AGAIN.

Once again, the BMJ gives a platform for Brian Deer's investigation of the research behind Dr Andrew Wakefield at el's 1998 Lancet paper. This time the BMJ editors criticise all 13 co-authors for failing to check the data, warn all medical researchers and ethics committees to check carefully before they publish, and urge scrutiny of all Wakefield published papers (presumably all 100 plus papers). The BMJ allies itself with Deer's potentially defamatory attack on Wakefield.

Autism study doctor a 'victim of smear campaign' Andrew Wakefield

2011-01-06T09:58:00.000-08:00

Autism study doctor a 'victim of smear campaign'

Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies.

2010-12-01T10:55:00.000-08:00

Mol Psychiatry. 2010 Nov 30. [Epub ahead of print]

Advancing paternal age and risk of autism: new evidence from a population-based study and a meta-analysis of epidemiological studies.
Hultman CM, Sandin S, Levine SZ, Lichtenstein P, Reichenberg A.

Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Abstract
Advanced paternal age has been suggested as a risk factor for autism, but empirical evidence is mixed. This study examines whether the association between paternal age and autism in the offspring (1) persists controlling for documented autism risk factors, including family psychiatric history, perinatal conditions, infant characteristics and demographic variables; (2) may be explained by familial traits associated with the autism phenotype, or confounding by parity; and (3) is consistent across epidemiological studies. Multiple study methods were adopted. First, a Swedish 10-year birth cohort (N=1 075 588) was established. Linkage to the National Patient Register ascertained all autism cases (N=883). Second, 660 families identified within the birth cohort had siblings discordant for autism. Finally, meta-analysis included population-based epidemiological studies. In the birth cohort, autism risk increased monotonically with increasing paternal age. Offspring of men aged 50 years were 2.2 times (95% confidence interval: 1.26-3.88: P=0.006) more likely to have autism than offspring of men aged 29 years, after controlling for maternal age and documented risk factors for autism. Within-family analysis of discordant siblings showed that affected siblings had older paternal age, adjusting for maternal age and parity (P<0.0001). Meta-analysis demonstrated advancing paternal age association with increased risk of autism across studies. These findings provide the strongest evidence to date that advanced paternal age is a risk factor for autism in the offspring. Possible biological mechanisms include de novo aberration and mutations or epigenetic alterations associated with aging.Molecular Psychiatry advance online publication, 30 November 2010; doi:10.1038/mp.2010.121

Andrew Wakefield Speaks to Parliament on Autism

2010-11-19T09:23:00.000-08:00

Andrew Wakefield Speaks to Parliament on Autism

Autism Risk Rises With Paternal Age

2010-09-29T07:32:00.000-07:00

Autism Risk Rises With Paternal Age http://www.docstoc.com/docs/55700709/Older-paternal-age-tied-to-autism-in-offspring(ChildAdolescent-Psychiatry)

These results support the claim that increased paternal age is associated with a birth of a child with autism spectrum disorders

2010-09-15T08:02:00.000-07:00

Pediatr Neurol. 2010 Oct;43(4):300-302.

Paternal Age in Autism Spectrum Disorders and ADHD.
Gabis L, Raz R, Kesner-Baruch Y.

Weinberg Child Development Center, Safra Children's Hospital, Sheba Medical Center (affiliated with the Sackler School of Medicine, Tel-Aviv University, Israel), Tel Hashomer, Israel.

Abstract
Increased paternal age has been associated with an increased risk for autism spectrum disorders. The present study compared the paternal age distribution in autism spectrum disorders children with that of the general population and among children with attention deficit hyperactivity disorder. Study participants were drawn from the records of children diagnosed with one of these conditions in the years 1998-2006 at the Weinberg Child Development Center, Israel. Data regarding paternal age distribution in the general Israeli population were drawn from the yearly official publications of the Central Bureau of Statistics, Israel. Paternal age at the child's birth was found for autism spectrum disorders children (n = 268) and attention deficit hyperactivity disorders children (n = 320). Paternal age distribution of the attention deficit hyperactivity disorder children was similar to that of the general population in Israel, whereas autism spectrum disorders children were born to older fathers, compared with either the general population (P < 0.001) or children with attention deficit hyperactivity disorder (P = 0.04). These results support the claim that increased paternal age is associated with a birth of a child with autism spectrum disorders, but indicate that this finding cannot be generalized to attention deficit hyperactivity disorder.

Father's age increase miscarriage, malformation, risk of autism, schizophrenia, and bipolar troubles in children.

2010-09-04T08:07:00.000-07:00

J Gynecol Obstet Biol Reprod (Paris). 2010 Apr;39(1 Suppl):36-8.

[Influence of paternal age]
[Article in French]

Velez de la Calle JF, Broussin B, Lelaidier C, Fallet C.

Unité FIV, Clinique Pasteur, 34, Rue du Moulin à Poudre, Brest, France.

Abstract
Father's age increase miscarriage, malformation, risk of autism, schizophrenia, and bipolar troubles in children.

PMID: 20728806 [PubMed - in process]

Publication Types

Older paternal age strongly increases the morbidity for schizophrenia in sisters of affected females.

2010-08-19T08:13:00.000-07:00

Am J Med Genet B Neuropsychiatr Genet. 2010 Aug 17. [Epub ahead of print]

Older paternal age strongly increases the morbidity for schizophrenia in sisters of affected females.
Perrin M, Harlap S, Kleinhaus K, Lichtenberg P, Manor O, Draiman B, Fennig S, Malaspina D.

Department of Psychiatry, New York University School of Medicine, New York, New York.

Abstract
The effect of a family history of schizophrenia on the risk for this disorder in the offspring has rarely been examined in a prospective population cohort accounting for the sex of the proband and the first-degree relatives, and certainly not with respect to later paternal age. The influence of affected relatives on offspring risk of schizophrenia was estimated using Cox proportional hazards regression in models that accounted for sex, relation of affected first degree relatives and paternal age in the prospective population-based cohort of the Jerusalem Perinatal Schizophrenia Study. Of all first-degree relatives, an affected mother conferred the highest risk to male and female offspring among the cases with paternal age <35 years, however, female offspring of fathers >/=35 years with an affected sister had the highest risk (RR = 8.8; 95% CI = 3.9-19.8). The risk seen between sisters of older fathers was fourfold greater than the risk to sisters of affected females of younger fathers (RR = 2.2, 95% CI 0.7-6.7). The test for interaction was significant (P = 0.03). By contrast, the risk of schizophrenia to brothers of affected males was only doubled between older (RR = 3.3, 95% 1.6-6.6) and younger fathers (RR = 1.6, 95% CI 0.7-3.5). The most striking finding from this study was the very large increase in risk of schizophrenia to sisters of affected females born to older fathers. The authors speculate that the hypothesized paternally expressed genes on the X chromosome might play some role in these observations. (c) 2010 Wiley-Liss, Inc.

PMID: 20718003 [PubMed - as supplied by publisher]

Paternal age increases the risk for autism in an Iranian population sample.

2010-08-04T09:34:00.001-07:00

Mol Autism. 2010 Feb 22;1(1):2.

Paternal age increases the risk for autism in an Iranian population sample.
Sasanfar R, Haddad SA, Tolouei A, Ghadami M, Yu D, Santangelo SL.

Department of Psychiatry, Harvard Medical School, Boston, MA, USA. ssantangelo@pngu.mgh.harvard.edu.

Abstract
ABSTRACT: BACKGROUND: Autism is a neurodevelopmental disorder which is known to have a strong genetic component and is most likely oligogenic. However, the necessary role of environmental factors has been well documented. Prior research suggests that parental characteristics, such as age and level of education, may be associated with a risk of autism. Parental age has been shown to be associated with many disorders, such as schizophrenia, childhood cancer and fetal death. However, results from studies of parental age and autism are inconsistent. METHODS: In the present study, we investigated the association of autism with parental age in 179 autism cases and 1611 matched cohort children from Iran. Each case was matched with nine cohort controls on parental education, sex, order of birth, consanguineous marriage, urbanism and province of residence. The Cox regression model was used to carry out conditional logistic regression on the matched data. RESULTS: There was a significant association between higher paternal age, but not maternal age, and an increasing risk of autism. An analysis of the combined effect of parental age and education also revealed that parents with higher education had an increased risk of having autistic children, with a dose-response effect of parental age. CONCLUSIONS: This study, which is the first epidemiological study of autism in Iran, provides evidence of the association of paternal age and risk of autism.

PMID: 20678245 [PubMed - in process]

Mercury in Vaccines

2010-07-06T08:00:00.000-07:00

Doctors Reject Calls for Enforced Pre-school Immunisation

2010-07-03T09:36:00.000-07:00

July 02, 2010
Doctors Reject Calls for Enforced Pre-school Immunisation
GMC panel chairman calls for compulsory MMR

From: News.Scotsman.Com DOCTORS have rejected calls for UK children to be fully immunised before they are allowed to start school.

The British Medical Association conference in Brighton heard that cases of measles had increased since uptake of the measles mumps and rubella jab (MMR) had fallen.

But doctors decided forcing parents to have their children vaccinated before starting school was not ethical or practical.

Dr Surendra Kumar, from the BMA's GPs committee, said measles had almost been eradicated until the publication of research, now discredited, linking the MMR vaccine to autism. He added: "As a result we have now started seeing children suffering and dying from measles.

"Let us send a clear message, that in a country like the UK we will not let our children suffer and we will not let our children be a source of risk of infection to others... we should not allow them to start schooling before they have been immunised."

Other doctors expressed concern about passing the motion.

Dr Hamish Meldrum, chairman of the BMA, said: "I want to make clear that we support immunisation but we are not in support of this means of compulsion for a whole lot of practical and ethical reasons. If it were ever to happen here we would have numerous opt-outs and it would be highly problematic."

IVF Linked to Autism, Israeli Study Suggests

2010-07-02T07:56:00.000-07:00

Science News IVF Linked to Autism, Israeli Study Suggests
ScienceDaily (June 30, 2010) — The first "test tube baby" was born in 1978. With advances in reproductive science, an estimated one percent of all American babies are now born each year through in vitro fertilization (IVF). But IVF and other assisted fertility treatments may be solving one problem by creating another, suggests new evidence from Tel Aviv University.

In a recent study, Dr. Ditza Zachor of Tel Aviv University's Sackler School of Medicine reported a strong link between IVF and mild to moderate cases of autism. Her findings were presented last month at the International Meeting for Autism Research in Philadelphia.

According to her research at the Autism Center at the Assaf Harofeh Medical Center in Israel, which Dr. Zachor directs, 10.5% of 461 children diagnosed with a disorder on the autism spectrum were conceived using IVF, a significantly higher number than the 3.5% autism rate in the general Israeli population.

Other factors in play

While the study doesn't draw any definitive conclusions, it presents some urgent questions, says Dr. Zachor. "It's too early to make a serious deduction based on that evidence alone," she says, citing other birth-related factors in her study, such as low birth rate and prematurity. Dr. Zachor's ongoing research will attempt to separate out these risk factors to come up with more precise numbers for autism and other prenatal conditions in IVF.

The key may be "imprinting," a biochemical procedure during cell division which determines which genes will be selected or "expressed" in the embryo. Research into epigenetics -- changes in gene expression that occur without a change in the DNA sequence -- suggest that the malformations may be caused by imprinting abnormalities introduced into the embryo while it's in a test tube environment, says Dr. Zachor. One such disorder linked with IVF appears to be Angelman syndrome.

However, Dr. Zachor does not want to discourage infertile couples from undergoing IVF implantation, which most often results in a healthy child.

Age-appropriate fertility treatments

Dr. Zachor notes that mothers in her study who had IVF tended to be older -- with a median age of 32.6 years. Also significantly, nearly 4% of the children with autism were born prematurely, and about 5% of those had a low birth weight. In the general population, only about 1% of all newborns are delivered with a low birth weight.

Aware of these risks, however, health practitioners may be able to intervene and find ways to avoid the problems, the researcher says. For example, they might recommend that IVF treatments be delayed for a longer period, despite any psychological stress this might cause to would-be parents. Some researchers believe that unassisted fertilization is a better way to avoid negative health effects.

"Many infertile couples choose this procedure, and they need to know whether there is a risk of autism," concludes Dr. Zachor. She stresses, however, that most women who undergo fertility treatments should not be scared away from IVF procedures: the majority of children born using IVF do not have autism, and most children who have autism were not conceived using IVF.

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Vaccines URGENT

2010-06-23T08:22:00.001-07:00

2010-06-20T14:15:00.001-07:00

"The only safe vaccine is one that is never used.----No vaccine can be proven safe before it is given to children."--- statements by the late James A. Shannon, while serving as Director of the US National Institutes of Health.

Men’s Biological Clock

2010-05-28T07:03:00.000-07:00

Naked Fatherhood
Parenting for Smart DadsCategory
Select Category Balanced Parenting The Recent Fathers’ Club (
Men’s Biological Clock
by justin on May 24, 2010

There were rumours a while back that Hugh Hefner, the octogenarian founder of the Playboy empire was planning to father a child with Holly Madison (53 years his junior), the alpha female of his three live-in girlfriends. Of course that was before the jam hit the fan and all three moved out of the mansion.

But, apropos the baby – why not? Charlie Chaplin and Picasso both fathered children well into their 70s, with no ill-effects. There are even anecdotal reports in the medical press of men in their 90s becoming fathers. Everyone knows that we men can just carry on having children until very late in life, (although it’s possible that having kids just makes you feel 100 hundred years old).

Photo by: judepics
But is it all true? It seems that medical evidence is mounting that men are not immune from the ticking of the biological clock (although we often battle to hear it quite as loudly as our partners).

The first part of the problem lies with the decline in fertility of men as they age. Testosterone levels fall over time which not only makes it harder for men to hold their tummies in at the beach, but also affects sexual performance. There is also a decline in sperm count and sperm quality which means that it takes men over 45 significantly longer to produce a pregnancy than men under 25 – up to 5 times longer according to some research.

Still, it was thought that even with a decline in fertility, any genetic issues with the pregnancy or resulting child lay with the mother. This was because while a woman is born with her full quota of eggs, men manufacture sperm continually without even having to think about it, so conception between an older couple might be the meeting of a forty-year-old egg with a three-month-old sperm (the time taken to manufacture mature spermatozoa).

However, it now seems that there’s also a deterioration in the quality of the genetic material that each sperm carries. This is first seen in an increase in the number of miscarriages – three times greater where fathers are older than 35 compared to those younger than 25. The incidence of pre-eclampsia also rises with increasing paternal age.

This deterioration of genetic material is thought to arise from a number of causes. The cells which divide to produce sperm cells replicate around 23 times per year starting from puberty, so by the time a man hits 50, those cells have divided about 800 times, increasing the risk of errors.

With age, the frequency of sporadic single-gene mutations also increases four to five times for a person over 45. On top of that, the enzymes that repair faulty DNA decrease in efficiency as one gets older.

All of which means an increase in a list of medical problems now totalling about 20.

A study of data from a huge Israeli health database showed that, for example, schizophrenia is twice as likely to occur in the children of men over forty as in those in their twenties. Men over fifty lead to a three-time increase in risk.

A further study on the same database showed that autism too is six times more frequent where fathers are over forty than those under 30.

An earlier study by Dr Harry Fisch (author of the book The Male Biological Clock) concluded that parents over 40 have a six-times higher risk of having a child affected by Down Syndrome than where both are under 35. And where a woman over forty has a child affected by Down Syndrome, the genetic blame is now thought to lie 50% with the father.

And the list goes on, with various studies linking advanced paternal age to disorders such as dwarfism, progeria (an extremely rare accelerated aging disease), skeletal disorders, congenital heart defects, certain types of cancer and even reduced scores in nonverbal IQ tests.

All of which helps explain why the cutoff age for sperm donors in The States is set at 40. So that’s another paying hobby limited to the youth – smacks of ageism, doesn’t it?

And yet more and more couples are leaving it later to have children for any number of reasons. Many want to feel like they’ve experienced something of a life and a career before the little tyrants arrive. Some prefer to wait until they’re in a more financially stable phase of their lives before committing. Maybe its just that there are more frogs to kiss nowadays in search of princes. Or even that the kiss-per-frog ratio has risen.

And really, what’s the downside? You may be more likely to spend time in casualty with a back problem from flinging your toddler around and there’s the danger of injuring yourself by tripping over your Zimmer frame when playing cricket with the young ‘uns.

Having kids later probably means that you’re going to have a bit less energy for them, but then again, that depends on how well you’ve looked after yourself in getting to where you are. Also, a decrease in the time available to spend with children can be offset to a certain degree by an increase in the quality of the time spent.

Many parents are finding that they’re having children later without even planning it that way – life often gets in the way of our plans. Then when one’s finally ready to make this life-altering commitment it takes a little while to get everything ready to even start trying (especially when you discover that the whole house has to be remodelled before you can even start).

And then it doesn’t just happen right away, and where there are miscarriages, recovery, both physical and emotional, takes time before you can start again.

All of which means an upswing in the number of parents who battle to remember where they left the children a few minutes before.

Then again, children of older parents should be more independent when they grow up, if only because they’re used to being able to easily outpace their pursuers.

From a selfish point of view, having kids later means that you’ll have someone around who is able to intuitively figure out how to use the new DVD player that has been standing unused because you can’t work out what the instruction manual is trying to tell you.

Also, you don’t resent the loss of your social life to the same degree as those that have their children while they are young (the parents, not the children) – you’re giving up a whole lot less when your idea of a good time is staying in with a good book and listening to Smooth Classics.

And when you’re lucky enough to have your mid-life crisis with small children you’re much less likely to embarrass yourself by running off and buying a convertible or any motorcycle that comes with tassles hanging from the handlebars.

The bottom line? Don’t leave it too late. While it is physiologically possible for a man to produce heirs at a very late stage of life, the risks do rise along the way.

And Hef? I think that at his age, he’s just perfected the art of saying ‘Yes Dear’ without really listening to what anyone is actually saying.

Share and Enjoy:

Tags: fathers, old dads, senior fathers

From: NY Alliance for Vaccination Choice nyvaccinechoiceAtgmail.com

2010-05-26T09:38:00.000-07:00

From: NY Alliance for Vaccination Choice

Dear All,

The NY Senate Health Committee just moved this bill along and we need to stop it in the Assembly and in the rest of the legislature. Please see below for details. Please ACT today, your call, email and visit COUNTS! ~Lisa, NYAVC

A bill to require meningitis vaccine for 7th graders and ALL college students is gaining momentum in Albany!

Bill S7156 passed the Senate Health Committee and is due for a floor vote.

Bill A10313 will be voted on the Assembly Health Committee any given Tuesday.

We have to FLOOD The Assembly & Senate with calls and e-mails. They must vote `no' on Bill S7156 and A10313

ASK FOR A CALL BACK

This bill is only steps away from LAW. We need to stop it. Our lawmakers will listen to these reasons:

* There is NO meningitis health `emergency'. Why the extreme measure?
* Less that .005% of the entire US contracts the disease yearly.
* Mandatory shots cost MILLION$$$. NY is $9.2B in debt. Financial pain is everywhere. We're increasing our burden?
* There is nothing stopping people from getting the shot right now.
* The vaccine does not address all strains.
* The vaccine can contain mercury-filled thimerosal

CALL THIS LIST of Assembly Health Committee Members

Find their e-mails at www.assembly.state.ny.us

ASSEMBLY HEALTH COMMITTEE

All phones numbers begin with 1-518-455- ####

Richard N. Gottfried, Chair, 4941
Jim Bacalles , 5791
Jonathan L. Bing , 4794
Kevin A. Cahill , 4436
Robert Castelli, 5397
James D. Conte , 5732
Steven Cymbrowitz , 5214
Jeffrey Dinowitz , 5965
Sandy Galef , 5348
Aileen M. Gunther , 5355
Andrew Hevesi , 4926
Rhoda Jacobs , 5385
Charles D. Lavine , 5456
William B. Magnarelli, 4826
Nettie Mayersohn , 4404
David G. McDonough , 4633
Joel M. Miller , 5725
Amy Paulin , 5585
Crystal D. Peoples , 5005
Jack Quinn , 4462
Naomi Rivera , 5844
Linda B. Rosenthal , 5802
Robin Schimminger , 4767
Lou Tobacco , 4495
Darryl C. Towns , 5821

AGE OF AUTISM

2010-05-26T06:46:00.001-07:00

May 26, 2010
Meet Dr. Andrew Wakefield at The American Rally for Personal Choice Today
From The American Rally for Personal Choice:

Join us TODAY in Chicago to show our support for vaccination choice and parental consent. Please join us live and meet Dr. Andrew Wakefield, or you can participate via satellite, or with balloons to represent all those who cannot attend but want to have their family counted.

Wednesday, May 26, 2010
3:00 - 5:00 pm
Grant Park, Downtown Chicago
Complete details here

Attend a Satellite Rally

Sign the petition in support of the Chicago Principles and Calls for Immediate Action.

Continue reading "Meet Dr. Andrew Wakefield at The American Rally for Personal Choice Today" »

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Autism Professor Needs Help

2010-05-26T06:43:00.000-07:00

5/26/10

Autism Professor Needs Help

Professor Gene Stubbs of the University of Oregon needs help with his study about vitamin D and autism. He is testing the theory that a mother with one child with autism will not have another if the mother takes vitamin D during her pregnancy. Women no longer need to come to the University of Oregon but can participate at a distance. Professor Stubbs writes:

"Can anyone assist us in recruiting mothers who already have children with autism and the mother is pregnant again before her third trimester? We are giving the mothers 5000 IU D3/day. So far every mother who has delivered has delivered within 1 week or on the date of expected delivery, and the babies are well within normal birth weights. They have not progressed far enough in age for us to screen for autism, but so far, the babies are interactive, have eye contact, are vocal etc..

However, we need more research families to participate. We have recruited other doctors to help us recruit and we have recruited doctors on the Vitamin D Council sites to help us recruit. We still need more families to participate to make our results significant. The families no longer have to come to our site to participate. If you know of any families who potentially might be eligible for our research, please give them my research assistant's phone number, 503-351-9255."

Thank you,

John Cannell, MD

The Vitamin D Council

1241 Johnson Ave., #134

San Luis Obispo, CA 93401

Geographic distribution of autism in California: a retrospective birth cohort analysis.

2010-05-25T07:43:00.001-07:00

Autism Res. 2010 Feb;3(1):19-29.

Geographic distribution of autism in California: a retrospective birth cohort analysis.
Van Meter KC, Christiansen LE, Delwiche LD, Azari R, Carpenter TE, Hertz-Picciotto I.

Department of Public Health Sciences, School of Medicine, and Medical Investigations of Neurodevelopmental Disorders Institute, University of California-Davis, One Shields Avenue, Davis, CA 95616, USA. vanmeter@pobox.com

Abstract
Prenatal environmental exposures are among the risk factors being explored for associations with autism. We applied a new procedure combining multiple scan cluster detection tests to identify geographically defined areas of increased autism incidence. This procedure can serve as a first hypothesis-generating step aimed at localized environmental exposures, but would not be useful for assessing widely distributed exposures, such as household products, nor for exposures from nonpoint sources, such as traffic. Geocoded mothers' residences on 2,453,717 California birth records, 1996-2000, were analyzed including 9,900 autism cases recorded in the California Department of Developmental Services (DDS) database through February 2006 which were matched to their corresponding birth records. We analyzed each of the 21 DDS Regional Center (RC) catchment areas separately because of the wide variation in diagnostic practices. Ten clusters of increased autism risk were identified in eight RC regions, and one Potential Cluster in each of two other RC regions.After determination of clusters, multiple mixed Poisson regression models were fit to assess differences in known demographic autism risk factors between the births within and outside areas of elevated autism incidence, independent of case status.Adjusted for other covariates, the majority of areas of autism clustering were characterized by high parental education, e.g. relative risks >4 for college-graduate vs. nonhigh-school graduate parents. This geographic association possibly occurs because RCs do not actively conduct case finding and parents with lower education are, for various reasons, less likely to successfully seek services.

2010-05-22T16:50:00.000-07:00

Dear All,

On Monday May 24th 2010 the GMC will convene to announce whether Andrew Wakefield is to be struck off. In light of the improprieties of the Legal Services Commission and GMC, it is hoped that the panel in Wakefield's case will be discharged pending a full inquiry.

We will gather to support Andrew Wakefield at 8:00am in 30 Rockefeller Center on Monday, May 24, 2010 in front of the NBC Studios on 49th St. Between 5th and 6th Ave. Andre w Wakefield will be interviewed by Matt Lauer and immediately following Andrew Wakefield will join our gathering outside the studio. Urgent attendance is requested and bring signs supporting Andrew Wakefield. PLEASE SEND TO ALL YOUR EMAIL LISTS!!

In 1998 Andrew Wakefield and 12 colleagues published a case series paper in the Lancet, describing bowel disease in twelve children diagnosed with autism spectrum disorders, a cautious article say the findings based on a study of 12 children did not prove for certain that there was an association between MMR-cited as the cause by the parent and the syndrome, but that further research should be carried out.

The significance of these finding has been overshadowed by a concerted systematic effort to discredit the work. This effort and an intense desire to subvert the inquiry into the issues of vaccine safety and legal redress for vaccine damage, has culminated in the longest running and most expensive fitness to pra ctice case ever to come before the GMC.

Thank you to all!!!

NY Alliance for Vaccination Choice (NYAVC)

Volume 47, Number 2, May 2010 Social Demographic Change and Autism

2010-05-14T11:49:00.000-07:00

Volume 47, Number 2, May 2010 Social Demographic Change and Autism
Journal Information

Volume 47, Number 2, May 2010
E-ISSN: 1533-7790 Print ISSN: 0070-3370

DOI: 10.1353/dem.0.0101

Social Demographic Change and Autism
Kayuet Liu
Noam Zerubavel
Peter Bearman

Demography, Volume 47, Number 2, May 2010, pp. 327-343 (Article)
DOI: 10.1353/dem.0.0101
HTML Version | PDF Version (616k)
Subject Headings:

■Autism -- Genetic aspects.
Abstract:

Parental age at child's birth—which has increased for U.S. children in the 1992-2000 birth cohorts—is strongly associated with an increased risk of autism. By turning a social demographic lens on the historical patterning of concordance among twin pairs, we identify a central mechanism for this association: de novo mutations, which are deletions, insertions, and duplications of DNA in the germ cells that are not present in the parents' DNA. Along the way, we show that a demographic eye on the rising prevalence of autism leads to three major discoveries. First, the estimated heritability of autism has been dramatically overstated. Second, heritability estimates can change over remarkably short periods of time because of increases in germ cell mutations. Third, social demographic change can yield genetic changes that, at the

Cancer vaccine programme suspended after 4 girls die

2010-05-10T14:50:00.000-07:00

Cancer vaccine programme suspended after 4 girls die
Vineeta Pandey / DNAThursday, April 8, 2010 0:39 IST Email

New Delhi: The Indian Council of Medical Research (ICMR) has told Andhra Pradesh and Gujarat to immediately suspend the cervical cancer control vaccination programme for girls. The programme is part of a two-year study to look into the utility of a vaccine in public health programmes and acceptability of Gardasil, the human papillomavirus (HPV) vaccine made by Merck. Gardasil, available in medical stores across the country, is marketed in India by MSD Pharmaceuticals Pvt Ltd.

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The programme was marred by controversy after four deaths and complications among 120 girls were reported after vaccination. The girls complained of stomach disorders, epilepsy, headaches and early menarche. Women activists fear the vaccine may impact the mental health of girls who have shown no signs of distress so far.

Health ministry sources said the vaccination programme is being conducted by Gardasil, jointly with PATH, a Seattle-based NGO, ICMR and the two state governments. About 32,000 girls, aged 10-14, were to be tested in the study.

ICMR chief Dr VM Katoch clarified ICMR was only a technical partner, with an advisory role, in the project. But Katoch said they were checking out who was at fault.

Questioning the study, CPM leader Brinda Karat said: “How has the government embarked on the study of giving three injections to the girls when it is also planning a massive multi-centric dose determination study to see if two doses will suffice?”

For a drug to be administered to children, Karat said, it has to go through stages of clinical trial, including phase 3 adult clinical trials. With Gardasil, only one trial has been carried out with a small sample of 110 girls, which has followed up with them for a month after completion of vaccination and that too only to look at the immune response post-vaccination, Karat said. The vaccine has also been approved for adult women aged 27, Karat said, without any trials on them.

Karat also alleged scientific logic and ethical guidelines have been violated at each step during drug and vaccine trials.

Australian Flu vaccination ban goes national after fever, convulsions in children

2010-05-10T07:38:00.000-07:00

Australian Flu vaccination ban goes national after fever, convulsions in children

submitted by Drew Kaplan on May 5, 2010 – 7:24 pm

In Australia Doctors are being advised to stop giving the flu vaccine to children.
Seasonal flu vaccinations across Australia for children under five have been suspended after 23 children in Western Australia were admitted to hospital with convulsions following their injections. One child, aged 1, remains in a coma in a Perth hospital. Commonwealth chief health officer Professor Jim Bishop yesterday announced the suspension while authorities urgently review data from around the country. WA’s chief public health officer Tarun Weeramanthri has defended the response time in closing down the state’s juvenile flu vaccine program amid revelations that children were presenting with convulsions more than two weeks ago.

Rogue batch may be to blame
National warning to GPs
Perth mum: ‘I was petrified’

WA free vaccine program suspended

More than 60 children around the state may have had adverse reactions to the vaccine, including fevers, vomiting and febrile convulsions – a type of fit brought on by a high fever.

One child remains in a critical condition in hospital after being given the vaccine. Dr Weeramanthri said he had few details on the child’s condition but they were “seriously ill”.

He said a national process set by the Therapeutic Goods Administration had been observed in responding to the reactions. Under the process the best clinical information was collected from as many doctors as possible and an assessment made on the “totality of that”.

“We take all reports very seriously and we believe we’ve acted in a very timely fashion,” Dr Weeramanthri said.

“We’ve been monitoring the situation, we’ve been talking to clinicians and we’ve acted as soon as we can.”

He said that since this year’s vaccine program started a month ago, 23 children under the age of 10 had presented to Princess Margaret Hospital with convulsions related to vaccinations they had received less than 12 hours before.

Another 40 convulsion cases had been detected in the past month in children at other metropolitan hospitals and in Bunbury. Doctors are now working to determine how many of those children received the flu vaccine.

Aside from the convulsions, affected children were suffering fever and vomiting within 12 hours of their flu shots.

A teleconference today with state, territory and TGA officials confirmed the picture in other states would not be available for “a few days”.

Dr Weeramanthri said the TGA was assessing the geographical spread of symptoms across Australia, and directly testing batches of vaccine for any impurity.

Rogue batch may be to blame

Health authorities are also working to determine if the entire Fluvax drug, or just batches, have caused the symptoms, and whether an alternative vaccine should be used.

University of Western Australia school of Paediatrics and Child Health Associate Professor Peter Richmond said that only Fluvax – produced by Australia’s biggest biopharmaceutical company CSL – was being used to vaccinate children in WA.

Dr Richmond said researchers were trying to determine whether it was the entire vaccine, or just batches, that had caused the problems which today prompted Australia’s chief medical officer to tell doctors to stop giving the vaccine to children.

He said the side effects had been largely limited to children under the age of five and he would not recommend that anybody in other groups – including elderly people – cancel their flu shots.

“This is not a long-term safety issue with vaccines,” Dr Richmond told WAtoday.com.au.

He recommended parents of young children who had received only the first of the required two vaccination doses hold off on the second dose for now.

This was despite the fact children who had no side effects from their first dose were unlikely to receive complications from their second.

Dr Richmond said the first dose provided partial protection against the flu anyway.

He said researchers were examining whether an alternative drug to Fluvax could be used for the second dose – generally scheduled for four weeks after the first.

Researchers were also trying to determine if the problem with Fluvax was temporary only – and whether the drug could still be used in coming weeks for the second dose.

He stressed that the vast majority of children receiving Fluvax had suffered no complications.

National warning to GPs

Commonwealth chief medical officer Jim Bishop issued a national warning to GPs not to use the vaccine followed a decision last night by the WA government to suspend the free vaccination program for children under five over concerns it was causing high fevers and convulsions.

“We suggest doctors and health professionals vaccinating children don’t use the seasonal flu vaccine for the moment, until we can get the Therapeutic Goods Administration (TGA) to investigate this in more detail,” Professor Bishop told ABC TV.

He said the concerns stemmed from a significant rise in the number of children developing a fever after receiving the vaccine.

“We need more information about what’s happened in WA, but also what we can now find out from all the other states from their experience,” Professor Bishop said.

“If this has been brought up as a possible side-effect of this drug, then we ought to at least suspend its use until we know more.”

In light of the seasonal flu shot suspension, Professor Bishop suggested children get vaccinated against swine flu instead, because that could be a health risk this winter too.

He said there did not appear to be any side effects from the swine flu vaccine Panvax.

“It is safe to have the swine flu vaccine,” Professor Bishop said.

“The TGA’s assessment of clinical trials and the advice of its expert committees is that Panvax is a safe, effective vaccine for prevention of the H1N1 influenza.

“It is expected that the dominant flu this winter season will be swine flu and the specific Panvax vaccine is available free for all Australians.”

‘I was petrified’

Perth mother of two Bea Flint said her 11-month-old boy Avery had a seizure after receiving the first dose of the two-dose flu vaccination on Saturday.

Mrs Flint said that after the 9am vaccination she noticed Avery had a minor temperature about 2pm. She treated him with Panadol and by Avery’s 7pm bedtime he seemed “OK”.

However, at 7.45pm, Avery started whimpering and moaning.

When Mrs Flint got to his cot the baby had vomited and was lying on his side having a seizure.

“In the car driving to the hospital he was just whimpering,” she said.

“He couldn’t cry – his head was hanging down in the car seat and he couldn’t move.

“I was petrified – it was one of the worst experiences of my life.”

By the time Avery arrived at St John of God Hospital in Murdoch, he was burning up with a fever of 39.5 degrees.

The doctor who treated Avery told Mrs Flint her baby was the fifth child with similar symptoms admitted to the hospital that day.

WA vaccine program suspended

Health Minister Kim Hames last night advised of the state-wide suspension as a precautionary measure.

He said the suspension came after a significant rise in the number of children who had developed a high temperature after receiving the vaccine.

He said some children had gone into febrile convulsions, a fit caused by a high fever, following the vaccinations.

Dr Hames said it was unclear if the fevers were related to the influenza vaccination but the precautionary measure was the most responsible course of action.

Fevers in most instances are treatable.

“People should give Paracetamol according to the instructions and tepid sponging to keep the temperature down.” Dr Hames said.

“On rare occasions children can have a convulsion as the result of the high temperature and sometimes that can be prolonged, which can be a risk to the child.”

He said parents should not take children under the age of five to be vaccinated against influenza until further notice

http://www.watoday.com.au/wa-news/flu-vaccination-ban-goes-national-after-fever-convulsions-in-children-20100423-tglp.html

Older Parents and Autism

2010-05-05T10:55:00.000-07:00

http://www.medscape.com/viewarticle/721007

From Medscape Pediatrics > Best Evidence Interviews in Pediatrics
Best Evidence Interview: Older Parents and Autism -- Questions on the Rise in Autism Continue
Expert Interview With Judith K. Grether, PhD
Carol Peckham

Posted: 05/04/2010

Information from Industry
Featuring New Content at the Pain Institute InfoSite Stay abreast of the latest topics in chronic pain assessment and management
Connect now The Best Evidence Study
Risk of Autism and Increasing Maternal and Paternal Age in a Large North American Population

Grether JK, Anderson MC, Croen LA, Smith D, Windham GC
Am J Epidemiol. 2009;170:1118-1126

This study was selected as the subject of this interview because of its high ranking in Medscape Best Evidence, which uses the McMaster Online Rating of Evidence System. Of a possible top score of 7, clinicians who used this system ranked this study as 5 for relevance and 7 for newsworthiness.

Abstract

About the Interviewee
Judith Grether, PhD, is Senior Epidemiologist in the Environmental Health Investigations Branch, California Department of Health Services. Dr. Grether is a perinatal epidemiologist who has had the opportunity over many years, within the California Department of Public Health, to conduct research studies on the prevalence of and risk factors for developmental disabilities, primarily cerebral palsy and autism spectrum disorders. She has recently retired and is now working to complete some analyses and manuscripts.

Medscape: Your study, "Risk of Autism and Increasing Maternal and Paternal Age in a Large North American Population," was highly ranked by pediatric clinicians. Could you just give a brief description of it and its significance?

Judith Grether, PhD: Our study was the largest that has yet been conducted -- and, I would guess, is probably the largest that will be conducted -- to specifically address the question of whether the risk for autism in offspring increases with the advancing age of the mother and/or the father. With our very large study, we were also able to obtain statistically precise estimates of how much of an increase in risk there is as parents get older. A number of prior studies have looked at the question of a parental age effect; to my knowledge, none have reported a decreasing risk as parents get older, but some have found an increased risk only for advancing maternal age and others only for advancing paternal age. A couple of studies have pretty dramatic estimates of the amount of that increased risk -- particularly one from Israel that found only father's age to be important. From a scientific perspective, to get clues to what may underlie any increase in risk for autism associated with older parents, it is important to answer the question: is it both age of the father and the mother, or is it only mothers or only fathers? There are some tricky statistical issues here and it is very helpful to have a large database like we had, in which the subjects are not self-selected for the study.

Medscape: Where did you get your data from?

Dr. Grether: We analyzed data from the California Department of Developmental Services (DDS), which is a statewide service system in California for people with developmental disabilities. It is a well-established, well-known program that has been around since, I believe, the late 1970s. Children and adults with autism, mental retardation, cerebral palsy, epilepsy, and related conditions are eligible to receive services if they meet diagnostic and severity criteria. It is an entitlement program, so there are no income or citizenship criteria. The program has a database that, I believe, has used the same data collection instrument since 1987 to document eligibility for services.

With the appropriate approvals from DDS and our institutional review board (IRB), we were able to obtain a data file that contained eligibility diagnoses for children born in 1989-2002. We then linked the DDS data to the statewide birth certificate files, again with IRB approval and strict requirements to maintain the confidentiality of the data, to obtain demographic data, such as parental age, [that had been] recorded before there was any concern that a child might have a developmental disability. The DDS data are assembled for administrative purposes, so the database has definite limits for research studies, especially with regard to diagnostic details and potential underlying causal factors. However, DDS data are extremely valuable for looking at broad-stroke time trends and demographic patterns. And so, it is really very useful for some types of studies.

After we had excluded multiple births and subjects with missing data, we were able to analyze the demographic characteristics of more than 20,000 singleton children born to California residents who were receiving DDS services for autism and compare them to the remaining 7.5 million singleton children born to California residents during those same 14 years.

Medscape: Did these children in your dataset have classic autism or were they part of the autism spectrum?

Dr. Grether: Well, that is part of the complexity here. According to DDS eligibility guidelines, a child is supposed to have autistic disorder or have mental retardation with sufficient severity to meet the criteria to be getting services. In reality, partly because the diagnosis of autism is based on behavioral criteria, the distinction between autistic disorder and other spectrum conditions can be rather "soft." We know through experience that there are some children receiving DDS services for autism who may not, in some clinicians' eyes, meet the full DSM-IV [Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition] criteria for autistic disorder. However, these are clearly not typically functioning children; they need services and there may be nowhere else to send them. So, sometimes the eligibility criteria likely get interpreted a bit leniently. None of this, I think, is particularly relevant to our concerns in this study. It has restricted some other analyses, but is not so relevant here.

Some unknown proportion of children enrolled with DDS are probably somewhere else on the spectrum, and there also children receiving services from DDS who have autism but whose eligibility diagnosis is mental retardation. We have no way of teasing this apart unless we actually go into the hard copy records, which we have done for some other studies, but not for this one, given the very large size of this study. The bottom line is that we can't make any claims about autistic disorder vs other spectrum disorders, so we have to be careful here, especially when looking at time trends.

Medscape: Would the fact that children are entering the system who actually don't meet the strict autism criteria be responsible for the increase observed over the past decades?

Dr. Grether: Clearly, there has been a huge increase in children with autism coming into the DDS system, and as epidemiologists, we have spent a lot of time trying to figure how much of that increase is likely attributable to children with other spectrum disorders coming into the system, and how much is likely due to other factors, such as more awareness or that there are now treatments for eligible children. We know all of those things go on, and also that diagnostic criteria have changed over time. The basic question is, from an etiologic standpoint, how much of the increase may be real, in the sense that something new is going on that was not there before and that contributes to some children having autism.

Medscape: So, you can't tell what percentage of the increase might be due to this broader diagnosis.

Dr. Grether: No, to really get a good handle on that, you would have to do a study in which you go into a community, you try to find every child who may be anywhere on the spectrum, and you give all of them the gold standard diagnostic evaluation. That is a very expensive and time-consuming kind of study.

Medscape: I suppose if you saw autism leveling off now, it would be some indication that a fairly significant percentage might be due to broader diagnostic or socioeconomic factors.

Dr. Grether: If the eligibility criteria for programs like the DDS included anybody anywhere on the spectrum, then you would expect there would be an influx of new kids coming in who meet the broader diagnostic criteria. The numbers would go up accordingly and then level off after that if nothing else was changing to lead to bigger numbers. Obviously, we cannot go backward in time and reconstruct such a scenario, so we have to live with uncertainty.

Medscape: Are there any other factors that you could hypothesize might be going into the increase in autism?

Dr. Grether: Many environmental factors have been raised as possibilities, because obviously, many things have changed in our environment. The difficulty is that most of the things that we worry about -- water and air contamination, plastic hardeners in the sports water bottles, etc. -- are very hard to study in a rigorous way. It is a huge methodological challenge and, fortunately for all of us, some talented scientists are trying to do these studies. Some years ago, after trying to tease out how-much-is-real-and-how-much-isn't kind of question, some of us got to the point of saying, you know, folks, we are never going to have the occurrence data to really figure this out in a satisfying way. Let's stop devoting some much of our precious time and energy to this question, and let's try to figure out what is going on in our environment that could be relevant here. Even if all these new environmental exposures and other changes in our environment are not contributing to autism, per se, we need to know more about them because autism is only one of many pediatric disorders that could be linked to environmental factors. Let's do our best to design studies to really try to narrow in on some of it. It is a huge challenge.

Medscape: What about genetic factors?

Dr. Grether: Genetic studies are going on, and talented researchers are finding more and more genetic factors that may contribute. But from everything we know about the human condition, environmental factors are likely to also play a role.

Medscape: To get back to your study, older parenting has been increasing, so might this also contribute to the increase in autism?

Dr. Grether: Yes, the typical age of parents has been going up somewhat. We have done an estimate, not yet published, in which we basically took the demographic profile of the statewide population in 1989 and applied it to the statewide population in 2002. This standardized the 2002 population for the demographic profile in 1989, permitting us to estimate how much of the increase in DDS-reported autism was either reduced or exacerbated by changing demographic patterns. It was somewhat reduced, but not by a lot. Overall, the changing demographics of the population, including increasing age at parenthood, seems to explain some small part of the increase we see. In a recent paper, colleagues at UC [University of California]-Davis used DDS data and came up with an estimate that 4.6% of the increase in DDS-reported autism from 1990-1999 may be attributable to changing parental age patterns. That's a very modest portion. Clearly, the fact that parents are typically somewhat older than they used to be is not the main explanation behind the increase in autism that we are seeing.[1]

Medscape: What was the significance of your results on older parenting and autism?

Dr. Grether: Our results were certainly consistent with what other people are reporting using California data and also with other studies conducted elsewhere in the world. Both mother's and father's age matter, there is both a maternal and a paternal age effect, and in our study, the maternal age effect is somewhat stronger. However, the increase in risk for autism in offspring born to older parents is pretty modest and probably not useful as a guide in personal decision-making. The real benefit of our study and similar ones is that we now have a scientific clue that may help point us toward underlying biological factors that contribute to the risk for autism in some children. We needed to pin down whether advancing parental age really matters or if it is just some kind of statistical artifact. We can now have confidence that there is a modest parental age effect for both mothers and fathers (at least in the US population). Our task now is to try to figure out why the risk of having a child with autism is greater for older parents.

Medscape: Can you give us some background on why parental age may affect the risk for autism?

Dr. Grether: There are 2 sets of factors, they are not mutually exclusive, and both may well be important. One set of factors involves biological changes that occur as men and women get older and that can affect the outcome of the pregnancy. Down syndrome would be an example of an outcome we know is sometimes related to maternal age. For women, as they get older, the hormonal balance of the womb changes in some ways, and older women are more likely to have infertility. There has been speculation that the hormonal changes that contribute to infertility, or the treatments for infertility, may increase the risk for autism, but we don't have very good data yet. As a woman ages, she will have an increased cumulative exposure to chemicals and toxins in her environment that may affect the neurodevelopment of the fetus. Again, there are not very much data there, but it makes good biological sense to conduct research on environmental factors to which the mother is exposed before or during pregnancy that may affect fetal neurodevelopment.

Medscape: How is male reproduction affected by aging that might influence the risk for autism?

Dr. Grether: Unlike eggs, which were formed during fetal development of the mother, the process of sperm creation and maturation is ongoing, and it is now recognized that as men get older, typically there are more new mutations that occur in the sperm, that are developing. Again, it could be related in some ways to cumulative toxic exposures as men get older. Several studies have demonstrated that, in families lacking a history of schizophrenia, there is an association between older age of fathers (but not mothers) and risk of having a child with schizophrenia, presumably due to more de novo mutations in sperm. These studies of young-adult schizophrenia provide a model that may be relevant to autism, but the studies needed to clarify this for autism have not yet been reported.

The data we and others report showing both a maternal and a paternal age effect for autism could indicate that genetic mutations to the sperm contribute to the risk for autism in the children, but clearly that is not the whole picture because we also see a maternal age effect. That is one reason why we are so interested in studying hormonal factors in the mother during or before pregnancy that may contribute to autism risk.

Medscape: Are there reasons, other than biology, why this risk exists in older parents?

Dr. Grether: There is another possibility here, another possible explanation that could also explain the parental age effect. Over and above whatever reproductive biological changes happen as people age, people who are predisposed to have an autistic child may be more likely to start having children later in life, for a variety of reasons. They may be going to college, pursuing more intensive careers, and putting off childbearing until later. We can speculate about these reasons, but we don't yet have studies on this and, unfortunately, we don't have relevant data from our study.

There is also speculation in the research literature that, to the extent there is a tendency for people to have children with a partner who is similar to themselves ("like marries like"), there may be a pattern for people with a genetic predisposition for autism to form a relationship with a partner who has a similar genetic predisposition. By waiting until later in life to have a family, perhaps there is more opportunity to find a partner with similar underlying genetics, thereby increasing the genetic risk in the child.

As I said, this is speculation at this point. The studies simply have not yet been done. The "takeaway" message here is that we now have some good hypotheses around which to conduct further studies that will help in disentangling the mix of genetic and environmental factors that contribute to autism.

Medscape: Did you find any greater association with autism and any ethnicity or race in older parents?

Dr. Grether: No, not with the increasing parental age. It was really very, very similar across racial ethnic groups, which is really interesting.

Medscape: What about socioeconomic groups?

Dr. Grether: We found an association with one SES [socioeconomic status] measure (private insurance payment for the delivery vs other sources of payment, primarily government programs for low income people) but not with another (educational level attained by the mother or father), so our findings must be considered to be inconclusive with regard to socioeconomic status.

Medscape: Haven't there been some studies indicating that higher economic groups are more prone to autism than lower?

Dr. Grether: Yes, but that is really a different question. Let me try to restate it, as this can be a real mind-twister. In our parental age study, we were trying to look at how much an increase in the age of parents is related to the risk for autism in a child. We were not looking at the baseline risk. So when I say that we did not see a difference in the increase in risk associated with age of parents for well-educated parents compared with less well-educated parents, what I am talking about is the increase associated with the parents being older. At any given age, well-educated parents are more likely to have children with autism than less well-educated parents (and we don't know why this is so), but the amount that the risk increases with increasing age of parents is the same for both groups. Their baseline risk may be different, but the rate of increase in risk represented by the upward slopes of the lines are parallel to each other.

Medscape: Are there any other factors that might affect the risk of having a child with autism among older vs younger parents?

Dr. Grether: One finding that we have, which most other studies have not examined, is that both the maternal and paternal age effect is stronger among first-born children than among later-born children. For first-born children, both for mothers and fathers, that slope with increasing parental age is steeper than for later-born children. So, if it is the first time a parent is having a child, the risk of that child having autism is greater than for a child of a parent of comparable age who already has children.

The explanation for this pattern may be that parents starting their families later in life have a pre-existing risk and so we would see this pattern more strongly among first-born children. It certainly should not matter if it is the first-born child for that older father or the fifth-born, since the sperm at that older age would still be going through the same genetic changes.

Medscape: Does the higher risk in first-born children hold up with women as well as men?

Dr. Grether: Yes, the maternal age effect is stronger in first-born than in later-born children. For a woman has had prior children, prior pregnancies may change the in utero environment in ways that affect her fetus differently than is typical for a women of the same age having her first child. Or perhaps the effect of toxic exposures from the environment is different, depending on the reproductive history of a woman giving birth for the first time compared with one who has given birth before.

My guess is that when we have the answers to all the questions raised by our study and others that have addressed the question of a parental age effect, we will see that both delayed childbearing and age-related biological changes contribute to the higher risk for older parents. But until the research is conducted, we won't know. A recent letter to the editor in the American Journal of Public Health by some colleagues basically said, and I fully agree, that studies, including ours, have consistently established a parental age effect. Now it is time to move on and figure out why.[2]

Medscape: Do you see prenatal screening anytime in the future?

Dr. Grether: No. I don't think we are close to having prenatal screening. In the meantime, as a society, we need to work through the deep ethical issues involved. Our current best understanding is that autism spectrum disorders are at one end of a human continuum, raising complex questions about the kind of society we want to fashion as science changes and the possibilities for medical interventions increase.

Medscape: Just as an aside, our news group covered the Lancet article that retracted the study associating autism with vaccinations. Do you have any thoughts on this and the problem of convincing fearful parents to immunize their children?

Dr. Grether: It has always surprised me how many people confuse the various concerns that have been raised regarding childhood immunizations and risk for autism. The Lancet retraction focused on the MMR [measles, mumps, and rubella] vaccination and the allegations by a team of researchers in Great Britain about MMR playing a role in autism in some children. The MMR-autism connection has now been demonstrated to have been based on very shoddy, perhaps even falsified, evidence. There is no scientific basis that I am aware of for being concerned about MMR and autism. Another issue about vaccines is the thimerosal preservative that was included in multidose vials of some other childhood vaccines (thimerosal was not in the MMR vaccine). Here there have been many studies and no credible study has found a link between thimerosal exposure through vaccines and autism. In the United States, thimerosal exposure from vaccines is no longer an issue, except perhaps through some flu shots. The other concern that I have heard voiced is that the recommended childhood vaccine schedule now includes so many vaccines and that children are thereby being exposed to more antigens than previously. Although there are now more vaccines recommended for children, the total antigen exposure from today's vaccines is considerably less than in earlier years because of advances in vaccine composition. And compared to the sheer volume and diversity of antigens in a typical environment, the antigen dose received in vaccines is minor. While it is understandable that parents, and perhaps some clinicians, have raised the alarm about vaccines, I am not aware of any credible evidence to support these concerns.

Medscape: To conclude, and I think you really answered this already, do your results have any implications for personal decision-making or clinical practice?

Dr. Grether: You know, I wish they did, but I really don't think that they do at this point. The increase in risk that comes with older parents is really quite modest and we don't know what is behind it. I think the main benefit of our study and other similar ones is to alert us to an important etiologic clue, and it is now time to find out what is going on.

References

Does Increased Parental Age Mean Increased Risk?

2010-04-26T10:51:00.000-07:00

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

2010-04-17T08:06:00.000-07:00

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…

A Newly published Study

2010-04-13T07:33:00.001-07:00

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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Grandparental Age and ASD
PLoS ONE

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

2010-04-10T10:32:00.000-07:00

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

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

2010-04-08T06:58:00.000-07:00

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

Do Men Have a Biological Clock Too?

2010-04-07T16:30:00.000-07:00

Do Men Have a Biological Clock Too?

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

2010-04-07T10:59:00.000-07:00

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

Medical Board Drops All Original Charges and Allegations

2010-04-07T07:30:00.000-07:00

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

2010-04-06T07:16:00.001-07:00

[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.

2010-04-05T07:20:00.001-07:00

A "RIGHT" TO HEALTH FREEDOM, NOT HEALTH CARE

By Attorney Jonathan Emord