Is the Rise in Neurocognitive Developmental Disorders Unexpected with the Rise in Paternal Age NO!

Not unexpected at all. There has been a 50 year game of blaming the mother's age or some mysterious cause.

What is the role of vaccinations?? What is the connection?

Who is well aware of the paternal age effect?


Why has paternal age risen so much in the last 20 years? Why does the myth that men can father at any age persist when autism, schizophrenia, diabetes, MS, prostate cancer, breast cancer, nervous system cancers, some leukemias, mental retardation, progeria, heart defects, low birth-weight, miscarriages, Down syndrome, epilepsy, kidney disease, fibromyalgia, hemophilia, fragile X, Alzheimer's, etc. etc. all rise in incidence in non-familial/spontaneous/sporadic cases with older paternal age and older maternal grandfather's age? It is also known that women who had fathers over 45 have significantly shorter life spans than those with younger fathers. What happens to the X-chromosome, what happens to the genes that form the brain and nervous system and the immune system? Why do Hispanics have significantly less autism on a population level than Caucasians and Asians in the USA, in California according to the CDC and the other studies? Why has it been known since the 1950s that olders fathers and schizophrenia/autism, etc. are related and the public is steered in late fathering. If you read the many epidemiologic studies or the studies on the increasing DNA breakage in sperm with a man's age you will find the warnings that older paternal age is the most potent cause of genetic disease that seems to come from nowhere. There are many studies that have to do with epidemiology and paternal age and with sperm and older age that are not funded. Why? Why do recent studies on autism not point out the paternal age connection. Even in plants mutations are known to arise predominantly in the paternal germ line, not the maternal germ line.

Who benefits? Who looses? Why are papers warning of the consequences of advanced paternal age (past 31) suppressed and ignored? The rise in "autism" is not unexpected or mysterious!

Journal of Epidemiology and Community Health 2006;60:851-853; doi:10.1136/jech.2005.045179Copyright © 2006 by the BMJ Publishing Group Ltd.


SHORT REPORT
Advanced paternal age: How old is too old? Isabelle Bray, David Gunnell, George Davey Smith
Department of Social Medicine, University of Bristol, UK
Correspondence to:Correspondence to: Dr I Bray Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK; Issy.Bray@bristol.ac.uk

"Average paternal age in the UK is increasing. The public health implications of this trend have not been widely anticipated or debated. This commentary aims to contribute to such a debate. Accumulated chromosomal aberrations and mutations occurring during the maturation of male germ cells are thought to be responsible for the increased risk of certain conditions with older fathers. Growing evidence shows that the offspring of older fathers have reduced fertility and an increased risk of birth defects, some cancers, and schizophrenia. Adverse health outcomes should be weighed up against advantages for children born to older parents, mindful that these societal advantages are likely to change over time."

Autism, schizophrenia, type 1 diabetes, MS, other autoimmunes, etc. had to rise because average paternal age over 31 rose so much

Since 1980. We are not told about the male biological clock. No will to prevent the average person from having autistic children. Those in the know do know about the paternal age effect but the political will is to have a weaker citizenry. We could have diminished the number of mentally ill, the diabetic, the autistic, the people with all kinds of genetic disorders, but instead the people who want to warn the public cannot do so.



Journal of Epidemiology and Community Health 2006;60:851-853; doi:10.1136/jech.2005.045179Copyright © 2006 by the BMJ Publishing Group Ltd.
Advanced paternal age: How old is too old? Isabelle Bray, David Gunnell and George Davey Smith
Department of Social Medicine, University of Bristol, UK
Correspondence to: Dr I Bray Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK; Issy.Bray@bristol.ac.uk


Average paternal age in the UK is increasing. The public health implications of this trend have not been widely anticipated or debated. This commentary aims to contribute to such a debate. Accumulated chromosomal aberrations and mutations occurring during the maturation of male germ cells are thought to be responsible for the increased risk of certain conditions with older fathers. Growing evidence shows that the offspring of older fathers have reduced fertility and an increased risk of birth defects, some cancers, and schizophrenia. Adverse health outcomes should be weighed up against advantages for children born to older parents, mindful that these societal advantages are likely to change over time.
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Autism, type 1 diabetes, Alzheimer's, schizophrenia in many, many cases could have been prevented by fathering babies before the age when the DNA breaks and mutations occur.
One third or more cases of schizophrenia are caused by increasing paternal age over 32. The risk goes up with the father's age. Vaccinations are an assault above and beyond paternal age.


The amount of neurocognitive disorders had to rise with rising average paternal age. Vaccinations are in addition to DNA strand breaks, and other damage. Still there is not a public health warning on paternal age and maternal age is falsely pointed to as the cause of sporadic autism. There have been studies for 50 years showing the effects of older paternal age. All kinds of disorders including non-familial mental retardation, fibromyalgia, progeria, Huntington chorea, heart defects, prostate cancer, breast cancer can be caused by mutations in the sperm of older fathers. These are non-familial, spontaneous mutations and cerebral palsy, low birth-weight and many conditions that are deleterious, and chronic life long disabilities including hemophilia, Duchennes, blindness, autism are carried by mothers who had an older father. 34 is an older father when these disorders start showing up in offspring.

Many disorders such as lupus, scleroderma, type 2 diabetes have not been studied for paternal age effects because there is no will to prevent these profitable diseases.

Any dose of ionizing radiation poses a risk and the body accomulates the damages and when enough damage is done, cancer will develop.

Paternal age and older maternal age also increases a child's risk of leukemia
Foodconsumer.org editor’s note: One of the biggest mistakes a consumer can make is to ask his doctor about the risk of ionizing radiations such as x-ray. The answer is standardized. He will be told that the risk is minimal, or the benefit overweighs the risk.
X-ray as an ionizing radiation is one of the most studied carcinogen and the U.S. government officially recognized it as a human carcinogen in 2005. Children who are exposed to a chest x-ray before 2 years have a 7 to 8 times higher risk of leukemia. Those who get exposed after two years of age will have 2 to 3 times higher risk of leukemia, according to the EPA data.
The risk is not just associated with radiotherapy used to treat cancer, which uses high doses of x-ray. Any dose of ionizing radiation poses a risk and the body accomulates the damages and when enough damage is done, cancer will develop.
X-ray does not only cause cancer, it also damage arteries causing heart disease which is less known to many ordinary consumers. According to John Gofman, PhD and MD, a nuclear physicist and a physician who retired now from The University fo California at Los Angeles, 75 percent breast cancer is related to the exposure to x-ray.
Ionizing Radiation and Childhood Leukemia
Environ Health Perspect 115:395-399 (2007). doi:10.1289/ehp.10080 available via http://dx.doi.org [Online 24 June 2007]
Referencing: Risk Factors for Acute Leukemia in Children: A Review
I read with interest the recent review by Belson et al. (2007) on childhood leukemia, particularly the sections dealing with radiation exposure. Like the authors, I believe that ionizing radiation is strongly associated with childhood acute leukemia. I would like to point out that several critical pieces of information were overlooked; these support stronger and more meaningful conclusions.
Although atomic bomb survivors offer the clearest evidence of leukemia risk after childhood exposures to ionizing radiation, studies of children exposed to fallout in other contexts should not be downplayed. Belson et al. (2007) stated that "radiation exposure secondary to the Chernobyl accident has not been shown to increase the risk of leukemia in children who were exposed after birth . . . ," but they failed to mention the case–control study of Noshchenko et al. (2002), which found significant increases in childhood and acute leukemias in association with estimated childhood exposures. Children living downwind of the Nevada Test Site have also shown a significant increase in leukemia related to estimated fallout exposure (Stevens et al. 1990).
In utero exposure to ionizing radiation has been a known causal factor for childhood cancer for > 50 years. Although Belson et al. (2007) stated that the lack of evidence for a childhood leukemia risk among atomic bomb survivors constitutes the "most notable reason for doubt of a true association," they overlooked the reviews of Wakeford and Little (2002, 2003); these authors demonstrated that the highly uncertain atomic bomb survivor data are statistically compatible with the robust set of data found in the Oxford Survey of Childhood Cancers and related X-ray exposure cohorts. There is no valid reason to doubt this association at present.
The association between preconception paternal irradiation (PPI) and childhood leukemia has always been controversial. Two of the major objections to the "Gardner hypothesis," as Belson et al. (2007) pointed out, have been mixed evidence from studies of radiation-exposed fathers and a lack of positive evidence in the children of the atomic bomb survivors. Regarding the first objection, Belson et al. overlooked the two largest studies of the children of radiation workers. Draper et al. (1997) conducted a UK-wide case–control study of childhood cancers in relation to paternal radiation exposure. This study showed, based on > 13,000 cases not included in the study of Gardner et al. (1990), that children with leukemia or non-Hodgkin lymphoma were significantly more likely than controls to have fathers who were radiation workers. Dickinson and Parker (2002) conducted a cohort study of > 250,000 births in Cumbria, England, including the cases of Gardner et al. (1990), and found a significant 2-fold increase in the risk of leukemia and non-Hodgkin lymphoma among the children of radiation workers. These and other studies, taken together, give statistical support to the idea that paternal radiation work is a risk factor for childhood leukemia.
When interpreting the evidence for a PPI effect in atomic bomb survivors, it is important to consider what is known about potential mechanisms. As reviewed by Niwa (2003), Nomura (2003), and others, animal studies have consistently demonstrated that PPI can cause or increase the susceptibility to leukemia in offspring. In addition to fascinating evidence of postconception genomic instability after preconception exposure, many studies suggest that there may a window of sensitivity corresponding to postmeiotic stages of spermatogenesis; in humans, this would mean the few months leading up to conception (Adler 1996). Of the roughly 30,000 children of atomic bomb survivors, only about 2% were conceived in the 6 months after the bombings. Based on the spontaneous leukemia rate reported by Yoshimoto (1990), the expected number of spontaneous cases in this subcohort would be < 1, and an excess on the order suggested by the radiation worker studies would not be statistically apparent. For this and other reasons, the atomic bomb survivors may not be an appropriate comparison group.
To summarize, it is not unreasonable to observe that the weight of evidence generated to date supports the idea that preconception, prenatal, and postnatal exposures to ionizing radiation are all risk factors for childhood leukemia.
The author declares he has no competing financial interests.
Abel Russ
George Perkins Marsh Institute
Worcester, Massachusetts
E-mail: abelruss@riseup.net
References
Adler ID. 1996. Comparison of the duration of spermatogenesis between male rodents and humans. Mutat Res 352(1-2):169–172.
Belson M, Kingsley B, Holmes A. 2007. Risk factors for acute leukemia in children: a review. Environ Health Perspect 115:138–145.
Dickinson HO, Parker L. 2002. Leukemia and non-Hodgkin's lymphoma in children of male Sellafield radiation workers. Int J Cancer 99:437–444.
Draper GJ, Little MP, Sorahan T, Kinlen LJ, Bunch KJ, Conquest AJ, et al. 1997. Cancer in the offspring of radiation workers: a record linkage study. BMJ 315(7117): 1181–1188.
Gardner MJ, Snee MP, Hall AJ, Powell CA, Downes S, Terrell JD. 1990. Results of case-control study of leukemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria. BMJ 300:423–429.
Niwa O. 2003. Induced genomic instability in irradiated germ cells and in the offspring: reconciling discrepancies among the human and animal studies. Oncogene 22: 7078–7086.
Nomura T. 2003. Transgenerational carcinogenesis: induction and transmission of genetic alterations and mechanisms of carcinogenesis. Mutat Res 544(2-3):425–432.
Noshchenko AG, Zamostyan PV, Bondar OY, Drozdova VD. 2002. Radiation-induced leukemia risk among those aged 0-20 at the time of the Chernobyl accident: a case-control study in the Ukraine. Int J Cancer 99(4):609–618.
Stevens W, Thomas DC, Lyon JL, Till JE, Kerber RA, Simon SL, et al. 1990. Leukemia in Utah and radioactive fallout from the Nevada test site. A case-control study. JAMA 264(5):585–591.
Wakeford R, Little MP. 2002. Childhood cancer after low-level intrauterine exposure to radiation. J Radiol Prot 22(3A):A123–A127.
Wakeford R, Little MP. 2003. Risk coefficients for childhood cancer after intrauterine irradiation: a review. Int J Radiat Biol 79(5):293–309.
Yoshimoto Y, Neel JV, Schull WJ, Kato H, Soda M, Eto R, et al. 1990. Malignant tumors during the first 2 decades of life in the offspring of atomic bomb survivors. Am J Hum Genet 46(6):1041–1052.
Editor's note: In accordance with journal policy, Belson et al. were asked whether they wanted to respond to this letter, but they chose not to do so.
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The Rise in Autism is Not a Mystery, but There is a PR Campaign to Make You Think it is, Older Fathers and Older Maternal Grandfathers Cause Mutations

Advanced Grandparental Age and Autism Survey


Many other lesser genetic disorders are also caused by genetic changes in sperm DNA that increase with a man's age. The Center for Disease Control will never inform the public, nor will the NIH, or NIMH, or NARSAD or NAMI. It is the inability of the child's immune system to handle the antigens that causes the problems when the children are vaccinated. Risk factors for autism and schizophrenia should be made public and new vaccinations schedules made if men insist on having babies past the age of 32. Also the mother's father's age should be noted and if higher than early 30s a special schedule should be used. Any family history of autoimmune disorders should put the baby in the high risk category as well as a family history of autism, schizophrenia or OCD.

If you want to do something to prevent autism get informed by reading about it. No one is going to tell the public that older paternal age is past 31 32 and it is that increasing genetic disorders in offspring is a result of the male biological clock caused by mutations in sperm DNA. Sperm come from somehere, they are not made fresh out of nothing. Everyone in the field of autism/schizophrenia research knows that the incidence increases with paternal age and maternal grandfather's age at the mother's birth. Most researchers are happy to keep this secret from the public and get funded to do research that does nothing postitive but make more money for themselves, pharmaceutical companies and genomic studies institutes. They will take your genes to make money for themselves and not help your child.

With the number of men fathering over 35, when over 33 is old and dangerous, there has to be more autism./schizophrenia, diabetes, MS, Lupus, fibromyalgia, endometriosis, Alzheimer's disease, heart disease, Crohn's disease, IBD, Duchenne's, hemophilia, prostate cancer, breast cancer, colon cancer, ovarian cancer, etc. etc. etc.

Some industries are very happy about the rise in autism/schizophrenia think pharmaceuticals, academia,psychiatric researchers on the whole special ed field etc. The March of Dimes is set up to distract from Paternal Age as the major cause of birth defects. Many researchers with big research departments know that their whole professional life revolves around the fact that no one informed the public in the 1950s that older paternal age causes birth defects and damaged children. Any researcher who tries or tried to inform of the connection was called crazy and not allowed to publish in any reputable journal. It is a bit like the connection between smoking and cancer, we have been taught that older fathers are wonderful and to be admired. This is pure PR.

For a good discussion on the paternal age roots of non-familial schizophrenia including childhood schizophrenia/autism, its name since 1994 read through the following paper by Dr. Dolores Malaspina, Chair of the Department of Psychiatry at NYU School of Medicine.

Schizophrenia Risk and the Paternal Germ LineBy Dolores Malaspina
Dolores Malaspina

Paternal age at conception is a robust risk factor for schizophrenia. Possible mechanisms include de novo point mutations or defective epigenetic regulation of paternal genes. The predisposing genetic events appear to occur probabilistically (stochastically) in proportion to advancing paternal age, but might also be induced by toxic exposures, nutritional deficiencies, suboptimal DNA repair enzymes, or other factors that influence the fidelity of genetic information in the constantly replicating male germ line. We propose that de novo genetic alterations in the paternal germ line cause an independent and common variant of schizophrenia.
Seminal findingsWe initially examined the relationship between paternal age and the risk for schizophrenia because it is well established that paternal age is the major source of de novo mutations in the human population, and most schizophrenia cases have no family history of psychosis. In 2001, we demonstrated a monotonic increase in the risk of schizophrenia as paternal age advanced in the rich database of the Jerusalem Perinatal Cohort. Compared with the offspring of fathers aged 20-24 years, in well-controlled analyses, each decade of paternal age multiplied the risk for schizophrenia by 1.4 (95 percent confidence interval: 1.2-1.7), so that the relative risk (RR) for offspring of fathers aged 45+ was 3.0 (1.6-5.5), with 1/46 of these offspring developing schizophrenia. There were no comparable maternal age effects (Malaspina et al., 2001).
Epidemiological evidenceThis finding has now been replicated in numerous cohorts from diverse populations (Sipos et al., 2004; El-Saadi et al., 2004; Zammit et al., 2003; Byrne et al., 2003; Dalman and Allenbeck, 2002; Brown et al., 2002; Tsuchiya et al., 2005). By and large, each study shows a tripling of the risk for schizophrenia for the offspring of the oldest group of fathers, in comparison to the risk in a reference group of younger fathers. There is also a "dosage effect" of increasing paternal age; risk is roughly doubled for the offspring of men in their forties and is tripled for paternal age >50 years. These studies are methodologically sound, and most of them have employed prospective exposure data and validated psychiatric diagnoses. Together they demonstrate that the paternal age effect is not explained by other factors, including family history, maternal age, parental education and social ability, family social integration, social class, birth order, birth weight, and birth complications. Furthermore, the paternal age effect is specific for schizophrenia versus other adult onset psychiatric disorders. This is not the case for any other known schizophrenia risk factor, including many of the putative susceptibility genes (Craddock et al., 2006).
There have been no failures to replicate the paternal age effect, nor its approximate magnitude, in any adequately powered study. The data support the hypothesis that paternal age increases schizophrenia risk through a de novo genetic mechanism. The remarkable uniformity of the results across different cultures lends further coherence to the conclusion that this robust relationship is likely to reflect an innate human biological phenomenon that progresses over aging in the male germ line, which is independent of regional environmental, infectious, or other routes.
Indeed, the consistency of these data is unparalleled in schizophrenia research, with the exception of the increase in risk to the relatives of schizophrenia probands (i.e., 10 percent for a sibling). Yet, while having an affected first-degree relative confers a relatively higher risk for illness than having a father >50 years (~10 percent versus ~2 percent), paternal age explains a far greater portion of the population attributable risk for schizophrenia. This is because a family history is infrequent among schizophrenia cases, whereas paternal age explained 26.6 percent of the schizophrenia cases in our Jerusalem cohort. If we had only considered the risk in the cases with paternal age >30 years, our risk would be equivalent to that reported by Sipos et al. (2004) in the Swedish study (15.5 percent). When paternal ages >25 years are considered, the calculated risk is much higher. Although the increment in risk for fathers age 26 through 30 years is small (~14 percent), this group is very large, which accounts for the magnitude of their contribution to the overall risk. The actual percentage of cases with paternal germ line-derived schizophrenia in a given population will depend on the demographics of paternal childbearing age, among other factors. With an upswing in paternal age, these cases would be expected to become more prevalent.
Biological plausibilityWe used several approaches to examine the biological plausibility of paternal age as a risk factor for schizophrenia. First, we established a translational animal model using inbred mice. Previously it had been reported that the offspring of aged male rodents had less spontaneous activity and worse learning capacity than those of mature rodents, despite having no noticeable physical anomalies (Auroux et al., 1983). Our model carefully compared behavioral performance between the progeny of 18-24-month-old sires with that of 4-month-old sires. We replicated Auroux's findings, demonstrating significantly decreased learning in an active avoidance test, less exploration in the open field, and a number of other behavioral decrements in the offspring of older sires (Bradley-Moore et al., 2002).
Next, we examined if parental age was related to intelligence in healthy adolescents. We reasoned that if de novo genetic changes can cause schizophrenia, there might be effects of later paternal age on cognitive function, since cognitive problems are intertwined with core aspects of schizophrenia. For this study, we cross-linked data from the Jerusalem birth cohort with the neuropsychological data from the Israeli draft board (Malaspina et al., 2005a). We found that maternal and paternal age had independent effects on IQ scores, each accounting for ~2 percent of the total variance. Older paternal age was exclusively associated with a decrement in nonverbal (performance) intelligence IQ, without effects on verbal ability, suggestive of a specific effect on cognitive processing. In controlled analyses, maternal age showed an inverted U-shaped association with both verbal and performance IQ, suggestive of a generalized effect.
Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.
A variant of schizophreniaA persistent question is whether the association of paternal age and schizophrenia could be explained by psychiatric problems in the parents that could both hinder their childbearing and be inherited by their offspring. If this were so, then cases with affected parents would have older paternal ages. This has not been demonstrated. To the contrary, we found that paternal age was 4.7 years older for sporadic than familial cases from our research unit at New York State Psychiatric Institute (Malaspina et al., 2002). In addition, epidemiological studies show that advancing paternal age is unrelated to the risk for familial schizophrenia (Byrne et al., 2003; Sipos et al., 2004). For example, Sipos found that each subsequent decade of paternal age increased the RR for sporadic schizophrenia by 1.60 (1.32 to 1.92), with no significant effect for familial cases (RR = 0.91, 0.44 to 1.89). The effect of late paternal age in sporadic cases was impressive. The offspring of the oldest fathers had a 5.85-fold risk for sporadic schizophrenia (Sipos et al., 2004); relative risks over 5.0 are very likely to reflect a true causal relationship (Breslow and Day, 1980).
It is possible that the genetic events that occur in the paternal germ line are affecting the same genes that influence the risk in familial cases. However, there is evidence that this is not the case. First, a number of the loci linked to familial schizophrenia are also associated with bipolar disorder (Craddock et al., 2006), ), whereas advancing paternal age is specific for schizophrenia (Malaspina et al., 2001). Next, a few genetic studies that separately examined familial and sporadic cases found that the "at-risk haplotypes" linked to familial schizophrenia were unassociated with sporadic cases, including dystrobrevin-binding protein (Van Den Bogaert et al., 2003) and neuregulin (Williams et al., 2003). Segregating sporadic cases from the analyses actually strengthened the magnitude of the genetic association in the familial cases, consistent with etiological heterogeneity between familial and sporadic groups.

Read Dr. Malaspina's whole paper and its sources.

See the following post for autism as an extreme autoimmune disorder related to a family history of autoimmune disorders caused by older paternal age in one generation or another.


Pediatrics. 2003 Nov;112(5):e420. Links
Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders.Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM, McDougle CJ.
Department of Psychiatry, Indiana University School of Medicine, and James Whitcomb Riley Hospital for Children Indianapolis 46202-4800, USA.
OBJECTIVES: Increased prevalence of familial autoimmune disease is a common finding among probands with various autoimmune disorders. Autistic disorder (autism) is a highly genetic disorder with known immune and immunogenetic abnormalities. Previous research has found an increased frequency of autoimmune disorders in families with autistic probands. We further investigated this association by determining the frequency of autoimmune disorders in families that have probands with pervasive developmental disorders (PDDs), including autism, compared with 2 control groups. METHODS: Three well-defined study groups, including 1) families that have a child with a PDD, 2) families that have a child with an autoimmune disorder, and 3) families with a healthy control child, constituted the sample. A questionnaire inquiring about which first- and second-degree family members had received a diagnosis of having specific autoimmune disorders was completed by 101 families in each group. RESULTS: The frequency of autoimmune disorders was significantly higher in families of the PDD probands compared with families of both the autoimmune and healthy control probands. Autoimmunity was highest among the parents of PDD probands compared with parents of the healthy control subjects. Hypothyroidism/Hashimoto's thyroiditis and rheumatic fever were significantly more common in families with PDD probands than in the healthy control families. CONCLUSIONS: Autoimmunity was increased significantly in families with PDD compared with those of healthy and autoimmune control subjects. These preliminary findings warrant additional investigation into immune and autoimmune mechanisms in autism.

PMID: 14595086 [PubMed - indexed for MEDLINE]


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Thanks to Ginger's blog Adventures in Autism

Since Autism Speaks is coming under such close examination, I thought I would bring to you the keen observation of an anonymous poster on the Evidence of Harm List.
Labels: autism prevention?, Autism Speaks, causes of autism, charities, follow the cash

posted by concerned heart at 12:13 PM 0 Comments Links to this post

Friday, June 8, 2007
I Found The Post Below the Picture This Morning on Adventures in Autism
The $2,000,000 for Mark Rothmeyer doesn't surprise me at all. Neither do the other expenses and salaries. If anyone is interested in the causes of autism and the history of its creation as a mysterious disorder go to the autism prevention blogspot. Autism, until 1994 used to be a diagnosis given for a very specific set of symptoms and it was sometimes considered the severest example of early childhood schizophrenia. The paper by Kanner on classical autism can be linked to on the site.


Autism Speaks never does anything to help anyone with autism, or prevent even one case of autism. The causes of autism are known, the way to prevent more autism is known in a percentage of cases. How to take a tragic disorder and turn it into a lucretive business venture is demonstrated again by Autism Speaks and the Institutions it funds.

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GINGER's Blog: ADVENTURES IN AUTISM

Thursday, June 07, 2007
I Take Back Every Nice Thing I Have Ever Said About Autism Speaks

"I read this today and it just made me sick. I don't even have the words to comment on it."~Ginger
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I am a professional that has reviewed many non profit organization's IRS Form 990s. Autism Speaks Form 990 raises serious red flags. Serious. This is all from the official filing for 2006.





1. Three members of the Board of Directors received $2.5 million for their own organizations.

2. The President Mark Rothmeyer, just received a 5 year contract for about $2,000,000 including bonuses with no prior background with autism.

3. The grants are primarily going to those representing institutions that are reviewing the grants. There is no indication that these conflicts are independently reviewed

4. The location of this small and new foundation is in very expensive downtown New York facilities rented for $200,000 by the institution that is run by the Chairman of Autism Speaks.

5. A expense of a Private Jet plane for $57,000 was noted. This is very unusual for a new non profit groups.

6. The head of the scientific review received the majority of the funds for 2005 for his institution for a data base - almost $3 million

Since the funding is now from the public - and the advertising and promotion tugs at the publics heart strings with images of families in need - the funds collected MUST be about those it raises the money for.

The following are all taken from the Form 990 filing

Web Site $830,000
Software for the computer $514,000
Lawyers $440,000
Computers $337,000
Public relations $285,000
Office annual rent $200,000
HR consultant $110,000
Editorial Consultant $76,000
Private Jet Plane for someone that entertained $57,000


Mark Rothmeyer* $360,000
Peter Bell [$240,000?]
Alison Singer $168,000
Mr Ringall $150,000
Andy Shik $110,000

Remember all the above also gets significant fring benefits that
probably add.

Mark Rothmayer also can get $50,000 more with a bonus a year benefits

ADVANCING PATERNAL AGE IS CONSISTENTLY ASSOCIATED WITH INCREASED RISK OF AUTISM AND ASDs

Alexander Kolevzon, MD; Raz Gross, MD, MPH; Abraham Reichenberg, PhD

Vol. 161 No. 4, April 2007



The results of this review show that 3 of the 4 population-based studies28-29,32 to examine paternal age reported a significant association with risk of autism and ASDs. The fourth study31 also found that paternal age was older in fathers of case patients with autism compared with fathers of controls, although this relationship was statistically weaker in the adjusted analysis. Thus, advancing paternal age is consistently associated with increased risk of autism and ASDs.
Advanced paternal age has been associated with several congenital disorders, including Apert syndrome,40 craniosynostosis,41 situs inversus,42 syndactyly,43 cleft lip and/or palate,44-45 hydrocephalus,44 neural tube defects,46 and Down syndrome.47 In addition, advanced paternal age has been associated with schizophrenia15 and decreased intellectual capacities in the offspring.48 The most widely proposed mechanism underlying these congenital anomalies is known as the "copy error" hypothesis, first proposed by Penrose.49 After puberty, spermatocytes divide every 16 days, and by the age of 35 years, approximately 540 cell divisions have occurred. As a result, de novo genetic mutations that result from replication errors and defective DNA repair mechanisms are believed to propagate in successive clones of spermatocytes. These mutations accumulate with advancing paternal age and thus help explain how this disorder, which has a large genetic component, can be maintained in the population despite reduced reproduction in affected individuals.



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Southwest Autism Research & Resource Center (SARRC)
PREVALENCE OF PSYCHIATRIC AND LEARNING DISORDERS IN MULTIPLEX, ONLY-CHILD, SINGLETON, AND CONTROL FAMILIES

S. E. Ober-Reynolds, R. D. Melmed, R. C. Bay, S. M. Stephens, J. J. Jones, S. E. Brautigam, J. E. Kirwan, T. A. Grebe
Enter abstract here-DON'T include authors or title
Background: While specific genes have been implicated in the etiology of autism, a history of psychiatric and learning disorders (psych/LD) in family members may increase a childs vulnerability to autism as well as these disorders.

Objectives: To compare the family history of psych/LD disorders in four groups: multiplex families, families whose only child has autism (only-child), families with one child with autism as well as unaffected children (singleton) and control families.

Methods: The prevalence of self-reported psych/LD was calculated using data from 1081 families who completed the SARRC Parent Questionnaire. Families were compared on reported history of the following: bipolar disorder, anxiety, depression, obsessive/compulsive disorder, ADHD, and learning disorders.

Results: Of the families, 52(4.8%) were multiplex, 131(12.1%) only-child, 584(54%) singleton, and 308(29.0%) controls. Prevalence of each psych/LD disorder differed across family type (chi-square exact tests, two-tailed), all p<0.001. The trend for prevalence was identical for all disorders analyzed; multiplex families reported the greatest prevalence (by family history) of each disorder followed by only-child families, singleton families, then control families.

Conclusion: Reported family history of psychiatric and learning disorders occurs most frequently in multiplex families and least in control families suggesting a genetic vulnerability which may predispose an individual to a spectrum of disorders, including autism.

"ADVANCED PATERNAL AGE IS CONSISTENTLY ASSOCIATED WITH INCREASED RISK OF AUTISM AND ASDS"

The results of this review show that 3 of the 4 population-based studies28-29,32 to examine paternal age reported a significant association with risk of autism and ASDs. The fourth study31 also found that paternal age was older in fathers of case patients with autism compared with fathers of controls, although this relationship was statistically weaker in the adjusted analysis. Thus, advancing paternal age is consistently associated with increased risk of autism and ASDs.
Advanced paternal age has been associated with several congenital disorders, including Apert syndrome,40 craniosynostosis,41 situs inversus,42 syndactyly,43 cleft lip and/or palate,44-45 hydrocephalus,44 neural tube defects,46 and Down syndrome.47 In addition, advanced paternal age has been associated with schizophrenia15 and decreased intellectual capacities in the offspring.48 The most widely proposed mechanism underlying these congenital anomalies is known as the "copy error" hypothesis, first proposed by Penrose.49 After puberty, spermatocytes divide every 16 days, and by the age of 35 years, approximately 540 cell divisions have occurred. As a result, de novo genetic mutations that result from replication errors and defective DNA repair mechanisms are believed to propagate in successive clones of spermatocytes. These mutations accumulate with advancing paternal age and thus help explain how this disorder, which has a large genetic component, can be maintained in the population despite reduced reproduction in affected individuals.