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