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

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

Monday, June 11, 2007

Vaccines and Autism Connection Controversy Heats Up, The Real Connection Between Autism and Vaccines Is Known, Kept Secret Read Below to Discover It





















Many many different combinations of mutations in DNA cause autism/schizophrenia but one cause is certain and that is older paternal age in one generation or another.



Autism Prevention- father your children 23-33 Autism today's term for various neurodevelopmental disorders.MOST AUTISM DUE TO AN OLDER FATHER IN ONE GENERATION OR ANOTHER The Autism Spectrum Disorders, have been devised to confuse any serious discussion of why there is an epidemic. Risk factors for non-familial autism are an older father over 32, autoimmune disorders in family, mother had old dad. Some autism is X-linked and some autosomal recessive. Childhood schizophrenia is now called autism. Older paternal age a major risk factor.


Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders.Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM, McDougle 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.







"The issue is that the older man will have sperm that has undergone more divisions and therefore had more chances to have mutations. The COMPLEXITY of the myelination process makes it more vulnerable to mutations. I am not talking of one specific mutation. Many things could MANIFEST in the myelination or myelin breakdown process because it is so vulnerable - something going slightly wrong will impact it while it will not impact bone growth or the heart. A good example is ApoE4 - whatever else it may affect, it manifests in the reduced capacity of myelin repair and earlier onset of AD." Prenatal and Perinatal Risk Factors for AutismA Review and Integration of Findings Alexander Kolevzon, MD; Raz Gross, MD, MPH; Abraham Reichenberg, PhD Arch Pediatr Adolesc Med. 2007;161:326-333. Objective To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders. Data Sources Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic. ....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.-----------------------------------------------------------------------------------



Thursday, April 12, 2007 AUTISM WAS RARE IN 1988 2-5 PER 10,000 Vol. 45 No. 10, Oct., 1988 Autism and genetics. A decade of research S. L. Smalley, R. F. Asarnow and M. A. Spence Department of Psychiatry, UCLA School of Medicine 90024. The last ten years of research on the genetics of infantile autism were critically reviewed. Epidemiologic findings have shown that autism is a rare disorder with a prevalence of two to five per 10,000, a male-female ratio of 3:1, and an association with mental retardation (66% to 75% of autistic subjects have full-scale IQ scores [70]). Autism is familial, as reflected in an empiric sibling recurrence risk of 3% and pooled monozygotic and dizygotic concordance rates of 64% and 9%, respectively, which are much greater than the population prevalence of 0.02% to 0.05%. Genetic heterogeneity is pronounced with potential genetic subgroups, including autosomal recessive inheritance, X-linked inheritance, and sporadic chromosomal anomalies. Studies of subclinical markers in autism have elucidated potential markers at various levels of phenotypic expression from the DNA to the behavioral level. Linkage and cytogenetic studies point to two chromosome regions as putative markers, 9q34 and Xq27. Results of family studies support a putative biochemical marker, low levels of plasma dopamine-beta-hydroxylase, and a putative cognitive marker, ie, normal visuospatial but low verbal functioning, in autism. The frequency of minor physical anomalies and presence or absence of mental retardation are two dimensions of the physical and behavioral phenotype that may demark etiologically distinct subgroups. Genetic heterogeneity is offered as one explanation of the observed sex difference in the prevalence of autism. Directions for potentially fruitful research should

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Wednesday, April 11, 2007

DO COPY NUMBER VARIATIONS FOUND IN SPORADIC AUTISM EXIST IN THE SPERMATAGONIA OF THE FATHERS? WILL ANYONE LOOK FOR THEM?

Jonathan Sebat and colleagues found the key to sporadic autism and it seems they will fail to follow up and look for the same CNVs in the father's sperm and spermatagonia. ESPECIALLY BE WARNED ABOUT AUTISM IF YOU HAVE AUTOIMMUNE DISORDERS OR YOUR CLOSE RELATIVES DO. DISEASE CAUSING MUTATIONS ACCUMULATE IN SPERM MAKING CELLS BETWEEN 33-35. YOUR RISK IS MUCH GREATER IF THERE IS ANY AUTISM OR OTHER BRAIN RELATED DISORDERS IN THE FAMILY. TRY TO FATHER YOUR BABIES BY 35-40 AT THE LATEST. IF YOU ARE ABLE TO AND YOUNGER THAN 35 CRYOPRESERVE YOUR SEMEN FOR ANY LATER FATHERING OF BABIES.

CANCERS, ALZHEIMER'S, AUTOIMMUNE DISEASES/ALL OF THEM, AUTISM, SCHIZOPHRENIA, AND MANY OTHER DISORDERS CAN BE CREATED DE NOVO IN OFFSPRING THROUGH SPONTANEOUS MUTATIONS IN SPERM MAKING CELLS. THESE MUTATIONS INCREASE WITH INCREASING PATERNAL AGE.



Finding the genes responsible for autism is one of the goals that Sebat and his colleagues have set for their next project. "We'll be screening at least 2,000 families over the next three years using a much higher resolution platform," Sebat said. He added that he hopes the data will provide a better estimate of the frequency of CNV in sporadic autism, as well as a view of a larger array of genes involved than when researchers restricted their studies to inherited cases. "I think this will be a study that really tips the balance in the field towards using technologies that can directly detect mutations, [and] focusing on the majority of cases that are sporadic."

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Monday, April 09, 2007

Dolores Malaspina "It is well established that paternal age is the major source of de novo mutations in the human population"

Seminal findings
We 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).

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Paternal age, size at birth, and size in young adulthood - risk factors for schizophrenia.Rasmussen F.
Child and Adolescent Public Health Epidemiology Group, Department of Public Health Sciences, Karolinska Institute, Norrbacka, SE-17176 Stockholm, Sweden.

It is appropriate to consider schizophrenia a neurodevelopmental disorder

In fully adjusted analyses, the risk of schizophrenia was 4.62 (95% confidence interval : 2.28; 9.36) times higher in subjects whose fathers were >/=50 years old and at time of conception than in subjects whose fathers were 21-24 years old. Growth and development in fetal life and childhood are influencing the risk of schizophrenia in adulthood, but the underlying causal pathways are still unknown. De novo mutations in the germ cells of older fathers may play a causal role in the etiology of some cases of schizophrenia.

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J Money WAS THE FIRST TO WRITE ABOUT THE CONNECTION BETWEEN AUTOIMMUNE DISORDERS AND AUTISM

J Autism Child Schizophr. 1971 Apr-Jun;1(2):146-60. Related Articles, Links
Autism and autoimmune disease: a family study.

Money J, Bobrow NA, Clarke FC.

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Friday, April 06, 2007

PATERNAL AGE DERIVED AUTISM COULD BE PREVENTED THROUGH BANKING ONES SPERM IN ONES MID 20S

The highest risks of autism were found in siblings of children with autism, or Asperger's syndrome and other pervasive developmental disorders (PDDs), with relative risks of 22 and 13, respectively. The relative risk of autism in the child was about twice as high if the mother had been diagnosed with a psychiatric disorder. The risk of autism was associated with increasing degree of urbanisation of the child's place of birth and with increasing paternal, but not maternal, age. An increased relative risk of 1.4 was found if the mother was born outside Europe, and in children of parents who were born in different countries. CONCLUSIONS: The highest risk of autism was found in families with a history of autism, or Asperger's syndrome and other PDDs in siblings, supporting the commonly accepted knowledge that genetic factors are involved in the etiology of autism.

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Thursday, April 05, 2007

OPRAH SPENDS AN ENTIRE HOUR ON AUTISM AND SHE DOESN'T MENTION PATERNAL AGE

I WONDER WHY? WHAT IS THE AGENDA OF ANDY SHIH AND AUTISM SPEAKS?

Dr. Dolores Malaspina in her excellent discussion of neural cogntive disorders and the paternal germ line wrote:

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.


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Maternal and Paternal Age and Risk of Autism Spectrum Disorders
Lisa A. Croen, PhD; Daniel V. Najjar, MS; Bruce Fireman, MA; Judith K. Grether, PhD

Arch Pediatr Adolesc Med. 2007;161:334-340.

Objective To explore the association between maternal and paternal age and risk of autism spectrum disorders (ASDs) in offspring.






Results Risk of ASDs increased significantly with each 10-year increase in maternal age (adjusted RR, 1.31; 95% confidence interval [CI], 1.07-1.62) and paternal age (RR, 1.28; 95% CI, 1.09-1.51). Adjusted RRs for both maternal and paternal age were elevated for children with autistic disorder (maternal age: RR, 1.18; 95% CI, 0.87-1.60; paternal age: RR, 1.34; 95% CI, 1.06-1.69) and children with Asperger disorder or pervasive developmental disorder not otherwise specified (maternal age: RR, 1.45; 95% CI, 1.09-1.93; paternal age: RR, 1.24; 95% CI, 0.99-1.55). Associations with parental age were somewhat stronger for girls than for boys, although sex differences were not statistically significant.

Conclusion Advanced maternal and paternal ages are independently associated with ASD risk.

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Tuesday, April 03, 2007

Low Birthweight and Advancing Paternal Age

Research and Practice
Paternal Age as a Risk Factor for Low Birthweight

Nancy E. Reichman 1* Julien O. Teitler 2


AJPH First Look, published online ahead of print March 29, 2006


©
American Journal of Public Health, 10.2105/AJPH.2005.066324


1 Robert Wood Johnson Medical School
2 Columbia University


Objectives. We examined associations between paternal age and low birthweight in the US urban population.

Methods. Using a population-based sample of 4621 births, we used multiple logistic regression analysis to estimate associations between paternal age and low birthweight, controlling for maternal age, other demographic factors, and the child's gender.

Results. When the child’s gender and the mother's race/ethnicity, birthplace, parity, marital status, and health insurance type were controlled, teenaged fathers were 20% less likely and fathers older than 34 years were 90% more likely than fathers aged 20 to 34 years to have low-birthweight babies. The associations were significant when maternal age was also controlled. No racial/ethnic differences in associations between paternal age and low birthweight were found.

Conclusions. We identified paternal age as an independent risk factor for low birthweight in the US urban population, suggesting that more attention needs to be paid to paternal influences on birth outcomes and to the interactive effects of urban environments and individual risk factors on health.

Key Words: Birth Outcomes, Socioeconomic Factors

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Paternal Age A Major Path To Autism

PRENATAL AND PERINATAL RISK FACTORS FOR AUTISM

A REVIEW and INTEGRATION OF FINDINGS

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


Arch Pediatr Adolesc Med. 2007;161:326-333.

Objective To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders.

Data Sources Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic.

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Main Exposures Parental characteristics and obstetric complications.

Main Outcome Measures Rates of autism and autism spectrum disorders.

Results Seven epidemiological studies were identified that fulfilled inclusion criteria. The parental characteristics associated with an increased risk of autism and autism spectrum disorders included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America. The obstetric conditions that emerged as significant fell into 2 categories: (1) birth weight and duration of gestation and (2) intrapartum hypoxia.

Conclusions Evidence to suggest that parental age and obstetric conditions are associated with an increased risk of autism and autism spectrum disorders is accumulating. Although not proven as independent risk factors for autism, these variables should be examined in future studies that use large, population-based birth cohorts with precise assessments of exposures and potential confounders.


Author Affiliations: Department of Psychiatry, Mount Sinai School of Medicine (Drs Kolevzon and Reichenberg), Department of Epidemiology, Mailman School of Public Health, Columbia University (Dr Gross), and Department of Psychiatry, College of Physicians and Surgeons, Columbia University (Dr Gross), New York, NY; Unit of Mental Health Epidemiology, The Gertner Institute of Epidemiology and Health Policy Research, Tel Hashomer, Israel (Dr Gross); and Department of Psychological Medicine, Institute of Psychiatry, King's College, London, England (Dr Reichenberg).



This study does not differeniate between familial and non-familial autism.

Low Birthweight and advancing paternal age have been found to go together.

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Saturday, March 31, 2007

FATHER'S AGE AND DEVASTATING DISORDERS

"Until recently, health care professionals have focused almost exclusively on the mother's age as a risk factor for health problems in the child. But we now know that the father's age also adds to the risk of potentially devastating diseases. And there is no practical way to detect these illnesses during pregnancy. For those weighing the risks, the decision can be wrenching. Adoption and in some instances a sperm donation may be acceptable alternatives to older fathers wanting to build a healthy family."

Michael Craig Miller, M.D. is Editor in Chief of the Harvard Mental Health Letter. He is also associate physician at Beth Israel Deaconess Medical Center and assistant professor at Harvard Medical School. He has been practicing psychiatry for more than 25 years and teaches in the Harvard Longwood Psychiatry Residency Program.

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Friday, March 30, 2007

Later Paternal Age Can Influence Neural Functioning

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.

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