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.

Friday, May 25, 2007

Children Born to Couples who have IVF are more likely to be autistic, have cancers, cerebral palsy and mental retardation

THE ARTICLE DOESN'T POINT OUT THAT THIS IS DUE TO THE AGE OF THE FATHER IN MOST CASES


Children born
after IVF treatment 'face higher health risks'


Ian Sample in New Orleans
Thursday October 26, 2006
The Guardian



Children born to couples who have undergone fertility treatment are more likely to be diagnosed with autism, cancer and other disorders such as cerebral palsy and mental retardation, researchers claimed yesterday.
The higher risk to child health is believed to be caused by medical problems in the parents, such as diabetes and hypertension, damaging the child in the womb, but doctors conducting the study said IVF and other fertility treatments may also play a role. Medical records of children born after their parents sought fertility treatment showed they were four times more likely to have autism than those born to fertile parents. Childhood cancers including leukaemia and brain tumours also rose.

The risk of more minor problems, such as attention deficit hyperactivity disorder, rose by 40%, and other medical conditions affecting hearing and sight nearly doubled. Children had a 30% higher chance of being admitted to neonatal intensive care units and to stay in hospital for more than three days if they were born following fertility treatment, the study found.

The researchers stressed the figures represent relative risks. In July researchers at Guy's and St Thomas' hospital in London reported the prevalence of autism to be 0.39% in the general population, a figure that will include some children born to parents aided by fertility treatment. A fourfold rise in the risk of autism would see a child's chances of having the condition increase to 1.56%.

Mary Croughan at the University of California in San Francisco studied 2,000 women who either gave birth naturally after a long period of infertility, or conceived after a variety of fertility treatments, and compared them with 2,000 fertile mothers who gave birth between 1994 and 1998. More than 19,000 medical records were used to build up a picture of the women's pregnancies and deliveries and the health of their children up to six years of age.

The researchers found infertile women had more complications such as pre-term labour and pre-eclampsia, more delivery difficulties and caesarean sections. Children born to infertile women were 20% more likely to have low birth weights and were twice as likely to show evidence of poor growth in the womb. Speaking at the American Association for Reproductive Medicine (ASRM) conference in New Orleans, Dr Croughan said that medical conditions more common in infertile couples may be to blame for the rise in childhood health problems. She said: "The vast majority of children born to infertile couples are healthy, but if a couple has any risk factors that could lead to a child not being born healthy, then those should of course be taken into consideration."

Clare Brown, chief executive of Infertility Network UK, said "continual research" was needed to ensure "treatment is safe for couples and potential children".

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Thursday, May 24, 2007

PATERNAL AGE EFFECT IN SOME CEREBRAL PALSY- ATHETOID/DYSTONIC - HEMIPLEGIC CEREBRAL PALSY

1: J Med Genet. 1993 Jan;30(1):44-6. Links
Parental age, genetic mutation, and cerebral palsy.Fletcher NA, Foley J.
Department of Neurological Sciences, St Bartholomew's Hospital, London.

Parental age and birth order were studied in 251 patients with cerebral palsy. No parental age or birth order effects were observed in spastic quadriplegia or diplegia, but a paternal age effect was detected in those with athetoid/dystonic cerebral palsy and congenital hemiplegia. These observations indicate that some cases of athetoid/dystonic or hemiplegic cerebral palsy might arise by fresh dominant genetic mutation.






Dev Med Child Neurol. 1996 Oct;38(10):873-80. Links
Comment in:
Dev Med Child Neurol. 1996 Oct;38(10):871-2.
Dyskinetic cerebral palsy: a clinical and genetic study.Fletcher NA, Marsden CD.
Walton Centre for Neurology and Neurosurgery, Liverpool, UK.


The clinical features and family histories of 20 adults with dyskinetic cerebral palsy from 20 families were studied. The majority of the patients showed progressive neurological deterioration in adult life. In only three did the condition stabilise by 10 years of age and in seven there was deterioration after the age of 30. Two patients developed a secondary cervical spondylotic myelopathy. Four patients had affected relatives and there were similar proportions of affected parents and siblings. The family data suggest genetic heterogeneity with autosomal recessive and The existence of an X-linked form cannot be excluded, and the demonstration of an increased paternal age effect among single cases suggests that some of these may arise because of fresh dominant genetic mutation.dominant variants. PMID: 8870609 [PubMed - indexed for MEDLINE]

1: Dev Med Child Neurol. 1977 Apr;19(2):179-91. Links
Recurrence risks in families of children with symmetrical spasticity.Bundey S
, Griffiths MI.
This study was undertaken to evaluate the recurrence risks for sibs of patients with symmetrical spasticity (either quadriplegia or diplegia) in the absence of factors known to cause spastic cerebral palsy (e.g. pre-term birth, perinatal hypoxia). Among 669 children in the West Midlands with spastic cerebral palsy, 24 had symmetrical spasticity and normal birth histories. This group was clinically and genetically heterogenous. Among their 55 sibs, six had a spastic disorder similar to that in the index patient, and one further sib, who had died young, had been mentally retarded. Of particular interest were two families with an autosomal recessive condition of post-natal microcephaly, myoclonic epilepsy and spastic quadriplegia; and one family, and possibly a sporadic case of X-linked athetoid cerebral palsy. The recurrence risk in this series of approximately 1 in 9 suggests that about half the children with symmetrical spastic cerebral palsy and a normal birth history may have a recessive condition.

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