Children whose fathers were over 33 were 1.8 times more likely to have autism than those fathers were under 29.

Father age link to autism in children
Older fathers are almost twice as likely to have autistic children as younger men, research has found.

By Rebecca Smith, Medical Editor
Last Updated: 12:31AM BST 01 Oct 2008

A small study of children with autism spectrum disorder, the umbrella term for a range of similar conditions, found they were more likely to have been fathered by men over the age of 33.

There was no link with the condition and the mother's age, the Japanese study found.

The research involved 84 children with high-functioning autism spectrum disorders, meaning they had the social impairments of the condition but had normal intelligence, and 208 children without the disorder.

Children whose fathers were over 33 were 1.8 times more likely to have autism than those fathers were under 29. Men who fathered children between the age of 29 and 32 were 30 per cent more likely to have an autistic child.

The research is published in the British Journal of Psychiatry.

This is the first study to explore the effect of paternal age on the risk of high-functioning autistic spectrum disorder. Its findings correspond with previous studies which have shown a link between older fathers and a low IQ in children.

Benet Middleton, director of communications at The National Autistic Society, said: "The causes of autism are still being investigated. Many experts believe that the pattern of behaviour from which autism is diagnosed may not result from a single cause. Autism affects around one in 100 people in the UK and does not solely affect children of older parents.

"Members of the NAS are made up of parents of children from a variety of ages and backgrounds; in addition there is evidence to suggest that complex genetic factors are responsible for some forms of autism."

Some experts have argued that the measles, mumps and rubella vaccination is linked to the development of autism but this has been widely discredited and other studies have failed to find any link.

Analysis of copy number variation using quantitative interspecies competitive PCR

Nucleic Acids Research Advance Access originally published online on August 12, 2008
Nucleic Acids Research 2008 36(17):e112; doi:10.1093/nar/gkn495


Nucleic Acids Research, 2008, Vol. 36, No. 17 e112
© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Methods Online


Analysis of copy number variation using quantitative interspecies competitive PCR
Nigel M. Williams1,*, Hywel Williams1, Elisa Majounie1, Nadine Norton1, Beate Glaser1, Huw R. Morris2, Michael J. Owen1 and Michael C. O’Donovan1
1Department of Psychological Medicine, Wales School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN and 2Department of Neurology, Ophthalmology and Audiological Medicine, Wales School of Medicine, Cardiff University, Cardiff, UK

*To whom correspondence should be addressed. Tel: +44(0)2920 687070; Fax: +44(0)2920 687068; Email: williamsnm@cf.ac.uk

Received May 23, 2008. Revised July 17, 2008. Accepted July 17, 2008.

Over recent years small submicroscopic DNA copy-number variants (CNVs) have been highlighted as an important source of variation in the human genome, human phenotypic diversity and disease susceptibility. Consequently, there is a pressing need for the development of methods that allow the efficient, accurate and cheap measurement of genomic copy number polymorphisms in clinical cohorts. We have developed a simple competitive PCR based method to determine DNA copy number which uses the entire genome of a single chimpanzee as a competitor thus eliminating the requirement for competitive sequences to be synthesized for each assay. This results in the requirement for only a single reference sample for all assays and dramatically increases the potential for large numbers of loci to be analysed in multiplex. In this study we establish proof of concept by accurately detecting previously characterized mutations at the PARK2 locus and then demonstrating the potential of quantitative interspecies competitive PCR (qicPCR) to accurately genotype CNVs in association studies by analysing chromosome 22q11 deletions in a sample of previously characterized patients and normal controls.

Paternal Age a major cause of new disorders in the population

Am J Med Genet A. 2008 Sep 15;146A(18):2385-9. Links
The population-based prevalence of achondroplasia and thanatophoric dysplasia in selected regions of the US.Waller DK, Correa A, Vo TM, Wang Y, Hobbs C, Langlois PH, Pearson K, Romitti PA, Shaw GM, Hecht JT.
Houston Health Science Center, The University of Texas, Houston, Texas 77030, USA. kim.waller@uth.tmc.edu

There have been no large population-based studies of the prevalence of achondroplasia and thanatophroic dysplasia in the United States. This study compared data from seven population-based birth defects monitoring programs in the United States. We also present data on the association between older paternal age and these birth defects, which has been described in earlier studies. The prevalence of achondroplasia ranged from 0.36 to 0.60 per 10,000 livebirths (1/27,780-1/16,670 livebirths). The prevalence of thanatophoric dysplasia ranged from 0.21 to 0.30 per 10,000 livebirths (1/33,330-1/47,620 livebirths). In Texas, fathers that were 25-29, 30-34, 35-39, and > or =40 years of age had significantly increased rates of de novo achondroplasia among their offspring compared with younger fathers. The adjusted prevalence odds ratios were 2.8 (95% CI; 1.2, 6.7), 2.8 (95% CI; 1.0, 7.6), 4.9 (95% CI; 1.7, 14.3), and 5.0 (95% CI; 1.5, 16.1), respectively. Using the same age categories, the crude prevalence odds ratios for de novo cases of thanatophoric dysplasia in Texas were 5.8 (95% CI; 1.7, 9.8), 3.9 (95% CI; 1.1, 6.7), 6.1 (95% CI; 1.6, 10.6), and 10.2 (95% CI; 2.6, 17.8), respectively. These data suggest that thanatophoric dysplasia is one-third to one-half as frequent as achondroplasia. The differences in the prevalence of these conditions across monitoring programs were consistent with random fluctuation. Birth defects monitoring programs may be a good source of ascertainment for population-based studies of achondroplasia and thanatophoric dysplasia, provided that diagnoses are confirmed by review of medical records. Copyright 2008 Wiley-Liss, Inc.

PMID: 18698630 [PubMed - indexed for MEDLINE]

Related ArticlesEffect of paternal age in achondroplasia, thanatophoric dysplasia, and osteogenesis imperfecta. [Am J Med Genet. 1995] The birth prevalence rates for the skeletal dysplasias. [J Med Genet. 1986] Thanatophoric dysplasia: an autosomal dominant condition? [Am J Med Genet. 1988] Association of paternal age with prevalence of selected birth defects. [Birth Defects Res A Clin Mol Teratol. 2007] Prevalence of spina bifida at birth--United States, 1983-1990: a comparison of two surveillance systems. [MMWR CDC Surveill Summ. 1996] » See all Related Articles...

Bipolar disorder: What you need to know

Bipolar disorder: What you need to know
By NIH
Sep 3, 2008 - 8:08:23 AM





Older men may be at risk of having children with bipolar disorder, according to a study published in the Sep. 2008 issue of Archives of General Psychiatry.


Emma M. Frans, M.Med.Sc., of the Karolinska Institutet, Stockholm, Sweden, and colleagues came to the conclusion after they compared 13,428 patients in Swedish registers with a diagnosis of bipolar disorder with those with sex and age matched, but without the condition.


They found the older an individual's father, the more likely he or she was to develop bipolar disorder. An increase risk was observed among children who were fathered by men age 29 or older.


"After controlling for parity [number of children], maternal age, socioeconomic status and family history of psychotic disorders, the offspring of men 55 years and older were 1.37 times more likely to be diagnosed as having bipolar disorder than the offspring of men aged 20 to 24 years," the authors wrote.


The ages of older mothers also had an effect on the risk, which was not as significant as the ages of older fathers. There was no association between the mother's age and early bipolar disorder (diagnosed before the age of 20). But the association existed for the father's age.


The researchers explained that de novo mutations occur in germ cell replications while women's eggs do not have as many replications and mutations may not be as common in eggs. Because of this, maternal age does not affect the risk of bipolar disorder in children as much as the father's age.


Few risk factors have been identified for bipolar disorder.


Older paternal age has been linked in previous studies to higher risk of complex neurodevelopmental disorders, including schizophrenia and autism, according to the press release by JAMA and Archives Journals.

Bipolar risk rises with father's age

Bipolar risk rises with father's age


Adam Cresswell, Health editor September 02, 2008
CHILDREN of older fathers are more likely to have bipolar disorder - a discovery that could explain the increasing numbers of people diagnosed with the condition.
Compared with the offspring of fathers aged 20 to 24, people whose fathers were aged 55 or over at the time of their birth are 37 per cent more likely to be diagnosed with bipolar disorder.
Children of fathers aged 30-34 had an 11 per cent increased risk of bipolar, while children of fathers aged 40-44 had a 15 per cent increased risk.
Having an older mother also increased the risk, but the effect was far less pronounced.
The research is based on nearly 13,500 Swedish people with bipolar disorder, a severe mood disorder that causes repeated peaks of euphoria and hyperactivity followed by troughs of depression.
The authors of the study, published in the US journal Archives of General Psychiatry, said paternal age was already known to be linked to other developmental disorders such as schizophrenia and autism. They suggested the findings might reflect the increased risk of DNA mutations in sperm cells, which, unlike a woman's eggs, undergo hundreds of replication cycles in which errors can occur.
Australian psychiatrist Gordon Parker, executive director of the Black Dog Institute, said the findings were important, and might explain why diagnoses of bipolar disorder had been rising.
In 1992, according to the Australian Bureau of Statistics, 35 per cent of fathers of children aged 0-14 were under 35. This fell to 26 per cent by 2003. The proportion of fathers aged 45 and over rose from 19 per cent in 1992 to 25 per cent in 2003.
However, Professor Parker said as the existing risk of bipolar disorder was thought to be between 4 and 6 per cent, the effect of the increases remained slight.
"I would hate to see any concern in the community that people shouldn't have babies because they have bipolar disorder in their family," he said.
"If you have bipolar disorder in your family, you are more likely to end up in Who's Who, because high intelligence and creativity is over-represented in families with bipolar disorder."