Fathers’ Age as Contributor to Risk for Autism
Leslie Feldman
The average age of fatherhood is increasing in the US and in Western Europe. Some research shows that offspring of older fathers are at increased risk for diseases and conditions (Bray et al., 2006). Some experts predict an upswing in cases of schizophrenia will accompany the increasing average paternal age. [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 (Malaspina et al., 2006).] Approximately 25-33% of all cases of schizophrenia may be due to the father’s age at conception, according to Malaspina (2006). Malaspina sees a connection between advancing paternal age and neural functioning difficulties in people with autism and with schizophrenia. According to Tarin et al. (1998), there are well over 30 known conditions that the offspring of older fathers are more at risk for (see chart on paternal aging in the linked article).
The diagnosis of autism is increasing in the US and elsewhere (Centers for Disease Control, 2006). In a population study of 1990 through 1999, a total of 669,995 children, Atladottir and colleagues (2007) reported increased diagnoses of autism, Torrette Syndrome, and hyperkinetic disorder. Is there a connection between increased cases of disorders such as autism and increased average paternal age? Psychiatrist Michael Craig Miller (2006), editor of the Harvard Mental Health Letter is convinced there is. Although a connection between the two would be corelational (not causal), the relationship encourages examination of the possibility that something related to paternal age (e.g. mutations in gametes) may contribute to the occurrence of autism. If there is a potential causal relationship, the new study by the Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) Network would provide a valuable opportunity to test the hypothesis.
Observations of a connection between advanced paternal age and difficulties for offspring go way back. Earlier research looking for a link between maternal age and autism also found the average paternal age (34) was much higher than the average age in the general population (Gillberg, 1980). Geneticist James F. Crow (1997) cites Wilhelm Weinberg (1862-1937) as noticing, during his 42 years of medical practice and helping 3,500 births, that the mutation rate might be a function of paternal age. Crow said, the evidence suggested that the greatest mutational health hazard in the population is fertile old men.
A study by Reichenberg et al. (2006) found a strong connection between cases of autism and advancing paternal age. Reichenberg and colleagues, who found more autism as paternal age increased, also found that the ratio of girls to boys in this cohort was 1:1, suggesting that this was a special subset of autism, maybe de novo rather than familial autism.
What might be the mechanism that produces higher rates of disorders among children of older fathers? The DNA in a 20 year-old male has been copied approximately100 times but in a 50 year-old father it has been copied over 800 times. Singh and colleagues (2003) studied differences in the sperm of older and younger men. Men over age 35 have sperm with lower motility and more highly damaged DNA in the form of double-strand breaks. The older group also had fewer apoptotic cells, an important discovery. (Apoptosis is form of cell death that protects the parent organism from problems or that permits differentiation, as in resorption of a tadpole’s tail.) A really key factor that differentiates sperm from other cells in the body is that they do not repair their DNA damage, as most other cells do. As a result, the only way to avoid passing DNA damage to a child is for the damaged cells to undergo apoptosis, a process that the study indicates declines with age. Singh is quoted in Science Blog (Sullivan, 2002) as explaining that, “In older men, the sperm are accumulating more damage, and those severely damaged sperm are not being eliminated.”
Sources
The following list of sources is for works cited in this document or for other studies finding a connection between age of fathers at conception and various disorders. Access to some of the Web-based resources may be limited because of the policies of the publishers.
Atladottir, H. O., Parner, E. T., Schendel, D., Dalsgaard, S., Thomsen, P. H., & Thorsen, P. (2007). Time trends in reported diagnoses of childhood neuropsychiatric disorders. Arch Pediatr Adolesc Med., 161, 193-198. Link
Brown et al. (2002): Paternal age and risk of schizophrenia in adult offspring. Am J Psychiatry, 159, 1528-1533. Link
Bray, I., Gunnell, D., & Smith, G. D. (2006). Advanced paternal age: How old is too old? Journal of Epidemiology and Community Health, 60, 851-853. Link
Burd et al., (1999). Prenatal and perinatal risk factors for autism. J. Perinatal. Med., 27, 441-450. Link
Byrne, M., Agerbo, E., Ewald, H., Easton, W. W., & Mortensen, P. D. (2003). Parental age and risk of schizophrenia, A case control study. Arch Gen Psychiatry, 60, 673-678. Link
Centers for Disease Control, (2006). How common are Autism Spectrum Disorders (ASD)? Link
Centers for Disease Control. (2002). Prevalence of the Autism Spectrum Disorders (ASDs) in multiple areas of the United States, 2000 and 2002. Atlanta, GA: Author. Link
Crow, J. F. (1997). The high spontaneous mutation rate: Is it a health risk? Proc. Natl. Acad. Sci. USA, 94, 8380-8386. Link
Dalman, C., & Allebeck, D. (2002). Paternal age and schizophrenia: Further support for an association. Am J Psychiatry, 159, 1591-1592. Link
Gillberg, C. (1980). Maternal age and infantile autism. J. Autism and Developmental Disorders, 10, 293-297. Link
Lauritsen M. B., Pedersen, C. B., & Mortensen, P. B. (2005) Effect of familial risk factors and place of birth on the risk of autism: a nationwide register-based study. J. Child Psychology and Psychiatry, 46, 963-971. Link
Miller, M. C. (2006) A new key to Autism. Aetna IntelliHealth, September 25. Link
Malaspina, D., et al. (2001): Advancing paternal age and the risk of schizophrenia. Arch Gen Psychiatry, 58, 361-367. Link
Malaspina, D. (2006). In session with Dolores Malaspina, MD, MSPH: Impact of childhood trauma on psychiatric illness (interview by N. Sussman). Primary Psychiatry, 13(7), 33-36. Link
Malaspina, D. (2006). Schizophrenia risk and the paternal germ line. Schizophrenia Research Forum. Link
Rasmussen, F. (2006) Paternal age, size at birth, size in young adulthood&mdashrisk factors for schizophrenia. Eur Journal of Endocrinology, 155 Suppl 1:S65-69. Link
Reichenburg, A., Gross, R., Weiser, M. Bresnahan, M., Silverman, J. Harlap, S., et al. (2006). Advancing paternal age and autism. Arch Gen Psychiatry, 63, 1026-1032. Link
Singh, N. P., Muller, C. H., & Burger, R. E. (2003). Effects of age on DNA double-strand breaks and apoptosis in human sperm. Fertility and Sterility, 80, 1420-1430. Link
Sipos, A., Rasmussen, R., Harrison, G., Tynelius, P., Lews, G., Leon, D. A., et al. (2004). Paternal age and schizophrenia: A population based cohort study. BMJ, 329, 1070. Link
Sullivan, B. J. (2002). Research reveals a cellular basis for a male biological clock. Science Blog, 2002-11-25 22:31. Link
Tarin, J. J., Brines, J., & Cano, A. (1998). Long-term effects of delayed parenthood. Human Reproduction, 13, 2371-2376. Link
Tsuchiya, K. J., Takagai, S., Kawai, M., Matsumoto, H., Nakamura, K., Minabe, Y., et al. (2005). Advanced paternal age associated with an elevated risk for schizophrenia in offspring in a Japanese population. Schizophrenia Research, 76, 337-342. Link
Wohl, M. & Gorwood, P. (2006). Paternal ages below or above 35 are associated with a different risk for schizophrenia in offspring. Eur. Psychiatry, Dec 1 [Epub ahead of print]. Link
Zammit, S., Allebeck, P., Dalman, C., Lundgerg, I., Hemming, T., Owen, M. J., et al. (2003). Paternal age and risk for schizophrenia. Br. J. Psychiatry, 183, 405-408. Link
http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5601a1.htm
February 9, 2007 / 56(SS01);1-11
Prevalence of Autism Spectrum Disorders — Autism and Developmental Disabilities Monitoring Network, Six Sites, United States, 2000
Corresponding author: Catherine Rice, PhD, Division of Birth Defects and Developmental Disabilities, National Center on Birth Defects and Developmental Disabilities, CDC, 1600 Clifton Road, N.E., MS E-86, Atlanta, GA 30333. Telephone: 404-498-3860; Fax: 404-498-3550; E-mail: crice@cdc.gov.
http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5601a1.htm
Dr. Narendra P.Singh suggested that I elaborate about what happens when the DNA in the primitive sperm making cells divides hundreds and hundreds of times as men age.
I will try.
Mutations arise with each cell division and the mutation rate increases with age. There are base substitutions and deletions and other copying errors. In a man of 45 there have been 770 cell divisions ancestral to a sperm. See James F. Crow’s paper, “The high spontaneous mutation rate: Is it a health risk? in the sources section of the paper.
There is an interesting discussion on the subject advancing paternal age on Salon.com http://www.salon.com/mwt/broadsheet/2007/02/27/clocks/index.html
My Father was 42 when I was born. Did he make a mistake? I THINK NOT. I am very healthy and have no health problems. Face it people, older dads will exist no matter what the so called experts in the field of medicine contend. I have learned from experience that Doctors are to be trusted to a rather limited extent.
Hi, Rihard. Thanks for taking the time to drop a comment. You’ve illustrated a good point. The research about paternal age doesn’t mean that every person sired by an elder father will have problems. It simply means that the chance of problems increases. That’s the nature of “risk.” Not every person who drives at 80 mph (~130 kph) while talking on a cell phone, for example, will have an accident. However, the risk of an accident is greater when a driver does so. It’s good that you reminded us of this difference.
Try this site for the 2000 and 2002 report on the Prevalence of Autism Spectrum Disorders…..
http://www.cdc.gov/mmwr/pdf/ss/ss5601.pdf
http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5601a2.htm
CDC Study 2002 html
Thank you John for your response to what I had earlier posted and I truly appreciate your positive feedback. You made many excellent points and forgive me for having previously misspelled my own name! I left out the C in Richard. I must admit that I was a bit wound up, and perhaps a bit defensive earlier.
A pre-publication abstract of a paper on Newborns at Risk for Special Education Placement: A population study was just released by Pub Med:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17142012&query_hl=7&itool=pubmed_docsu
CONCLUSIONS: Among the known risk factors for learning disabilities (LD), our study highlighted the importance of a higher paternal age and a lower SES especially in the familial forms of LD.
OOps wrong abstract. Try this instead.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17346999&query_hl=1&itool=pubmed_docsum
Some more TV coverage of the the paternal age relationship to risk of schizophrenia and autism in offspring.
http://allday.msnbc.msn.com/archive/2007/03/13/88225.aspx
http://video.msn.com/v/us/msnbc.htm?g=b6bf1a0b-bdc2-4414-b7bd-553ff4e55fc9
Very important news today from scientists in Cold Springs Harbor
CSHL Scientists Confirm Genetic Distinction Between Heritable and Sporadic Cases of Autism
Science Publishes ‘Strong association of de novo copy number variation with
autism’
COLD SPRING HARBOR, N.Y., March 15 /PRNewswire/ — Autism is thought to
be the most highly heritable of all neuro-psychiatric disorders. Yet, most
cases of this childhood developmental disorder that severely affects social
interaction and communication are “sporadic” and come with no family history.
“Sporadic autism is the more common form of the disease, and even the
inherited form might derive from a mutation that occurred in a parent or
grandparent,” explained Wigler. Using a high-resolution method for
analyzing DNA called microarray technology, the researchers found that
spontaneous copy number mutations occur primarily in sporadic cases. The
study reports that these new mutations were found less frequently in
families that have more than one child with autism.
For the complete press release look here:
http://www.prnewswire.com/cgi-bin/stories.pl?ACCT=104&STORY=/www/story/03-15-2007/0004547169&EDATE=
history. New research, led by Cold Spring Harbor Laboratory (CSHL)
comment:
Spontaneous Mutations and Autism
by Leslie Feldman
[Comment posted 2007-03-16 03:51:16]
I have researched, in the existing scientific literature, the hypothesis that de novo autism is caused by the increasing spontaneous mutations in sperms cells and ancestral sperm making cells of ageing men.
http://ebdblog.com/paternalage/
There could also be other causes of mutations in the spermatagonia of men such a radiation. Mutations in sperm have been found to increase with age in prior research that is not included in my paper such as:
http://www.sciencedaily.com/releases/2002/10/021018080014.htm
“It makes sense that the mutations causing these diseases would occur more frequently in older men, and indeed that’s what we saw for Apert syndrome,” says Ethylin Jabs, M.D., director of the Center for Craniofacial Development and Disorders at Johns Hopkins.
Importantly, disorders linked to advancing paternal age begin to increase rapidly at about the same time as maternal risks increase — age 33 to 35. Until now, the only evidence for paternal age effects has come from determining how many children with these dise\ases are born to fathers of various ages….”
http://www.the-scientist.com/news/home/52940/
The Scientist had news on the Copy Number Linked to Autism
Some new research on the effect of age on sperm DNA:
Hum Reprod. 2007 Jan;22(1):180-7. Epub 2006 Oct 19. Links
The effects of male age on sperm DNA damage in healthy non-smokers.Schmid TE, Eskenazi B, Baumgartner A, Marchetti F, Young S, Weldon R, Anderson D, Wyrobek AJ.
Lawrence Livermore National Laboratory, Livermore, CA, USA.
BACKGROUND: The trend for men to have children at older age raises concerns that advancing age may increase the production of genetically defective sperm, increasing the risks of transmitting germ-line mutations. METHODS: We investigated the associations between male age and sperm DNA damage and the influence of several lifestyle factors ….
CONCLUSIONS: Our findings indicate that (i) older men have increased sperm DNA damage associated with alkali-labile sites or single-strand DNA breaks and (ii) independent of age, men with substantial daily caffeine consumption have increased sperm DNA damage associated with double-strand DNA breaks. DNA damage in sperm can be converted to chromosomal aberrations and gene mutations after fertilization, increasing the risks of developmental defects and genetic diseases among offspring.
PMID: 17053003 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17053003&itool=pubmed_DocSum
A 2002 article on a presentation by Ethylin Wang Jabs MD on Disease Causing Sperm Mutations Increasing With Age in Aperts Syndrome
http://www.sciencedaily.com/releases/2002/10/021018080014.htm
“It makes sense that the mutations causing these diseases would occur more frequently in older men, and indeed that’s what we saw for Apert syndrome,” says Ethylin Jabs, M.D., director of the Center for Craniofacial Development and Disorders at Johns Hopkins.
Importantly, disorders linked to advancing paternal age begin to increase rapidly at about the same time as maternal risks increase — age 33 to 35. Until now, the only evidence for paternal age effects has come from determining how many children with these diseases are born to fathers of various ages.
To obtain the first genetic explanation for these effects, the scientists studied sperm from about 60 men of various ages and looked for two genetic changes responsible for 99 percent of the cases of Apert syndrome. They found that men over 50 were, on average, three times as likely as men under 30 to have sperm with at least one of these changes. The mutations were not more common in blood samples as men aged.
The scientists say it’s likely that the number of cell divisions that go into making a sperm plays a large role in the link between Apert syndrome and paternal age, and represents a fundamental difference between how aging egg and sperm can impact the health of a child.”
Richard wrote:
No prob. You’re welcome.
I’m also reminded that there is another caution about risk factors worth noting: Even though a risk factor might indicate greater likelihood of a given outcome, the reverse does not necessarily hold. For example, using the present topics as an illustration, even if older paternity is associated with higher risk of Autism, that does not mean that a child with Autism must have been sired by an elder father.
If some p ==> q, not all q are caused by p.
Wheeee!
I recently have come across the work of Dr. Maurice Auroux is studying the effects on paternal age on the cerebral function of man and of rat.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8515089&query_hl=1&itool=pubmed_docsumThe quality of conceptus as a function of father’s age][Article in French]
Auroux M.
Biologie de la Reproduction et du Developpement, CHU Bicetre, Le Kremlin-Bicetre.
Testicular ageing affects at the same time the individual and his lineage. In the individual, vascular, endocrine, blood testis barrier and Sertoli cells changes because of age lead a decrease of spermatozoa number and an alteration in their form and motility. These changes lead a gradual decrease of fertility. In the progeny, paternal ageing is responsible for new dominant autosomic mutations which themselves cause different malformations and perhaps for certain chromosome X linked recessive mutations. Moreover, in animal and man, paternal ageing seems responsible for a gradual lowering in the level of progeny cerebral functions. In man, very youthful age was also related to these effects. Maternal age did not appear to play a part in this event. On the whole, these results pose the problem of the optimum age for fatherhood.
PMID: 8515089 [PubMed - indexed for MEDLINE]
This is another abstract of a relevant paper by Dr. Auroux from 1992.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12286001&query_hl=1&itool=pubmed_docsum
: Contracept Fertil Sex (Paris). 1992 Oct;20(10):942-5. Links
[Age of the father and development potential][Article in French]
Auroux MR.
PIP: Testicular aging, like ovarian aging, concerns not just the individual but also the quality of the gametes and hence of the offspring. The 1st signs of testicular aging appear early. Beginning around the age of 30, the vascularization begins to thin, with a progressive decline in the density of the capillaries. The membrane of the seminiferous tubules, an essential element of the hematotesticular barrier, begins to thicken and the number of Sertoli cells begins to decline. Endocrine effects usually appear a decade later, but individual variations are considerable. These modifications are accompanied by a slow decline in the number of sperm and alterations in their morphology and motility. Male fertility declines progressively with age. The quality of the gametes is lower among very young males and increases to a maximum at about age 30. Paternal aging may be responsible for well-defined syndromes in the offspring. Paternal aging has long been recognized as a factor in dominant autosomal mutations causing macroscopic malformations such as achondroplasia, Apert syndrome, Marfan’s syndrome, fibrodysplasia ossificans progressiva, and others. The frequency of each disorder is very low, but the total number of recognized disorders of this type exceeds 1000, multiplying the risks so that the .3-.5% risk of anomalies due to paternal aging after 40 is comparable to the risk of trisomy 21 for women aged 35-40. Dominant autosomal mutations can also be responsible for less marked anomalies such as Recklinghausen’s neurofibromatosis. Some authors believe that recessive mutations linked to the X chromosome causing hemophilia or Duchenne muscular dystrophy can also result from paternal aging. Some evidence suggests that for a given maternal age, paternal age results in subtle and continuous declines in cerebral functioning. A psychometric study of 1700 military recruits in Nancy, France, in 1985 who were 18 years old showed that sons of very young fathers and of older fathers did less well on the tests. The study is being repeated on 12,000 recruits in the Paris area in 1989-90 to verify the results. Efforts will be made to separate the influence of socioeconomic status and birth order on the results.
PMID: 12286001 [PubMed - indexed for MEDLINE]
1: Contracept Fertil Sex. 1993 May;21(5):382-5. Links
[Age of the father and development][Article in French]
Auroux M.
Biologie de la Reproduction et du Developpement, CHU Bicetre.
Testicular ageing affects at the same time the individual and his lineage. In the individual, vascular, endocrine, blood testis barrier and Sertoli cells changes because of age lead a decrease of spermatozoa number and an alteration in their
form and motility. These changes lead a gradual decrease of fertility. In the progeny, paternal ageing is responsible for
Recklinghausen disease, Marfan Syndrome etc. and perhaps for certain chromosome X linked recessive mutations as Duchenne myopathy or hemophily A. Moreover, in animal and man, paternal ageing seems responsible for a gradual lowering in the level of progeny cerebral functions. In man, very youthful age is also related to these effects. Thus, the curve corresponding to this phenomenon presents an inverted U-Shape, of which the top corresponds to about thirty years of paternal age. Maternal age does not appear to play a part in this event. On the whole, these results pose the problem of the optimum age for fatherhood.
PMID: 7920923 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7920923&query_hl=1&itool=pubmed_docsum
I would like to add one more paper by Dr. Maurice Auroux:
: Contracept Fertil Sex (Paris). 1991 Nov;19(11):945-9. Links
[Evolution of male fertility as a function of age and risks in progeny][Article in French]
Auroux MR.
PIP: Testicular aging starts form age 30 with progressive deterioration of vascularization, the density of capillaries, the diminution of the efficacy of the blood-testis barrier, the aging of Sertoli cells, which results in fall of production of androgen-binding protein. These changes lead to a slow reduction of the number of spermatozoa, although it is their quality that is responsible for male fertility. Analysis of the number, morphology, and mobility of spermatozoa of men aged 25-59 showed that the quality varies depending on age: the maximum values are reached between age 25 and 35, decreasing afterwards. The aging finally results in a degradation of the number and especially in the quality of spermatozoa, which is not satisfactory in individuals of very young age either. Whether male of female, parental aging poses a problem, because fertility diminishes and the risk of anomalies of the conceptus increase with the age of parents. It has been demonstrated that the new, autosomal dominant mutations responsible for fetal deaths or the numerous malformation syndromes, such as achondroplasia, Apert’s disease, ossifying fibrodysplasia, and Marfan’s syndrome, may be linked to paternal aging. The frequency of each of these syndromes is very low: 15-28 cases per million births for achondroplasia. Also, the frequency of anomalies attributable to paternal aging after the 40s reaches .3-.5% of births. Neurofibromatosis or von Recklinghausen’s disease, hemophilia A, the myopathy of Duchenne, schizophrenia, and the performance of 18-year-old males on psychometric tests have been associated with paternal aging. The aging of gonads cannot be prevented, but one could avoid the consequences of the aging of gametes by avoiding having children after 35 or 40 years of age. This has been recommended to women for about 15 years, and perhaps should also be recommended to men.
PMID: 12284763 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12284763&query_hl=1&itool=pubmed_DocSum
I am gonna buy that tank and freeze my sperm. Maybe I’ll get an extra big one and throw a side of beef in there also.
This is purely anecdotal, but the special ed kids in my district tend to:
1. Have very young parents. (Do some young parents have “bad genes” or do they lack the ability to create a good environment for their offspring?)
2. be poor.
3. be minorities – the school looks like a melting pot, but special ed looks very minority.
I do wish that the Israeli study had a much larger sample of older fathers.
davev,
You are absolutely right with your observation about the offspring of very young fathers being at risk of problems relating to cerebral functioning. Please read the abstract listed in comment #19.
Leslie, can you help me out with that #19? I’m intrigued by the “young fathers” and “lower cerebral functioning”, but the abstract is very light on detail. What exactly constitutes a “very young” father?
I think that it is important to look at the overall picture. Do older PARENTS offer the child a more stable environment? Older men and women are more likely to have children with genetic defects, but from what I have seen, it seems like the OVERALL majority of special ed type exceptionalities seem to be linked to the home environment. (Poverty, abusive parents, etc.) I wonder if the anecdotal connection that I see between young parents (particularly poor, minority parents) is due to the fact that the home environment is often so chaotic. Some parents are too busy trying to survive to actually raise kids.
I speak only from what I see in special ed at my school. Anecdotal evidence is not rock solid, but it is not entirely without merit . . . if I were forced to bet on a basketball game between five guys who are 5’2″ and five guys who are are 6’6″ I would pick the second group. Anecdotally speaking, the taller team usually wins.
I think that the age of the parents as it relates to the the health of the offspring is a very important topic. We must consider ALL risks and weigh them carefully.
Keep up the good work!
davev,
Thanks davev.
A stable environment is not in any way as important as genetic health for any child. Healthy children have resilience and the ability to overcome all kinds of adversity. Better to father children in ones mid 20s to 32 it seems. My research has turned up quite a few studies, (1971, 1999, 2003) that connect a high risk of autism in families with autoimmune disorders. There seems to be, in some families, a gradual build up of genetic mutations to first cause diabetes, SLE, Hashimotos, Rheumatoid Arthritis, etc.and then as the mutations in the spermatagonia DNA increase, schizophrenia and autism.
In terms of what is a very young father, under 20 is indicated.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7619937&query_hl=35&itool=pubmed_DocSum “Men under 20 years of age were also at increased risk for fathering children with birth defects such as neural tube defects, hypospadias, cystic kidney, and Down syndrome.
Leslie
Two recent papers have been published on the paternal and maternal age issues in autism.
The first one is a large study of all the children born to Kaiser of Northern California patients from 1995-1999.
http://archpedi.ama-assn.org/cgi/content/short/161/4/334
The second paper is a review of seven epidemiological studies of the prenatal and perinatal risk factors for autism. Ony four of the papers looked at paternal age. 3 of the 4 found that rising paternal age was a potent risk factor for autism, the fourth from Western Australia, also found that increasing paternal age is a risk factor for autism (the people with autism had significantly older parents.
http://archpedi.ama-assn.org/cgi/content/abstract/161/4/326
Some more research has been published on paternal age and autism. Maternal age is found to be a risk factor also in some research.
http://archpedi.ama-assn.org/cgi/content/abstract/161/4/326
http://archpedi.ama-assn.org/cgi/content/short/161/4/334
thanks for stopping by my blog!
i have a two year old son, and my partner was 42 when he was conceived. so far, so good. he’s incredibly healthy and happy… he’s been speaking in sentences for a couple of months now.
this info is interesting. i’ve long questioned the increase in autism in children, and have wondered about the link between vaccines and autism/sids/etc, though the scientific community seems to be saying there is no such correlation. i just don’t know. metals and other additives can do a tremendous amount of damage in a person’s system. i’ve also found mention of independently tested vaccines that are touted as being thimersol-free aren’t.
i can’t help but wonder also, about the role of culture and society in the prevalence of the dis-eases you’ve brought up – maybe not so much autism, but with schizophrenia and the so-called add/adhd.
Kara, thanks for stopping by here. Sorry I’m slow in responding, but I’ve been out and about a bit…not minding the store as much as I should!
The contributions of factors such as environment (family, social, cultural, etc) and biology (genetic, disease, etc.) to Emotional and Behavioral Disorders vary with disorder, I’m pretty sure. There are some very clear examples of each. Huntington’s disease, which has a genetic basis but appears after a person is 20 years old in most cases, is a fascinating example (see here, here and here> for more content). Many more specific problems clearly are at least affected by environmental processes (e.g., some of the challenging behaviors of children such as stereotypies that are apparently maintained by environmental factors; see, for example, a study by Craig Kennedy and his colleagues: Analyzing the multiple functions of stereotypical behavior for students with autism: Implications for assessment and treatment. Journal of Applied Behavior Analysis, 33, 559-571).
In most cases, I would hazard a guess that there are combinations of causes. If there is a genetic component, that component is going to produce some behavioral differences that will affect the environment, that is change the way people interact with the individual. In turn, those changes in the environment will affect the behavior of the individual. So, the hen-or-egg question really should be seen as a hen-and-egg issue. In considering the individual, what we have from our genetic endowment is what we have; we’re left with the task of addressing the social-environmental factors as directly, efficiently, and humanely as we can. We may be able to modify something in the individual’s body chemistry to counteract some of the effects of disease, but we’re still likely to have to teach the individual, and that’s done by modifying the environment.
Now, at the level beyond the individual, when we consider Autism instead of a child who has Autism, we need to pursue these various paths differently. That’s the role of strong biomedical research.
This comments starting to seem rambling and aimless….sorry.
May 2007 PATERNAL AGE AND AUTISM ARE ASSOCIATED IN A FAMILY-BASED SAMPLE
: Mol Psychiatry. 2007 May;12(5):419-421.Paternal age and autism are associated in a family-based sample.Cantor RM, Yoon JL, Furr J, Lajonchere CM.
[1] 1Department of Human Genetics, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, USA [2] 2Department of Pediatrics, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA, USA [3] 3AGRE Consortium, Los Angeles, CA, USA.
PMID: 17453057 [PubMed - as supplied by publisher]
The paternal age distribution of the AGRE fathers, whose first child is autistic differs significantly from that of the ‘control’ sample (P=0.005). A 2 goodness-of-fit test with 2 degrees of freedom was conducted using percents in the ‘control’ group age categories to calculate the expected values in the AGRE sample. The shift toward higher paternal ages in those with an affected first-born is seen most dramatically in the group of AGRE fathers who are 30–39 years inclusive, which is 54.7% of the distribution compared with the 41.9 % that is expected. We interpret this shifted age distribution to provide support for the recently reported finding by Reichenberg and co-workers that autism risk is associated with advancing paternal age.
A must read article on sperm fragmentation, genetic disorders and increasing paternal age: http://psychologytoday.com/articles/pto-20070830-000004.xml
Here’s a good summary on the age of the father and sperm DNA health. http://psychologytoday.com/articles/pto-20070925-000003.html