Irrefutable evidence of a paternal age effect on genetic disorders in offspring

There is as much evidence that sperm mutations increase with paternal age as there are repercussions if you drink and drive at the same time. There is irrefutable evidence that genetic disorders increase in offspring of older fathers with increasing paternal age. Look up paternal age and genetic disorders on this blog or google it.


Paternal age effect
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The paternal age effect describes the influence that a father's age has on the chances of conferring a genetic defect to his offspring. Generally, older men have a greater probability of fathering children with a genetic defect than younger men do.[citation needed] This is seen as likely due to genetic copying errors which may increase in number after repeated spermatogenesis cycles over a man's lifetime.
Contents[hide]
1 Disorders correlated with paternal age
2 See also
3 References
4 External links
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Disorders correlated with paternal age
Achondroplasia (dwarfism); craniofacial disorders such as Apert syndrome and Crouzon Syndrome; mental retardation of unknown etiologies; autism; and 25% of schizophrenia cases are correlated with advanced paternal age.
Other disorders related to advanced paternal age are:
Wilms' tumor
Thanatophoric dysplasia
Retinitis pigmentosa
Osteogenesis imperfecta type IIA
Acrodysostosis
Fibrodysplasia ossificans progressiva
Aniridia
Bilateral retinoblastoma
Multiple exostoses
Marfan Syndrome
Lesch-Nyhan syndrome
Pfeiffer Syndrome
Wardenburg Syndrome
Treacher-Collins Syndrome
Soto’s basal cell nevus
Cleidocranial dysostosis
Polyposis coli
Oculodentodigital syndrome
Costello syndrome
Progeria
Recklinghausen’s neurofibromatosis
Tuberous sclerosis
Polycystic kidney disease
Hemophilia A
Duchenne muscular dystrophy
Athetoid Cerebral Palsy
Dystonic Cerebral Palsy
Congenital Hemiplegia

See also
Maternal age effect

References
Crow JF (1997). "The high spontaneous mutation rate: Is it a health risk?". PNAS 94: 8380–6.
Bertram L, Busch R, Spiegl M, Lautenschlager NT, Müller U, Kurz A (1998). "Paternal age is a risk factor for Alzheimer disease in the absence of a major gene". Neuroscience 1 (4): 277–80.
Sipos A, Rasmussen F, Harrison G, Tynelius P, Lewis G, Leon DA, Gunnell D (2004). "Paternal age and schizophrenia: a population based (sic) cohort study". BMJ Online.
DNA repair activity linked to paternal age effect. University of Texas Health Science Center at San Antonio (2000-08-28).
Bray I, Gunnell D, Smith GD (2006). "Advanced paternal age: How old is too old?". Journal of Epidemiology and Community Health 60: 851–3.
Montgomery SM, Lambe M, Tomas O, Ekbom A (2004). "Paternal age, family size, and risk of multiple sclerosis". Epidemiology 15 (6): 717–23.
Reichenberg A, Gross R, Weiser M, Bresnahan M, Silverman J, Harlap S, Rabinowitz J, Shulman C, Malaspina D, Lubin G, Knobler HY, Davidson M, Susser E (2006). "Advancing paternal age and autism". Archives of General Psychiatry 63 (9): 1026–32.
Sanders L (2005). College scientist named Ellison Senior Scholar. University of Southern California College of Letters, Arts & Sciences.
Fisch H, Hyun G, Golden R, Hensle TW, Olsson CA, Liberson GL (2003). "The influence of paternal age on down syndrome (sic)". J Urol 169 (6): 2275–8. PMID 12771769.
Rami B, Schneider U, Imhof A, Waldhör T, Schober E (1999). "Risk factors for type I diabetes mellitus in children in Austria" 158 (5): 362–6. PMID 10333115.
Singh NP, Muller CH, Berger RE (2003). "Effects of age on DNA double-strand breaks and apoptosis in human sperm". Fertility and sterility 80 (6): 1420–30.
Lauritsen MB, Pedersen CB, Mortensen PB (2005). "Effects of familial risk factors and place of birth on the risk of autism: a nationwide register-based study". J Child Psychol Psychiatry 46 (9): 963–71. PMID 16108999.
Wohl M, Gorwood P (2007). "Paternal ages below or above 35 years old are associated with a different risk of schizophrenia in the offspring". Eur Psychiatry 22 (1): 22–6. PMID 17142012.
Schizophrenia Research Forum: Current Hypotheses (2006-03-28).
Choi J-Y, Lee K-M, Park SK, Noh D-Y, Ahn S-H, Yoo K-Y, Kang D (2005). "Association of paternal age at birth and the risk of breast cancer in offspring: a case control study". BMC Cancer 5: 143.
NW Andrology & Cryobank.
Croen LA, Najjar DV, Fireman B, Grether JK (2007). "Maternal and paternal age and risk of autism spectrum disorders". Archives of Pediatrics and Adolescent Medicine 161 (4): 334–40.
Tarin JJ, Brines J, Cano A (1998). "Long-term effects of delayed parenthood". Human Reproduction 13 (9): 2371–6

It is also apparent that DNA damage in spermatozoa is associated with adverse impacts on the health and wellbeing of children.

Soc Reprod Fertil Suppl. 2007;65:81-92.Value of DNA integrity assays for fertility evaluation.Aitken RJ, De Luliis GN.
ARC Centre of Excellence in Biotechnology and Development and Discipline of Biological Sciences, University of Newcastle, NSW 2308, Australia. jaitken@mail.newcastle.edu.au
DNA damage in the male germ line is associated with failed fertilisation, impaired preimplantation development and poor pregnancy outcomes, whether the insemination is natural or artificial. It is also apparent that DNA damage in spermatozoa is associated with adverse impacts on the health and wellbeing of children. This may be particularly important in the case of conceptions involving intracytoplasmic sperm injection. With this technique DNA damaged spermatozoa that would, under physiological circumstances, be excluded from the conception process are able to initiate pregnancies. Although the oocyte actively repairs the DNA damage brought into the zygote by the fertilising spermatozoon, errors in this repair process would generate mutations that might in turn be linked to the increased incidence of dominant genetic disease and childhood cancer seen in the offspring of fathers possessing DNA damaged spermatozoa. Significantly, the incidence of such mutations is so low that it might be several generations before the full consequences of using DNA damaged spermatozoa in assisted conception cycles are realised. The factors modulating DNA damage in the male germ line are complex and largely unresolved. They involve advanced paternal age, exposure to xenobiotics and male genital tract infection. The types of damage being measured by the assays used in most laboratories (SCSA, Comet and TUNEL) are also uncertain. Molecular characterization of this DNA damage might provide insights into the underlying aetiologies, facilitate the development of optimised diagnostic methods for its detection and suggest logical avenues to pursue for its correction and ultimate prevention.

PMID: 17644956 [PubMed - in process]

Related LinksDNA damage to spermatozoa has impacts on fertilization and pregnancy. [Cell Tissue Res. 2005]Pregnancy outcomes after assisted reproductive technology. [J Obstet Gynaecol Can. 2006]The effect of sperm DNA damage on assisted reproduction outcomes. A review. [Minerva Ginecol. 2004]Late, but not early, paternal effect on human embryo development is related to sperm DNA fragmentation. [Hum Reprod. 2004]Founders' Lecture. Human spermatozoa: fruits of creation, seeds of doubt. [Reprod Fertil Dev. 2004]See all Related Articles...