Old Eggs do not cause autism --The Hockey Stick ignores the Medieval Warm Period and the Little Ice Age.

Loads of papers report that increasing paternal age causes new mutations and new genetic disorders in offspring. Ovum do not accumulate spontaneous mutations because they do not divide more than a few times until fertilized. There is a good reason not to ignore this fact. It is not old eggs. It is increasing paternal age causing spontaneous mutations in sperm stem cells and sperm, hundreds and hundreds of divisions take place and genetic DNA errors do accumulate. CO2 emissions are not the cause of global warming; the change is caused by solar activity. This is a natural cycle. http://www.co2science.org/scripts/CO2ScienceB2C/subject/c/summaries/co2climatehistory.jsp

The general public does not know that the hockey stick is inaccurate, CO2 is not the culprite it is painted to be or that a warming period follows a colder period in approximately 1500 year cycles. They don't know that older fathering of babies is risky for the genetic health of the child; that paternal age is a known risk factor for neurocognitive disorders such as what is called "autism" today. The public does not know that the hockey stick is not accurate. There is no public health advisory urging men to father in their 20s and early thirties, even though epidemiologists and some psychiatrists would like the public to know about advancing paternal age past 32 and genetic disorders. Leslie B. Raschka,M.D., Isabelle Bray Ph.D., Philip Gorwood,M.D., Michael Craig Miller, M.D. Why is the information we receive about these matters contrary to the findings in epidemiology and climatology? I don't know. Dolores Malaspina predicts that there will be a greater percentage of offspring with neurocognitive disorders as the demographics of paternal age shifts ever higher. Is the rise in autism really surprising? Not to those who know the science of de novo/spontaneous/germ line mutations.


October 23, 2006
Tropical Seas Sink Hockey Stick
Filed under: Temperature History, Paleo/Proxy —
Defending the “Hockey Stick” depiction of hemispheric or global temperature for the past 1,000 years just got a lot tougher. The “Hockey Stick” curiously wipes out the “Medieval Warm Period” of 1,000 years ago and the “Little Ice Age” that began 450 years ago and ended around 1900. We are supposed to look at the blade of the stick and conclude that the warming of the past 100 years is completely unlike anything seen for at least 1,000 years. It comes as no surprise that the “Hockey Stick” is prominently presented in many of the documents of the Intergovernmental Panel on Climate Change (IPCC). Defenders of the “Hockey Stick” make claims that the Medieval Warm Period and Little Ice Age were confined to the mid-to-high latitudes of the Northern Hemisphere and not felt throughout the rest of the world. This always seemed odd to us at World Climate Report given that variations of solar output seem to explain the higher temperatures 1,000 years ago and the colder temperatures of the Little Ice Age......



Mutation Rate: Sex Biases
Standard Article
Laurence D Hurst, University of Bath, Bath, UK
Copyright © 2006 John Wiley & Sons, Ltd. All rights reserved.DOI: 10.1038/npg.els.0006093Article Online Posting Date: January 27, 2006

Abstract Full Text: HTML PDF (76K)

At least in humans, more spontaneous point mutations occur in the male germ line than in the female germ line. One explanation for this is the greater number of germ-cell divisions in males than in females.
Keywords: point mutations; germ-cell divisions; sex chromosomes; methylation; neutral evolution; dominance




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Study: Autism linked to genetic mutations, mother's age

"The older the mother, the more likely she has acquired spontaneous mutations" in her chromosomes, and will transmit them at conception, Dr. Wigler said. Less frequently, but just as likely, Dr. Wigler said, fathers can transmit autism traits as well.



Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8380-6.
Related Articles,
Links
The high spontaneous mutation rate: is it a health risk?Crow JF.Genetics Laboratory, University of Wisconsin, Madison, WI 53706, USA.The human mutation rate for base substitutions is much higher in males than in females and increases with paternal age. This effect is mainly, if not entirely, due to the large number of cell divisions in the male germ line. The mutation-rate increase is considerably greater than expected if the mutation rate were simply proportional to the number of cell divisions. In contrast, those mutations that are small deletions or rearrangements do not show the paternal age effect. The observed increase with the age of the father in the incidence of children with different dominant mutations is variable, presumably the result of different mixtures of base substitutions and deletions. In Drosophila, the rate of mutations causing minor deleterious effects is estimated to be about one new mutation per zygote. Because of a larger number of genes and a much larger amount of DNA, the human rate is presumably higher. Recently, the Drosophila data have been reanalyzed and the mutation-rate estimate questioned, but I believe that the totality of evidence supports the original conclusion. The most reasonable way in which a species can cope with a high mutation rate is by quasi-truncation selection, whereby a number of mutant genes are eliminated by one "genetic death."
"I conclude that for a number of diseases the mutation rate increases with age and at a rate much faster than linear. This suggests that the greatest mutational health hazard in the human population at present is fertile old males. If males reproduced shortly after puberty (or the equivalent result were attained by early collection of sperm and cold storage for later use) the mutation rate could be greatly reduced. (I am not advocating this. For one thing, until many more diseases are studied, the generality of the conclusion is not established. Furthermore, one does not lightly suggest such socially disruptive procedures, even if there were a well-established health benefit.) " 1997 James F. Crow

Myth Advancing Maternal Age Causes Spontaneous Mutations That Cause Autism-A Political View Not Backed By 50 Years of Science

Why do people believe that sperm don't mutate with every division (840 divisions by age 50) and eggs get old?

Bravo Dr. Higgs of the Independent Institute for explaning how science works.


Peer Review and Scientific Consensus
Dr Robert Higgs of the Independent Institute, writes:
Journalists, politicians and advocacy groups refer to “peer-reviewed research” and “scientific consensus” as the authoritative last words on controversial matters involving the natural sciences, from climate change to stem-cell research and genetically engineered foods. But many people have an unrealistic view of how the scientific community actually works.The peer-review process is not, contrary to popular belief, a nearly flawless system of Olympian scrutiny. Any editor of a peer-reviewed journal who desires to reject or accept a submission can easily do so by choosing appropriate referees.Unfortunately, personal vendettas, ideological conflicts, professional jealousies, methodological disagreements, sheer self-promotion and irresponsibility are as much part of the scientific world as any other. Peer review cannot ensure that research is correct in its procedures and conclusions. A part of the work in every discipline – from the physical sciences to economics –consists of correcting previous mistakes.At any given time, “scientific consensus” may exist about various matters. Over time, however, new interpretations, tests or observations may demolish that consensus. For instance, in the mid-1970s, an apparent scientific consensus existed that our planet was about to enter another Ice Age. Drastic proposals, such as exploding hydrogen bombs over polar icecaps to melt them. and damming the Bering Strait to prevent icy waters from entering the Pacific, were put forth by reputable scientists and seriously considered by the US government.The truth is that scientific research at the upper echelons occurs within a fairly small world. Leading researchers attend the same conferences, belong to the same societies, review one another’s work for funding organizations, and so forth. If you do not belong to this tight fraternity, it becomes extremely difficult to gain a hearing for your work, to publish in a “top” journal, to acquire a government grant, to receive an invitation to participate in a scientific conference, or even to place your grad students in decent positions. “Scientific consensus” often emerges because the members of this exclusive club, and those who support them, have too much invested in the reigning ideas to let go. In this context, it behooves bright young scientists not to rock the boat by challenging anything fundamental or dear to the hearts of those who constitute review committees of funders or journals. The terms "peer review" and "scientific consensus" often serve to suggest a process of disinterested neutrality and saintly pursuit of truth. Like every other human endeavour, however, science is conducted by people with the full range of human emotions and motives.Good rules of thumb for the non-scientist might be the following: government-funded research that is used to justify that government’s policy should be suspect, whether or not it’s peer-reviewed; and the research of scientists who appear at press conferences in the company of politicians or activists whose agendas they are there to support should be suspect, whether or not the work upholds the consensus opinion.
Robert Higgs is Senior Fellow in Political Economy at the Independent Institute, editor of the quarterly journal The Independent Review, and the author of Depression War and Cold War, as well as numerous books and more than 100 articles in scholarly journals.

One Faulty Copy Tips the Balance

Nature Reviews Cancer 7, 725 (October 2007) doi:10.1038/nrc2239
Tumour suppressors: One faulty copy tips the balance
Patrick Goymer
TIP60 is an acetyl-transferase that co-regulates MYC and p53, and modulates the MYC-induced DNA-damage response (DDR). A new study shows that loss of a single copy of Tip60 is associated with tumorigenesis, and that this is caused by impairment of the DDR and is independent of p53

Don't Be Fooled Father Your Babies in your 20s if possible to 33

The Times
From
September 5, 2006
Children of older fathers at risk of autism
/
By David Rose
OLDER men are far more likely to father autistic children, according to new research.
A study involving more than 100,000 children found that those born to fathers aged 40 and over were nearly six times more likely to suffer from autism and related disorders than those with a father under 30.
Scientists from the Institute of Psychiatry at King’s College, London and Mount Sinai School of Medicine in New York, said that their research supported the theory that men also have a “biolog-ical clock” when it comes to producing healthy babies.
They described the findings as “the first convincing evidence that advanced paternal age is a risk factor for autism spectrum disorder”. However the authors could not find a link between a mother’s advancing age and autism.
The exact causes of autism remain unknown, but cases of it and related conditions such as Asperger’s syndrome — known collectively as autism spectrum disorders (ASDs) — have increased tenfold in the past two decades. They now affect the lives of more than half a million families in Britain. A recent study suggested that the rate could be as high as 116 ASD cases per 10,000 children.
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'No regrets over my autistic son – but I still want answers'
According to the Office of National Statistics, the number of new fathers aged over 40 rose by about a third in the five years to 2004, when 75,810 older men became parents. Only 32,000 men aged over 40 became fathers in 1983.
Abraham Reichenberg, lead researcher in the latest study, said that genetic mutations in the sperm of older men may be responsible for the increased risk of their children developing ASDs.
Autism is a lifelong disability affecting the way that a person communicates and relates to others. People with autism have impaired social interactions, communication and imagination, including repetitive patterns of behaviour.
Better diagnosis has contributed to the rising rates of autism, but experts also believe that there may be more cases. Scientists have dismissed suggestions that the increase might be linked to the use of MMR, the combined childhood vaccine given to protect against measles, mumps and rubella.
The latest study, published in the Archives of General Psychiatry, analysed 132,271 Jewish children born during the 1980s in Israel. The researchers found that, if the father was aged 15 to 29 when the child was born, the risk of autism was 6 in every 10,000 children. If the father was 30 to 39, then 9 in 10,000 children suffered autism (1.6 times higher), going up to 32 in 10,000 (5.75 times higher) for fathers aged 40 to 49. The risk was even higher for older fathers.
“This research adds to our knowledge that men also have a biological clock when it comes to reproducing,” Dr Reichenberg said. “The sample size for the over-50s was small, so we added it to the results for fathers aged over 40, but our research suggests that very old fathers have around nine times the risk. “The research shows a linear effect — with every ten years, the risk doubles.”
The researchers emphasised that the results related to autism and could not necessarily be generalised to apply to related disorders such as Asperger’s syndrome. But they added: “This data suggests a significant association between advancing paternal age and risk of ASD.”
They said that there were several genetic factors which could be at play, including spontaneous mutations in sperm-producing cells, or discrepancies in how genes are expressed.
Although the fact that all the children were Jewish was a limitation of the study, Dr Reichenberg did not believe it affected the results. More research was needed to see if the findings were replicated across other racial and ethnic backgrounds.
ASDs have been linked with abnormalities in children’s brain development which occur before, during, or soon after birth. The advancing age of parents has also been linked to brain development.
Dr Reichenberg and his team discuss several possible genetic mechanisms to explain the paternal age effect but add: “It is important to keep in mind, however, that age at paternity is influenced by the sociocultural environment and varies across societies and over time.”
The National Autistic Society (NAS), Britain’s leading charity for the condition, said yesterday that the causes of autism were complex and required further investigatiopn.

This has been known for a long long time but that is not what we are all taught to believe: autism is not a mystery

Male biological clock is ticking

Sperm cells accumulate damage over time
The chances of a man having children dip past his 35th birthday, researchers have found.
The researchers, from the University of Washington in Seattle, found that damage to the genetic material containing sperm cells increases with age.
We found there is a significant change by the age of 35
Dr Narendra SinghUnlike most other cells in the body, sperm cells are unable to repair this damage.
In addition, the researchers found that as a man gets older he loses his natural ability to weed out unhealthy sperm cells through a process known as apoptosis.
This means that there is a greater chance that a damaged sperm cell will successfully fertilise the female egg.
This could mean that the risk of miscarriage is increased or, at the other end of the scale, that children have a greater chance of developing mild abnormalities such as uneven teeth, or asymmetrical limbs.
Lead researcher Dr Narendra Singh told the BBC: "We found there is a significant change by the age of 35."
Sperm quality
Dr Singh's team examined sperm quality in 60 men aged between 22 and 60. All had healthy sperm counts.
The researchers found that men aged 35 and older had higher concentrations of sperm with broken strands of DNA, and that the damage was greater.
In general, older men's sperm was less active so they had less chance of fertilising an egg.
A recent study found that male infertility was just as likely as female infertility to prevent couples from having a family.
The proportion of British men aged over 40 becoming fathers increased by half in the 1990s. In 1999 one in 10 children was born to a father aged over 40.
It is known that a healthy lifestyle can have a positive effect on male fertility.
The findings are to be presented at a meeting of the American Society of Reproductive Medicine in Seattle.
Society president William Keye said: "While there is nothing anyone can do about getting older, men who want to retain their own best capacity to father children should try to minimise contact with toxic agents and maintain a healthy lifestyle."
WATCH/LISTEN
ON THIS STORY
University of Washington's Dr Narendra Singh"Damage to the sperm increases with age"
See also:
17 Mar 02 UK
River 'pollution' sparks fertility fears
01 Jun 00 Health
'No fertility crisis' despite sperm decline
01 Aug 00 Health
Men 'have a biological clock'
Internet links:
University of Washington at Seattle
American Society for Reproductive MedicineThe BBC is not responsible for the content of external internet sites
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Links to more Health stories are at the foot of the page.

WHY NEVER PUBLISH THE PROMISED RESULTS?

http://asdcarc.com/index.php/publisher/articleview/?PHXSESSID=9d49c2c06dc3d79f3c97c63e6130b22f&/1/frmArticleID/170/staticId/847/


Older Dads and Autism SurveyUpdate: Sept 13 2006The research study by Reichenberg et al (2006) attracted a lot of attention from both the scientific community and the autism community, with many comments supporting and others criticising the results. Such a reaction is important because it helps us to explore new areas of research and to design better studies. Our Older Dads and Autism Survey is not a rigorous scientific study. BUT we are trying to see whether there is merit in conducting a more in-depth study. This survey taught us many things - the most important of which is that so many families want to participate in research to find answers. Within one hour and 20 minutes of posting, we had 100 responses! By the end of the first day (only 7 hours), we had 300! The word has spread and you helped make that happen - Thank you. We had more than 1000 responses in only 5 days! We are sharing some of those findings with you now, and the analysis of our results will be posted early next week. Please continue to invite others to participate and we hope that you will come back to participate in other surveys.



Why is the autism rate so high?
Friday, September 28th, 2007
Change in diagnostic standards - Broadened awareness - and maybe there is an increase in children being born to older fathers.1. Autism used to mean people that would be institutionalized, could never have meaningful jobs and would hardly even know how to talk (Like Rainman at best)Now the definition is so broad it includes people […]

http://www.autism-world.com/index.php/category/what-is-autism/what-causes-autism/

SLE Autoimmune disorder in families with autism other autoimmune disorders also found in family history

20 September 2007 Genetic cause discovered for systemic lupus erythematosus
Mutations in a gene researchers call TREX1 is one cause for systemic lupus erythematosus (SLE), a severe and incurable autoimmune disease. This is the result of a new study headed by Professor Norbert Hübner from the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and Dr. Min Ae Lee-Kirsch from the Technical University Dresden, (both in Germany) in collaboration with scientists from Finland, Sweden, the United Kingdom, and the USA. The study has now been published in the latest issue of Nature Genetics (Vol. 39, No. 9, pp. 1065-1067, 2007). The exact causes for SLE are still unknown. Triggers are thought to include viruses, the sunlight, drug reactions, or a specific genetic predisposition. Symptoms of SLE can be inflammations of the skin, the joints, the heart, the lungs, the kidney, and the nervous system. The name of the disease refers to red spots on the skin which resemble the bites of a wolfe (latin: lupus). As the disease can affect any part of the body, it is “systemic”. SLE belongs to the group of autoimmune diseases, because the body’s immune system attacks its own healthy cells and tissues, causing inflammations. About 40,000 individuals are affected in Germany, most of them are women. In a family suffering from a rare form of lupus, Dr. Lee-Kirsch and Professor Hübner discovered various mutations in the gene TREX1. Hence, they wanted to know if mutations in TREX1 also play a role in SLE, the most common form of lupus. Collecting blood samples from patients with SLE from the UK, Germany, and Finland, the researcher compared them with samples from healthy individuals. As suspected, patients with SLE carried mutations in the TREX1 gene whereas healthy individuals did not. Nevertheless, the mutations found in TREX1 are not responsible for all types of SLE. The product of the gene TREX1 is a protein which plays a role in apoptosis, a program in which cells literally induce their own death when defective. Thus, apoptosis protects the body from harm. Once apoptosis starts, TREX1 gets rid of its junctions in the cytoplasm and translocates into the nucleus of a damaged cell to digest its DNA.Mutations in TREX1, however, change part of the protein with which it is chained to the cell’s cytoplasm. In the case of apoptosis, TREX1 gets rid of its molecular chains, translocates into the cell’s nucleus, and spreads to other parts of the cell too. The immune system seems to be mislead as it produces autoantibodies against these cell particles and also against other healthy cells. Why autoantibodies are produced still remains unclear. “Further studies will have to shed light onto this problem“, stresses Professor Hübner.
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Reference URL
http://www.nature.com/ng/journal/v39/n9/pdf/ng2091.pdf
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Medical, Life Sciences
Peer reviewed publication and references
*Mutations in the 3´-5´ DNA exonuclease TREX1 are associated with systemic lupus erythematosusMin Ae Lee-Kirsch1, Maolian Gong2#, Dipanjan Chowdhury3#, Lydia Senenko1#, Kerstin Engel1#, Young-Ae Lee2,4#, Udesh de Silva5, Suzanna L. Bailey5, Torsten Witte6, Timothy J. Vyse7, Juha Kere8, Christiane Pfeiffer9, Scott Harvey10, Andrew Wong7, Sari Koskenmies11,12, Oliver Hummel2, Klaus Rohde2, Reinhold E. Schmidt6, Anna F. Dominiczak13, Manfred Gahr1, Thomas Hollis5, Fred W. Perrino10, Judy Lieberman3, & Norbert Hübner2 1Klinik für Kinder- und Jugendmedizin, Technische Universität Dresden, 01307 Dresden, Germany2Max-Delbrück-Center for Molecular Medicine (MDC), Berlin-Buch, Germany3CBR Institute for Biomedical Research, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts 01225, USA4Charité - Universitätsmedizin Berlin, Pediatric Pneumology and Immunology, Campus Virchow-Klinikum, 13553 Berlin, Germany5Center for Structural Biology, Department of Biochemistry, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA6Medizinische Hochschule Hannover, Klinische Immunologie, 30625 Hannover, Germany7Imperial College, Faculty of Medicine, Section of Rheumatology and Molecular Genetics, Hammersmith Hospital, London W12 0NN, UK.8Karolinska Institute, Department of Biosciences and Nutrition, and Clinical Research Centre, 14157 Huddinge, Sweden9Klinik für Dermatologie, Technische Universität Dresden, 01307 Dresden, Germany10Department of Biochemistry, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA11University of Helsinki, Department of Medical Genetics and 12Department of Dermatology, 00014 Helsinki, Finland13Department of Medicine and Therapeutics, Western Infirmary, Glasgow University, Glasgow G11 6NT, UK#These authors contributed equally.Correspondence requests should be addressed to M. L.-K. (minae.lee-kirsch@uniklinikum-dresden.de) and N. H. (nhuebner@mdc-berlin.de)

Lack of normal myelination is involved with neurocognitive developmental orders due to sperm mutations and maybe vaccinations

Also read: http://autism-prevention.blogspot.com/search?q=Alzheimer%27s+and+myelination


Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine

Vaccine Induced Demyelination
Myelination is an essential part of human brain development. Nerves can only conduct pulses of energy efficiently if covered by myelin. Like insulation on an electric wire, the fatty coating of myelin keeps the pulses confined and maintains the integrity of the electrical signal so that it has a high signal-to-noise ratio. When the insulation on a wire is damaged or destroyed, the flow of electrical current may be interrupted and a short-circuit occurs.
Oligodendrocyte cells give white matter its color by manufacturing myelin. If myelin falls into disrepair, nerve axons cease to function, even though they themselves aren't damaged. Protecting oligodendrocytes after brain or spinal cord injury might keep nerve cells intact.
At birth, relatively few pathways have myelin insulation. Myelination in the human brain continues from before birth until at least 20 years of age. Up until the age of 10 or so, vast areas of the cortex are not yet myelinated. Up to the age of 20, large areas of the frontal lobes are not yet myelinated.1
Myelination begins in the developmentally oldest parts of the brain, like the brain stem, moving to the areas of the nervous system that have developed more recently, like the prefrontal lobe and cortex. Myelin spreads throughout the nervous system in stages, which vary slightly in each individual. Impairment of myelination can alter neural communication without necessarily causing severe CNS (central nervous system) damage.
The prefrontal portions of the cerebrum have a profound influence on human behavior.2 If an individual is injected with vaccines,most of which have adjuvants like mercury and aluminum compounds, as well as foreign proteins (some from other species in which the vaccines were grown) and biological organisms, unprotected nerves may be impacted. The argument for a role of vaccines in the development of autistic disorders hinges on these biological effects upon nerves, damaging them in a way that influences behavior and learning patterns.
The argument for adjuvants evoking an auto-immune response does not hinge on any inherent neuro-toxicity of these compounds, but on the initiation of an allergic response.
The model by which adjuvants initiate an immune response is that of Experimental Allergic Encephalomyelitis (EAE). To date, EAE is recognized as the best available animal model of several degenerative human diseases, like multiple sclerosis and post-vaccinal encephalopathies. EAE3 is generally thought to be an autoimmune response to myelin basic protein (MBP). Oddly, MBP can also suppress EAE, and many observations suggest that an independent immune response to so-called "adjuvant" material is also necessary to EAE induction. Of course, this is why adjuvants are used in vaccines, to dramatically increase the likelihood of an immune response to the administered biological material.
Thus, EAE may be a result of a pair of interactive immune responses, one against MBP, and one against the adjuvant. If so, the adjuvant should, like MBP, suppress EAE. Root-Bernstein, et al. (1986) presented data from experiments on strain 13 guinea pigs demonstrating EAE suppression by muramyl dipeptide, an active component of complete Freund's adjuvant. In the past, adjuvants have only been classified as immunopotentiators, not immunosuppressants. Apparently, adjuvants are both. This study strengthens the argument that adjuvants may be crucial to initiating an auto-immune response leading to post-vaccine neurological symptoms.
[Return to "Quick-Index" of Vaccines]

References

Edwards KM, Meade BD, Decker MD, et al. Comparison of 13 acellular pertussis vaccines: overview and serologic responses. Pediatrics 1995;96:548-57.
Orenstein WA, Brugliera PD. Preface: Immunization in medical education. Am J Prev Med 1994; 10(suppl):v-viii.
Root-Bernstein RS; Yurochko F; Westall FC. Clinical suppression of experimental allergic encephalomyelitis by muramyl dipeptide "adjuvant". Brain Res Bull, 17: 4, 1986 Oct, 473-6.
Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine
Website designed, hosted and maintained by The Healing Center On-Line © 2001

Myelin Sheath -Vaccines- Autism- Autoimmunity Discussed

What is in vaccines that might not be great for babies etc.

Auto-Immunity, Vaccines and Autism
V.K. Singh has studied autism as an autoimmune disorder for over fifteen years. He believes that up to eighty percent (and possibly all) cases of autism are caused by an abnormal immune reaction, commonly known as autoimmunity. The autoimmune process in autism results from a complex interaction between the immune system and the nervous system. He hypothesizes that an auto-immune reaction to basic brain structures, especially the myelin sheath, plays a critical role in causing the neurological impairments of patients with autism. He has suggested that an immune insult to developing myelin (after a natural infection or vaccination) causes "nicks" or small changes in the myelin sheath. These changes ultimately lead to life-long disturbances of higher mental functions such as learning, memory, communication, social interaction, etc.1
A disease is sometimes referred to as "autoimmune" when the etiology and pathogenesis is not well known or established. Autoimmunity is an abnormal immune reaction in which the immune system becomes primed to react against body organs, and the end result is autoimmune disease. Several factors contribute to the pathogenic mechanism of autoimmune diseases. These illnesses are commonly believed to be triggered by infectious agents; further, they are generally linked to genes that control immune responses. They cause immune abnormalities of T lymphocytes (one type of white blood cell); they induce the production of autoantibodies; they involve hormonal factors; and they generally show a gender preference.
This is also the case with autism: several autoimmune factors have been identified in patients with autism, suggesting the pathogenetic role of autoimmunity in autism. Some generalities regarding the genetics and immunology of autism are below:
Autism displays increased frequency of genetic factors for immune responses, e.g., HLA, C4B null allele and extended haplotypes. Autism involves a gender factor, i.e., it affects males about four times more than females. Autism often occurs in conjunction with a family history of autoimmune diseases, e.g., multiple sclerosis, rheumatoid arthritis, etc. Autism also involves hormonal factors, e.g., secretin, beta-endorphin, etc. Autism shows an association with infectious agents, in particular, viruses. Autistic patients have immune abnormalities, especially those that characterize an autoimmune reaction in a disease. Autistic patients also respond well to immune therapies.
The linkage of vaccines to neurological disorders comes through the promotion of an auto-immune process, triggered by the virus present in the vaccine together with the adjuvant used to sensitize the body to this virus. Wild viruses have also been linked to autism. Certain viral infections can easily be acquired during fetal life, infancy or early childhood. They can enter the brain through the nasopharyngeal membranes or induce an autoimmune response against the brain, thereby altering the development of brain function.
Since autism is an early-onset disorder, usually diagnosed before the age of 30 months, it has been suggested that viruses might serve as teratogens (agents that cause developmental malfunctions) contributing to autism.
Earlier studies implicated congenital rubella virus (RV), simply because children with this infection also showed autistic behaviors. Moreover, several autistic children did not produce antibodies to rubella vaccine even after the repeated rubella immunization. Although the reason for this problem has not been investigated, Singh believes it due to a defect in T lymphocytes reducing their functionality. In support of this, RV-induced lymphocyte proliferation response in autistic children was only one-fourth of the response in normal children.
A few cases of autism have also been described among children with congenital cytomegalovirus (CMV). Interestingly, an autistic child with CMV responded favorably to treatment with transfer factor, but there was no follow-up to the study in which this was reported. Singh and co-workers conducted a study of IgG antibodies to CMV. They found no statistical difference between autistic children and normal children.2 Simply put, this means that CMV is probably not related to autism.
Singh conducted a study of measles virus (MV) and human herpes virus-6 (HHV-6) in autism. This was done by two types of laboratory analysis: (a) virus antibody levels of MV and HHV-6; and (b) brain autoantibody titers in the same samples as those assayed for virus antibodies. This study showed that the virus antibody levels in the blood of autistic children were much higher when compared to normal children; and that the elevated virus antibody levels were associated with brain autoantibody titer. Interestingly, the viral antibody and brain autoantibody association was particularly true of MV antibody and MBP autoantibody (i.e., 90 percent of autistic children showed this association).
This observation led Singh to hypothesize that a measles virus-induced autoimmune response was a causal factor in autism, whereas HHV-6 via co-infection could also contribute to pathophysiology of the disorder. Although as yet unproven, Singh thinks it is an excellent working hypothesis to explain autism, and may also explain why some children show autistic regression after the measles-mumps-rubella (MMR) immunization. A small but significant proportion of children develop autism as a result of pre-or post-natal infections - for example, with rubella, cytomegalovirus, herpes simplex, HIV, and so on.3
William Shaw reports that he found none of the signs characteristic of known, inborn (genetic) metabolic disorders among children with autism and PDD (pages 31; 35-37; 68-9; 129). On pages 103-4 Shaw noted, "In several cases, electron microscopy has revealed live measles virus in the intestinal lining of children with the gastrointestinal abnormalities common in children with autism."
Since the brain is the affected organ in autism and other vaccine-induced neurological disorders, the autoimmune response will be directed against this organ. This response is commonly identified by certain autoimmune factors that have been identified in autistic children. The list includes brain-specific autoantibodies, viral antibodies, cytokine profile, immune activation markers, and antinuclear antibodies. Collectively, these are essential for identifying a brain-specific autoimmune response.
Brain autoantibody studies detect antibodies to two brain proteins - the myelin basic protein (MBP) and neuron-axon filament proteins (NAFP). The incidence of MBP antibody in the autistic population (70% positive) is over twenty times higher than that of the normal population (3% positive); hence, it serves as a primary marker of the autoimmune reaction in autism. In contrast, the incidence of NAFP antibody in autistic patients (55% positive) is only about twice that of normal controls (27% positive), making it a secondary marker of autoimmunity in autism.
Two immune activation markers or cytokines, namely interleukin-12 (IL-12) and interferon gamma (IFN-g), play key roles in the induction of autoimmune diseases, i.e., they initiate an autoimmune reaction. They are selectively elevated in autistic patients and should be measured as a sign of altered cellular autoimmunity - a function of Th-1 type white blood cells.
Virus serology measures levels of antibodies to measles (rubeola) virus (MV) and human herpes virus-6 (HHV-6). The antibody levels are elevated, which is a sign of a present infection, past infection, or reaction to measles-mumps-rubella (MMR) vaccine. The HHV-6 and measles viruses are etiologically-linked to autism because they are related to brain autoantibodies and demyelinating diseases.
Antinuclear antibodies (ANA) are non-specific antibodies often present in patients with autoimmune diseases. Approximately one-third of autistic children tested have positive titers of ANA. [Reference: V. Singh, 1992; unpublished data].
The induction of an auto-immune process against the central nervous system (particularly the myelin basic protein) may be the way that vaccines - coupled with their adjuvants - cause neurological damage, including seizures, autism, and encephalitis.4 Recently thirty-three autistic children (less than or equal to 10 years of age) were compared to controls which included 18 normal children (of the same ages), 20 children with idiopathic mental retardation (MR) of the same ages, 12 children with Down's syndrome (DS) of the same age, and 38 normal adults in the age range of 20 to 40 years.5
Antibodies to myelin basic protein were found in 19 of 33 (58%) sera from autistic children. In contrast, only 8 of 88 (9%) control sera were positive. Among these control sera, 3 of 20 (15%) sera were from MR children, 4 of 18 (22%) sera were from normal children, only one of 38 sera was from normal adults (25 to 40 years of age), but none of the 12 sera from the DS children showed this antibody positive reaction.
The authors suggested that the humoral, immune response to myelin basic protein (MBP) could be related in some way to mental retardation, since approximately 60% of autistic children had an IQ of 70 of lower. Seizure activity or antipsychotic drugs were not thought to relate to the production of anti-MBP, since there was neither the history of seizures nor the intake of antipsychotics (at least not at the time of blood drawing) among autistic or retarded children that were studied.
Immunological studies of autistic patients have revealed certain features that are also found in patients with other autoimmune diseases. There is a genetic predisposition for several autoimmune diseases6 , like grave's thyroid disease, rheumatoid arthritis, and insulin-dependant diabetes. Likewise, autism shows a greater concordance rate in monozygotic twins than in the normal population.7 Autism is also four to five times more prevalent in boys than in girls Ç a gender factor which is also seen in systemic lupus erythematosus (SLE), Grave's disease, and ankylosing spondylintis (though this is more common with women than men).
Triggering by microorganisms is thought to be an important feature of autoimmune diseases. Whether a similar event is associated with autism is not known but there are coincidental findings of congenital rubella8 and cytomegalovirus,9,10 indicating prior exposure to these microbial agents. Certain soluble antigens of immunocyte activation are elevated in the sera of autistic children,11 which is in concordance with similar findings in other autoimmune diseases, like SLE12 and multiple sclerosis.13
Forty to fifty percent of autistic patients show signs of depressed immunity, including reduced lymphocyte proliferation by phytohemagglutinin, concanavalin A, and pokeweed mitogens14,15,16 along with depression of the proportion of CD4+ T helper cells to suppresor-inducer (CD4CD45RA+) cells.17,18,19 They also showed reduced numbers of CD2+ T cells, CD4+ cells, and CD4+CD45RA+ lymphocytes,20 along with reduced B cells (CD20+) and a lower percentage of total lymphocytes than siblings and normal children.21
The level of blood values for female subjects appeared lower than those for males as compared to normal subjects of the same sex. While family and twin studies support a genetic component for autistic spectrum disorders, children with autism, also have increased eosinophil and basophil response to IgE-mediated reactions.22
A cause and effect relationship between antibodies to myelin basic protein (MBP) and autism has not yet been definitively established. There may be many routes to autism, of which auto-immunity is only one. Nevertheless, the development of antibodies to MBP may be a major route through which vaccination contributes to autism.
Another possibility for post-vaccine related damage is delayed or incomplete myelination in the corpus callosum (the largest myelinated area of the brain), which has been suggested as a basis for auditory processing problems in some children with learning disabilities (LD).23 Immunological assaults from wild virus infection or vaccine virus infection could theoretically result in poor myelination or abnormal function of the neuron-axon myelin.
[Return to "Quick-Index" of Vaccines]

References

Singh VK. Autism, Autoimmunity and Immunotherapy: a Commentary, Autism Autoimmunity Project.
V. Singh, D. Schubert and R. Warren, 1992; unpublished data.
Cohen and Volkmar, eds., Handbook of Autism and Pervasive Developmental Disorders, 2nd edition, 1997: p. 398.
Singh VK. CD4+ Helper T Cell Depression in Autism. Immunology Letters, 1990; 25(4): 341-5.
Brain, Behavior, and Immunity 7, 97-103 (1993).
Shoenfeld, Y., & Isenberg, D. (1989). The genetic components in autoimmunity. In The Mosaic of Autoimmunity, chap. 5, pp. 169-228. Elsevier: Amsterdam.
Folstein, S., & Rutter M. (1988). Autism: Familial aggregation and genetic implications. J. Aut. Develop. Disord. 18, 3-30.
Chess, S. (1971). Autism in children with congenital rubella. J. Aut. Childh. Schizophr. 1, 33-47.
Ivarsson, S. A., Bjerre, I., Vegfors, P., & Ahlfors, K. (1990). Autism as one of several abnormalities in two children with congenital cytomegalovirus infection. Neuropediatrics 21, 102-103.
Stubbs, E.G. (1987). Does intrauterine cytomegalovirs plus autoantibodies contribute to autism? In L. Wing (Ed.), Aspects of Autism: Biological Research, Gaskell Psychiatry Series, pp. 91-101.
Singh, V. K., Warren, R.P., Odell, J.D., & Cole, P. (1991). Changes of soluble interleukin-2, interleukin-2 receptor, T8 antigen, and interleukin-1 in the serum of autistic children. Clin. Immunol. Immunopath. 61, 448-455.
Huang, Y.P., Perrin, L.H., Miescher, P.A., & Zubler, R.H. (1988). Coorelation of T and B cell activites in vitro and serum IL-2 levels in systemic lupus erythematosus. J. Immunol. 141, 827-833.
Trotter, J.L., Clifford, D. B., Anderson, C. B., van der Veen, R. C., Hicks, B.C., & Banks, G. (1988). Elevated serum interleukin-2 levels in chronic progressive multiple sclerosis. N. Engl. J. Med. 318, 1206.
Singh, V. K., Fudenberg, H.H., Emerson, D., & Coleman, M. (1988). Immunodiagnosis and immunotherapy in autistic children. Ann. N.Y. Acad. Sci. 540, 602-604.
Stubbs, E.G. Crawford, M. L., Burger, D.R., & Vandenbark, A. A. (1977). Depressed lymphocyte responsiveness in autistic children. J. Aut. Childh. Schizophr. 7, 49-55.
Warren, R. P., Foster, A., Margretten, N. C., & Pace, N. C. (1986). Immune abnormalities in patients with autism. J. Aut. Dev. Disord. 16, 189-197.
Warren, R. P., Yonk, L. J., Burger, R.A., Cole, P., Odell, J. D., Warren, W. L., White, E., & Singh, V. K. (1990). Deficiency of suppressor-inducer (CD4 + Cd45RA + ) T cells in autism. Immunol. Invest. 19, 245-251.
Yonk, L. J., Warren, R. P., Burger, R. A., Cole, P., Odell, J. D., Warren, W. L., White, E., & Singh, V. K. (1990). CD4+ helper T cell depression in autism. Immunol. Lett. 25, 341-346.
Singh VK. Changes of Soluble Interleukin-2, Interleukin-2 Receptor, T8 Antigen, and Interleukin-1 in the Serum of Autistic Children. Clinical Immunology and Immunopathology, 1991; 61(3): 448-455.
Singh VK. Deficiency of Suppressor-inducer (CD4+CD45RA+) T Cells in Autism. Immunological Investigations, 1990; 19(3): 245-51.
Singh VK. CD4+ Helper T Cell Depression in Autism. Immunology Letters, 1990; 25(4): 341-5.
Trottier G. Etiology of infantile autism: a review of recent advances in genetic and neurobiological research. Journal of Psychiatry and Neuroscience, 1999; 24(2): 103-15.
Musiek, F. E., Gollegly, K. M., & Baran, J. A. (1984). Myelination of the corpus callosum and auditory processing problems in children: theoretical and clinical correlates. Semin. Hearing 5, 231-241.
Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,Beth Israel Hospital / Albert Einstein School of Medicine
Website designed, hosted and maintained by The Healing Center On-Line © 2001

Is the Rise in Neurocognitive Developmental Disorders Unexpected with the Rise in Paternal Age NO!

Not unexpected at all. There has been a 50 year game of blaming the mother's age or some mysterious cause.

What is the role of vaccinations?? What is the connection?

Who is well aware of the paternal age effect?


Why has paternal age risen so much in the last 20 years? Why does the myth that men can father at any age persist when autism, schizophrenia, diabetes, MS, prostate cancer, breast cancer, nervous system cancers, some leukemias, mental retardation, progeria, heart defects, low birth-weight, miscarriages, Down syndrome, epilepsy, kidney disease, fibromyalgia, hemophilia, fragile X, Alzheimer's, etc. etc. all rise in incidence in non-familial/spontaneous/sporadic cases with older paternal age and older maternal grandfather's age? It is also known that women who had fathers over 45 have significantly shorter life spans than those with younger fathers. What happens to the X-chromosome, what happens to the genes that form the brain and nervous system and the immune system? Why do Hispanics have significantly less autism on a population level than Caucasians and Asians in the USA, in California according to the CDC and the other studies? Why has it been known since the 1950s that olders fathers and schizophrenia/autism, etc. are related and the public is steered in late fathering. If you read the many epidemiologic studies or the studies on the increasing DNA breakage in sperm with a man's age you will find the warnings that older paternal age is the most potent cause of genetic disease that seems to come from nowhere. There are many studies that have to do with epidemiology and paternal age and with sperm and older age that are not funded. Why? Why do recent studies on autism not point out the paternal age connection. Even in plants mutations are known to arise predominantly in the paternal germ line, not the maternal germ line.

Who benefits? Who looses? Why are papers warning of the consequences of advanced paternal age (past 31) suppressed and ignored? The rise in "autism" is not unexpected or mysterious!

Journal of Epidemiology and Community Health 2006;60:851-853; doi:10.1136/jech.2005.045179Copyright © 2006 by the BMJ Publishing Group Ltd.


SHORT REPORT
Advanced paternal age: How old is too old? Isabelle Bray, David Gunnell, George Davey Smith
Department of Social Medicine, University of Bristol, UK
Correspondence to:Correspondence to: Dr I Bray Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK; Issy.Bray@bristol.ac.uk

"Average paternal age in the UK is increasing. The public health implications of this trend have not been widely anticipated or debated. This commentary aims to contribute to such a debate. Accumulated chromosomal aberrations and mutations occurring during the maturation of male germ cells are thought to be responsible for the increased risk of certain conditions with older fathers. Growing evidence shows that the offspring of older fathers have reduced fertility and an increased risk of birth defects, some cancers, and schizophrenia. Adverse health outcomes should be weighed up against advantages for children born to older parents, mindful that these societal advantages are likely to change over time."

"But in men, sperm are being made continuously throughout adult life from precursor germ cells that have much more time to be damaged..."

This is not well-known but this site reveals that testes have a preference for mutated sperm.


Sperm mutate more often as men get older - not because it helps their resulting offspring, but because it appears to help sperm survive in the testes, researchers have found. The discovery was made by accident - while seeking to understand a rare inherited condition known as Apert syndrome, which is more likely to develop in children born to older men, said the report in the journal Science."Striking male biases in mutation rates are observed in many human genetic disorders," said Dr Anne Goriely of the Weatherall Institute of Molecular Medicine at the University of Oxford, who led the British and Swedish research team.In the case of Apert syndrome, mutations in a gene known as FGFR2 "arise exclusively from the unaffected father and are associated with increased paternal age." The syndrome often results in affected children having distortions of the head and face, and fused fingers and toes - conditions that require multiple corrective surgeries.The team found that the mutation, although harmful to a foetus if the sperm were to fertilise one, appears to be beneficial to the sperm within the cellular environment of the testes. The mutation is preferentially selected even before meiosis, the two-cell division that lead to the production of a sperm cell.The researchers developed a special technique to measure mutation rates in sperm, and found that FGFR2 mutations occur infrequently. They had suspected these might be common events that accumulate with age and become amplified through natural selection.But their relative rareness, and their proliferation - with serious consequences for children who inherit them - seems to be at odds with natural selection as it usually understood.Dr Jim Cummins, a spermatologist at the school of health sciences at Murdoch University in Perth, argues that sperm mutations may be more common than is currently thought, but are rarely harmful: natural selection would weed out only those mutations that reduce or impair fertility."In this case, however, because the kids are badly affected, natural selection would prevent them from passing on the defective gene," Cummins told ABC Science Online.Similar problems are far less likely to occur in women, he said, because their lifetime egg supply - and the process of cell division required to produce eggs - is completed before they are born.But in men, sperm are being made continuously throughout adult life from precursor germ cells that have much more time to be damaged - by exposure to radiation, toxins or disease - in ways that may give rise to mutations."The likelihood of congenital defects arising through faulty cell division in the egg precursors doesn't increase with maternal age," he said. "Of course, advancing age leads to increased random damage to DNA from radiation or chemical exposure, so if this is not repaired, there could be an increased risk of a defect from that source."

By the time a man is 60 years old, sperm deterioration is so great that 85% of sperm is considered to be abnormal.

Furthermore, medical conditions such as obesity, cancer and cystic fibrosis can also impact male fertility, such as hormone deficiencies as well as genetic diseases.
Studies have found that both sperm quality and sperm mobility decrease as men age, leading to a reduced chance of conception. In addition, the natural process during which damaged sperm die and are flushed from the body slows down with age, impacting sperm quality. Sperm damage is also more common as men age.
A recent study has found that advanced age in men carries similar risks as advanced age in women with regard to passing on birth defects to their offspring as well as with reducing an individual’s chances of getting pregnant. The study was conducted over a fourteen-year period and found that were was an increased risk of Down’s syndrome in patients, particularly in cases when both the mother and father were over the age of 40.
Studies have also found that there is a link between a father’s age and the risk of schizophrenia and autism, as well as achondroplasia, a genetic disorder that often results in dwarfism. This is because sperm DNA fragmentation increases with male age, leading to a higher risk of gene mutation.
A study conducted by the University of California Berkeley in the United States also supports the relationship between male age and fertility. The study found that sperm began to deteriorate during a man’s twenties, and that sperm function, including sperm motility, slowed down 0.7% annually. By the time a man is 60 years old, sperm deterioration is so great that 85% of sperm is considered to be abnormal. The study was based on the analysis of sperm of 100 men ranging in age from 22 to 80.

"The optimal time for a man to father a healthy child is the same as for a woman — 25 or so," says Dolores Malaspina,

But you don't have to carry a genetic disease to pass one on — the trouble can start in your testicles. There, sperm-generating cells divide about 23 times a year, in the process slowly accumulating copying errors.


"Older fathers are more likely to have children with autism. Researchers tracked 387,000 people born in Israel and concluded the odds of fathering an autistic child are about 6 in 1,000 for men under 20. When a man reaches 50, those odds shoot up to about 52 in 1,000.
"The optimal time for a man to father a healthy child is the same as for a woman — 25 or so," says Dolores Malaspina, a psychiatry professor at New York University and coauthor of the study.
Malaspina led an earlier study showing a connection between paternal age and schizophrenia. She found children born to fathers over 50 carried about three times the risk of developing schizophrenia as those born to fathers in their 20s.
Autism and schizophrenia both arise from a little-understood combination of genetic and environmental triggers. Both disorders tend to run in families, suggesting that genetic risk factors can be inherited.
But you don't have to carry a genetic disease to pass one on — the trouble can start in your testicles. There, sperm-generating cells divide about 23 times a year, in the process slowly accumulating copying errors.
Older fathers are more likely to have children with achondroplasia (dwarfism) and several other conditions caused by spelling errors in the DNA. So for a man, the older you get, the less your child's genetic endowment will resemble your own.
For women, aging isn't as likely to lead to spelling errors because we make no new eggs after we're born. But that leads to other problems. The million or so we begin life with die at a rate of about 30 a day, and as the remaining eggs age, they get less adept at one of their critical jobs — dividing their 46 chromosomes in half. Eggs don't do this until after they're penetrated by a sperm."

1826 was the first mention in western scientific literature that there was a paternal age effect

"The first mention in the historical literature suggesting a possible life-shortening effect on offspring of delayed parenting was made by the French naturalist Buffon(1826), who noted that when old men procreate "they often engender monsters, deformed children, still more defective than their father"(see Robine and Allard 1997)


What is the first mention in historical literature of the paternal age effect? From a paper, "Human Longevity and Parental Age at Conception",by L.A. Gavrilov and N.S. Gavrilova, 2000 Thank you to Dr. Leonid Gavrilov for sending me the link to his paper because I was wondering what the early written observations of the problems of children of advanced paternal age were.
\Isn't it about time that prospective dads and biology students were informed? Prospective moms too?

Paternal age effect
From Wikipedia, the free encyclopedia
• Ten things you didn't know about Wikipedia •
Jump to: navigation, search
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
//

[edit] 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

[edit] See also
Maternal age effect

[edit] 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.

[edit] External links

Irrefutable truth about spontaneous mutations in sperm and neurocognitive disorders

Dolores Malaspina, M.D. Chair of NYU Medical School Department of Psychiatry


"The most irrefutable finding is our demonstration that a father’s age is a major risk factor for schizophrenia. We were the first group to show that schizophrenia is linearly related to paternal age and that the risk is tripled for the offspring of the oldest groups of fathers.7 This finding has been born out in every single cohort study that has looked at paternal age and the risk for schizophrenia. The only other finding that has been as consistently replicated in schizophrenia research is that there is an increased risk associated with a family history of schizophrenia. Since only 10% to 15% of schizophrenia cases have a family history, family history does not explain much of the population risk for schizophrenia. However, we think that approximately one third or one quarter of all schizophrenia cases may be attributable to paternal age. Paternal age is the major source of de novo genetic diseases in the human population, which was first described by Penrose8 in the 1950s. He hypothesized that this was due to copy errors that arose in the male germ line over the many cycles of sperm cell replications. These mutations accumulate as paternal age advances. After the Penrose report, medical researchers identified scores of sporadic diseases in the offspring of older fathers, suggesting that these could occur from gene mutations. Particular attention was paid to conditions in last-born children. In the 1960s, an excess of schizophrenia in last-born children was also reported."

Spontaneous Mutations in Human Testes

Molecular Anatomy of SPONTANEOUS MUTATIONS in Human Testes


The Molecular Anatomy of Spontaneous Germline Mutations in Human Testes
ABSTRACT
The frequency of the most common sporadic Apert syndrome mutation (C755G) in the human fibroblast growth factor receptor 2 gene (FGFR2) is 100–1,000 times higher than expected from average nucleotide substitution rates based on evolutionary studies and the incidence of human genetic diseases. To determine if this increased frequency was due to the nucleotide site having the properties of a mutation hot spot, or some other explanation, we developed a new experimental approach.
We examined the spatial distribution of the frequency of the C755G mutation in the germline by dividing four testes from two normal individuals each into several hundred pieces, and, using a highly sensitive PCR assay, we measured the mutation frequency of each piece. We discovered that each testis was characterized by rare foci with mutation frequencies 103 to >104 times higher than the rest of the testis regions.
Using a model based on what is known about human germline development forced us to reject (p < 10−6) the idea that the C755G mutation arises more frequently because this nucleotide simply has a higher than average mutation rate (hot spot model). This is true regardless of whether mutation is dependent or independent of cell division.
An alternate model was examined where positive selection acts on adult self-renewing Ap spermatogonial cells (SrAp) carrying this mutation such that, instead of only replacing themselves, they occasionally produce two SrAp cells. This model could not be rejected given our observed data. Unlike the disease site, similar analysis of C-to-G mutations at a control nucleotide site in one testis pair failed to find any foci with high mutation frequencies.
The rejection of the hot spot model and lack of rejection of a selection model for the C755G mutation, along with other data, provides strong support for the proposal that positive selection in the testis can act to increase the frequency of premeiotic germ cells carrying a mutation deleterious to an offspring, thereby unfavorably altering the mutational load in humans.
Studying the anatomical distribution of germline mutations can provide new insights into genetic disease and evolutionary change.
Authors: Jian Qin, Peter Calabrese, Irene Tiemann-Boege, Deepali Narendra Shinde, Song-Ro Yoon, David Gelfand, Keith Bauer, Norman Arnheim

Would Families Have Children At Younger Ages If It Was Clear That By the Age of 33 Sperm DNA mutations Are Rapidly Accumulating?

Is the mutated gene due to paternal contribution ?

The Wellcome Trust does not mention whether paternal or maternal age is involved.

Mutations in the Insulin Gene Can Cause Neonatal Diabetes
• Diabetes news • Sep 11, 2007
Ten previously unknown mMutations in the insulin gene can cause permanent neonatal diabetes, an unusual form of type 1 diabetes that affects very young children and results in lifelong dependence on insulin injections, report researchers from the University of Chicago and Peninsula University (Exeter, UK) in Sept. 18, 2007, issue of the Proceedings of the National Academy of Sciences, published early online.
Although abnormal insulin has been associated with milder cases of type 2 diabetes since the discovery of “insulin Chicago” in 1979, this is the first time that an insulin mutation has been connected to severe diabetes with onset early in life.type-1 diabetes.
The researchers describe the10 mutations, found in 221 patients from 16 families., and show how several of the mutations alter the way the protein folds, disrupting insulin synthesis. They suspect that the mutations alter the way insulin folds during its synthesis. TThey suggest that these improperly folded proteins interfere with other cellular processes in ways that eventually kill the cells that produce insulin.
“This is a novel and potentially treatable cause of diabetes in infants,” said study author Louis Philipson, MD, PhD, professor of medicine at the University of Chicago. “It’s exciting because each of these patients has one normal insulin gene as well as one mutated gene. If we could detect the disease early enough and somehow silence the abnormal gene, or just protect insulin-producing cells from the damage caused by misfolding, we might be able to preserve or restore the patient’s own insulin production.” .....

Vaccines and autoimmune disorders

Vaccines and autoimmune disease, this is from an insert for a rabies vaccine for dogs and cats:


SAFETY AND EFFICACY: Because Defensor 3 is produced on an established cell line, it has safety advantages over inactivated brain-origin rabies vaccines. Tissue-origin vaccines contain extraneous protein in addition to rabies antigen that can lead to autoimmune disease.

It is the father's age that causes spontaneous mutations that cause autism, etc. not the mother's

By age 27 a man's sperm has divided 300 times One new mutation in sperm. each time it replicates.

Geneticist James F. Crow wrote in 1994: "I don't find this nonlinear effect at all surprising. Everything gets worse with age, so I fully expect fidelity of replication, efficiency of editing, and error correction to deteriorate with age. For a man of age 20, the male mutation rate is about 8 times the female rate. With a linear increase, in a man at age 30, the ratio is 430/24 = 18, at age 45 it is 770/24 = 32. With nonlinearity, these ratios are much larger, some 30-fold at age 30 and as much as two orders of magnitude at age 40. Examples such as MEN2A, MEN2B, and Apert syndrome, in which a total of 92 new mutations were all paternal, are therefore not so surprising. Whatever selective forces reduced the mutation rate in our distant past, at a time when most reproduction must have been very early, were not effective for older males.
I conclude that for a number of diseases the mutation rate increases with age and at a rate much faster than linear. This suggests that the greatest mutational health hazard in the human population at present is fertile old males. If males reproduced shortly after puberty (or the equivalent result were attained by early collection of sperm and cold storage for later use) the mutation rate could be greatly reduced. (I am not advocating this. For one thing, until many more diseases are studied, the generality of the conclusion is not established. Furthermore, one does not lightly suggest such socially disruptive procedures, even if there were a well-established health benefit.)"

Autism, schizophrenia, type 1 diabetes, MS, other autoimmunes, etc. had to rise because average paternal age over 31 rose so much

Since 1980. We are not told about the male biological clock. No will to prevent the average person from having autistic children. Those in the know do know about the paternal age effect but the political will is to have a weaker citizenry. We could have diminished the number of mentally ill, the diabetic, the autistic, the people with all kinds of genetic disorders, but instead the people who want to warn the public cannot do so.



Journal of Epidemiology and Community Health 2006;60:851-853; doi:10.1136/jech.2005.045179Copyright © 2006 by the BMJ Publishing Group Ltd.
Advanced paternal age: How old is too old? Isabelle Bray, David Gunnell and George Davey Smith
Department of Social Medicine, University of Bristol, UK
Correspondence to: Dr I Bray Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK; Issy.Bray@bristol.ac.uk


Average paternal age in the UK is increasing. The public health implications of this trend have not been widely anticipated or debated. This commentary aims to contribute to such a debate. Accumulated chromosomal aberrations and mutations occurring during the maturation of male germ cells are thought to be responsible for the increased risk of certain conditions with older fathers. Growing evidence shows that the offspring of older fathers have reduced fertility and an increased risk of birth defects, some cancers, and schizophrenia. Adverse health outcomes should be weighed up against advantages for children born to older parents, mindful that these societal advantages are likely to change over time.
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Autism, type 1 diabetes, Alzheimer's, schizophrenia in many, many cases could have been prevented by fathering babies before the age when the DNA breaks and mutations occur.
One third or more cases of schizophrenia are caused by increasing paternal age over 32. The risk goes up with the father's age. Vaccinations are an assault above and beyond paternal age.


The amount of neurocognitive disorders had to rise with rising average paternal age. Vaccinations are in addition to DNA strand breaks, and other damage. Still there is not a public health warning on paternal age and maternal age is falsely pointed to as the cause of sporadic autism. There have been studies for 50 years showing the effects of older paternal age. All kinds of disorders including non-familial mental retardation, fibromyalgia, progeria, Huntington chorea, heart defects, prostate cancer, breast cancer can be caused by mutations in the sperm of older fathers. These are non-familial, spontaneous mutations and cerebral palsy, low birth-weight and many conditions that are deleterious, and chronic life long disabilities including hemophilia, Duchennes, blindness, autism are carried by mothers who had an older father. 34 is an older father when these disorders start showing up in offspring.

Many disorders such as lupus, scleroderma, type 2 diabetes have not been studied for paternal age effects because there is no will to prevent these profitable diseases.

Men Your Sperm Becomes Fragmented Autism Can Be the Result for Babies

No Doubt That Father's Age and Habits are Crucial The 20s to very early 30s are the time to conceive babies.


"But the bottom line in all of this is that couples should consider conceiving earlier when their fertility is at optimum levels," she said.


Fat, smokes, booze will hurt sperm


By Tamara McLean
September 10, 2007 04:09pm
MEN over 40 are being warned that their stomach fat, smoking habits and love of alcohol will damage their sperm and their chance of fatherhood.
Reproductive experts say there is emerging evidence that a man's fertility declines steadily with age just as it does for a woman, seriously impairing the couple's chance of having a baby.
It was well documented that the window of opportunity for women to conceive falls quickly in their late 30s, but evidence for men has been less clear, said Dr Anne Clark, chairwoman of the Fertility Society of Australia's fertility protection group.
"While the amber light of infertility comes on at the age of 35 for women, it is not so well known that it starts to shine for men at around 40," Dr Clark said at the fertility society's conference in Hobart.
Sperm count, shape and "travel path" has been the traditional method of analysing male fertility but new evidence suggests that DNA breakages in sperm may be a principal reason for male infertility problems.
For men with more than 20 per cent of their sperm "fragmented" the chance of pregnancy is significantly reduced, chance of miscarriage increased three to four times and there is also increased risk of birth defects.

No Public Health Warning About Escalating Risks of Autism and Schizophrenia, etc. with Paternal Aging

"Defining a cut-off at which the risk is significantly increased in the offspring could have an important impact on public health." A link between older fathers and neurodevelopmental disorders seen since the 1950s

1: Eur Psychiatry. 2007 Jan;22(1):22-6. Epub 2006 Dec 4.
Links
Paternal ages below or above 35 years old are associated with a different risk of schizophrenia in the offspring.
Wohl M, Gorwood P.
INSERM U675, 16 rue Henri Huchard 75018 Paris, France.
BACKGROUND: A link between older age of fatherhood and an increased risk of schizophrenia was detected in 1958. Since then, 10 studies attempted to replicate this result with different methods, on samples with different origins, using different age classes. Defining a cut-off at which the risk is significantly increased in the offspring could have an important impact on public health. METHODS: A meta-analysis (Meta Win) was performed, assessing the mean effect size for each age class, taking into account the difference in age class references, and the study design. RESULTS: An increased risk is detected when paternal age is below 20 (compared to 20-24), over 35 (compared to below 35), 39 (compared to less than 30), and 54 years old (compared to less than 25). Interestingly, 35 years appears nevertheless to be the lowest cut-off where the OR is always above 1, whatever the age class reference, and the smallest value where offspring of fathers below or above this age have a significantly different risk of schizophrenia. CONCLUSION: No threshold can be precisely defined, but convergent elements indicate ages below or above 35 years. Using homogeneous age ranges in future studies could help to clarify a precise threshold.
PMID: 17142012 [PubMed - indexed for MEDLINE]1: Eur Psychiatry. 2007 Jan;22(1):22-6. Epub 2006 Dec 4.
Links

New Mutations and Paternal Age 1979 It is old news that paternal age causes spontaneous mutations meaning germ line mutations

: J Med Genet. 1979 Apr;16(2):147-8.Links
Paternal age effect in fibrodysplasia ossificans progressiva.Rogers JG, Chase GA.
Analysis by the method of Smith (1972) of birth order and parental age data collected from 38 of 42 patients with fibrodysplasia ossificans progressive shows a significant paternal age effect. This finding among the sporadically occurring cases would support the proposition that this condition usually arises as a new dominant mutation.

PMID: 287808 [PubMed - indexed for MEDLINE]

Critique of FDA's proposal for evaluation of health claims

PRESS AND PUBLIC INFORMATION RELEASE

PLEASE FORWARD WIDELY!

US FDA Guidance on health claims signals
possible end-run of DSHEA

The American Association for Health Freedom (AAHF) in association with its international affiliate, the Alliance for Natural Health (ANH) have today submitted a powerful critique of the US Food & Drug Administration’s (FDA) proposal for evaluation of health claims which has been open to public consultation.

Since the passage of the Dietary Supplement Health & Education Act in 1994, American citizens have enjoyed one of the most liberal regimes for dietary supplements anywhere in the world. This legal regime was won only after unprecedented public lobbying of Congress, stimulated by concerns over unnecessary restrictions on natural products.

The FDA was forced to re-consider its approach to health claims following a Court of Appeals decision which followed the Pearson v Shalala case in 1999. The AAHF acted as joint plaintiffs in this ground-breaking case which challenged the FDA’s decision to disallow four substance/disease relationship claims. However, this latest proposal by the FDA is set to create a situation where only the largest, most well funded companies, such as pharmaceutical corporations, will be able to afford the evidence-based, stringent data requirements for health claims. These requirements would prevent smaller companies, which have historically been the key pioneers and innovators in the natural health field, from making claims as they would not be able to afford the cost of substantiation.

Dr Robert Verkerk, Scientific Advisor to AAHF and Executive and Scientific Director of the ANH, who was the lead author of the AAHF’s critique of the FDA Guidance, said:

“The FDA is in danger of being swayed by processes in Europe which, if followed into law in the US, could have catastrophic effects on the US natural health industry. Consumers need adequate information which tells them which substances are beneficial in reducing the risk of particular diseases to help them make informed choices, but the FDA seems to want to raise the bar so high that much of this vital, health-giving information will be lost from product labels and supporting material. If smaller manufacturers are forced to omit information even if it is supported by scientific and clinical evidence, there is no doubt that this would be a fundamental infringement on our human right to freedom of information and choice”.

The FDA’s proposed system which is almost exclusively reliant on evidence from human trials and observational studies, would likely ditch claims which were based on in vitro and biochemical studies, as well as animal studies, which are cheaper and have formed the basis of many structure/function claims to-date.

The AAHF and ANH are deeply concerned that the tone of the FDA Guidance document suggests a move by the FDA towards classic orthodox medicinal models, which will dispense of the framework that has led so many Americans towards taking responsibility for their own health.

ENDS.

CONTACTS

Alliance for Natural Health
Dr Robert Verkerk
The Alliance for Natural Health,
The Atrium, Dorking, Surrey RH4 1XA,
United Kingdom
Phone: +44 (0)1306 646 600
Fax: + 44 (0)1306 646 552
E-mail: info@anhcampaign.org


American Association for Health Freedom
Brenna Hill
American Association for Health Freedom and The Health Freedom
Foundation
4620 Lee Highway, Suite 210
Arlington, VA 2220
Phone: 1.800.230.2762 or 703.294.6244
Fax: 703.624.6380
E-mail: healthfreedom2000@yahoo.com


EDITOR’S NOTES

Food & Drug Administration (FDA)
FDA Guidance document is entitled “Guidance for Industry: Evidence-Based Review System for the Evaluation of Health Claims”

See full Guidance document at: http://www.cfsan.fda.gov/~dms/hclmgui5.html

Alliance for Natural Health (ANH)
The ANH is a UK-based, internationally-active, non-governmental organization working to positively shape regulatory and scientific frameworks affecting natural health. As an alliance, the ANH brings together scientists, medical doctors, integrative practitioners, lawyers and consumers, as well as suppliers of food and dietary supplements, globally as a means of working towards the development of sustainable approaches to healthcare. The ANH has been extensively involved in inputs to European Member State governments, the European Commission and the European Food Safety Authority (EFSA) with regard to the EU Nutrition & Health Claims Regulation which came into force across Europe on 1 July 2007.
www.anhcampaign.org


American Association for Health Freedom (AAHF)
The American Association for Health Freedom (AAHF) is a 501(c)4 nonprofit organization serving as the politically active voice at federal and state levels to protect Americans’ rights to access integrative medicine and dietary supplements. AAHF protects the right of the consumer to choose and the practitioner to practice by lobbying Congress and state legislature and crafting legislation; acting as a government watchdog and filing comments on proposed rulings; educating the public, press, and decision-makers on integrative medicine; initiating legal activities and joining and forming significant coalitions.
www.healthfreedom.net

NOTE:
The full critique by the AAHF/ANH can be downloaded at:
http://www.alliance-natural-health.org/_docs/ANHwebsiteDoc_278.pdf





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