AUTISM PREVENTION FATHER BABIES 24-34 PATERNAL AGE IS KEY IN NON-FAMILIAL AUTISMVaccines

"It is very possible that PATERNAL AGE is the major predictor of(non-familial) autism." Harry Fisch, M.D., author "The Male Biological Clock". Sperm DNA mutates and autism, schizophrenia bipolar etc. results. What is the connection with autoimmune disorders? Having Type 1 diabetes, SLE,etc. in the family, also if mother had older father. NW Cryobank will not accept a sperm donor past 35th BD to minimize genetic abnormalities.VACCINATIONS also cause autism.

Saturday, June 30, 2007

Cryopreservation of Sperm is Not Without Some Hazards for Some Offspring

There has not been enough follow-up study of the effects of cryopreservation on the children.

It is best to father all babies before the age of 33. The prior family history and toxic exposures of all kinds add to the paternal age effect. This is radically different from what we have been taught.

Some papers on the subject:



This paper has no abstract: 1: Hum Reprod. 2006 Jul;21(7):1943-4. Links
The child of problems.Auroux M.
PMID: 16818965 [PubMed - indexed for MEDLINE]




Long-term effects in progeny of paternal environment and of gamete/embryo cryopreservation. Human Reproduction Update 2000, 6, 550-563


The full text is available for free at the above address this is the abstract. A MUST READ

1: Hum Reprod Update. 2000 Nov-Dec;6(6):550-63. Links
Erratum in:
Hum Reprod Update 2001 Jan-Feb;7(1):112.
Long-term effects in progeny of paternal environment and of gamete/embryo cryopreservation.Auroux M.
CHU de Bicêtre (Université Paris-Sud), Andrologie et Biologie de la Procreation, Le Kremlin-Bicêtre, France.

In addition to gross malformations, many problems relating to the formation of gametes and embryos can generate, within a continuum of abnormalities, a number of problems that are less evident. On the basis of genetic and/or biochemical or cytological changes, these effects generally appear long after birth as functional difficulties that range from growth changes and altered endocrine functions and cancer to very late behavioural disorders. Such problems may have effects on males and females before conception, on the embryo during gestation, and may also impact on the success of assisted reproduction techniques. For this reason, we have examined the experimental and clinical data that indicate the long-term consequences, for progeny, of iatrogenic and toxic environmental factors on the male reproductive system, and in particular the effect that one specific condition-cryopreservation-may have on gametes and the conceptus. We then focus on the interpretation given to these data which, in general, emphasize the need not only for further experiments to help understand the mechanism of anomalies and increase the level of vigilance in humans, but also to extend follow-up investigations in children.
PMID: 11129688 [PubMed - indexed for MEDLINE]





Human Reproduction, Vol. 14, No. 5, 1141-1145, May 1999
© 1999 European Society of Human Reproduction and Embryology

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Debates Continued

Embryo cryopreservation and development: facts, questions and responsibility
Emmanuel Dulioust1,3, Marie-Claire Busnel2, Michele Carlier2, Pierre Roubertoux2 and Maurice Auroux1
1 Biologie de la Reproduction et du Développement, CHU de Bicêtre, Universite Paris-Sud, 94275 Le Kremlin-Bicêtre, and 2 Genétique, Neurogenétique, Comportement, CNRS UPR 9074, Institut de Transgénose, 3B rue de la Férollerie, 45071 Orleans Cedex 02, France

Four years ago, the results of an experimental study led us to conclude that in the mouse, cryopreservation of preimplantation embryo induced post-natal effects and thus could not be considered as neutral for the long-term development (Dulioust et al., 1995). This raised some concern in the scientific community and in the public about the safety of embryo cryopreservation in human assisted procreation. It has even been said that we had withdrawn our conclusions (Human Fertilisation and Embryology Authority, 1996); this was unfounded. Since then, only few studies have focused on this issue. Recently, a severe attack of our work was published (Testart, 1998). Here, we examine these criticisms and discuss the state of the art in the light of recent clinical and experimental studies.

Methodological criticisms

Principles of the study
According to Testart (1998), our research was limited to some kind of statistical fishing, lacking rational hypotheses, since `it appears that the clinical risk of freezing human embryos is only to slightly decrease the pregnancy rate' (Testart, 1998). In other words, while acknowledging that the embryo's ability to implant may be impaired by the freeze–thaw process, it is supposed that no other feature is altered. We thought that this common viewpoint was far from being substantiated and that, besides more detailed and long-term clinical investigations, additional experimental studies were needed.

Screening for various possible effects is common in toxicology, especially in reproductive and developmental toxicology. More precisely, our reflection and strategy were based on several facts and hypotheses: (i) freezing, cryoprotectants and finally, cryopreservation as a whole induce in cells a wide spectrum of chemical and metabolic disorders (Dulioust, 1995); these effects could in turn alter, through several pathways, developmental determinants like nuclear or mitochondrial DNA; (ii) although neither the practice of embryo cryopreservation in humans and cattle nor previous experimental studies have evidenced genotoxic or teratogenic effects, other works have reported genetic effects either in bacteria or somatic cells (Dulioust, 1995). This suggested the possibility of a still undetected genotoxic potential; (iii) assessment of post-natal development after embryo cryopreservation has mainly focused on patent anomalies at birth or in early life, and has not been carried out on adult and senescent individuals. However, many mutations can have mild or delayed phenotypic effects, and numerous clinical and experimental observations show that developmental disturbances can respect viability and macromorphological appearance while altering physiological processes, including behaviour and cognitive functions, through biochemical or microstructural anomalies (Auroux, 1997). Besides classic morphological examination, neural and behavioural screening has been recommended, for instance, by the National Institutes for Mental Health (NIMH), for transgenic and knock-out mice. There was thus a serious gap between the wide range of potential long-term effects of embryo cryopreservation and the means by which they had been investigated until then.

These facts, plus our past experience, prompted us to use, besides basic physical examination, sensori-motor and behavioural tests in an experiment comparing mice derived from cryopreserved versus non-cryopreserved embryos. We used classical tests (Carlier et al., 1983; Roubertoux et al., 1992) most of which are cited in a recently published list of behavioural tests (Crawley et al., 1997). In addition, we assessed mandible morphology, a classic teratological test, as an indicator of micromalformations (Festing, 1972; Bailey, 1985). We also programmed a long-term study, postulating that some anomalies could be undetected in youth but become detectable in adults or in old subjects. Furthermore, the experiment was carried out in parallel on two hybrid strains. This caution had two purposes. Since it is well known that genetic background can modulate the susceptibility to environmental modifications, affects, for instance embryo tolerance to cryopreservation (Schmidt et al., 1985, 1987; Dinnyes et al., 1995), we wished to be able to detect a possible variability of the results in relation with genotype. We also wanted to compare the intensity of eventual effects of cryopreservation with that of genotype-related differences. Similarly, sex-related differences have been documented in various situations (Auroux, 1997). So, in our experiment three main factors, genotype, sex and cryopreservation, were considered and various tests or evaluations were performed at different periods up to 67 weeks of age.

Statistical analysis
Testart has apparently understood that our analysis only consisted in numerous paired comparisons (Testart, 1998). According to him, this would explain why some significant differences were found. This explanation is invalid; as mentioned in our paper, all data (excepted those evaluating pre-weaning development for which sexes were not separated) were analysed in a three-way analysis of variance, according to the experimental design. Paired comparisons were made only when the analysis of variance (ANOVA) showed a significant main effect or an interaction between cryopreservation and one of the other studied factors.

No report of some negative results
Testart also suggested that we intentionally omitted negative results, especially regarding body weight (Testart, 1998). The debate deserves better arguments than such insinuations. All the results that were not presented in tables or figures were mentioned in the text, and we confirm that body weight was only recorded at the ages that we mentioned.

Discussion of the results

Maternal factor as a possible source of bias
The use of outbred mice as recipient females has been questioned, as they could have provided an heterogeneous uterine environment that might have contributed to the observed differences. Although Naval Medical Research Institute (NMRI) mice are not inbred, they show high consanguinity and histocompatibility. Additionally, we carefully controlled their age (8 weeks) and weight (28–30 g) and we verified that offspring's adult weights were not correlated with maternal ones. Moreover, this alternative explanation itself implies other hypotheses; the embryos from one category (for instance, the cryopreserved ones) should have been preferentially transferred to females having particular characteristics. This seems very unlikely, because the foster females were chosen at random and the transfers alternated embryos from the different groups. Furthermore, there should be specific relationships between this hypothetical particular type of females and the various differences that we observed. So, is such a hypothesis really less speculative than a relationship with cryopreservation?

Variability of the observed differences
Testart pointed out the variability of the effects of cryopreservation in relation to sex, genotype or age (Testart, 1998). According to him, this pattern revealed that there were only sampling variations giving rise, occasionally, to statistically significant differences. This view is based on a misunderstanding of our statistical procedures, as mentioned above. More fundamentally, it also seems to assume that true biological effects of cryopreservation should be similar whatever the genetic background. This is refuted by common experience with embryo freezing and, more generally, by numerous observations in biological research (Fraser and Fainstat, 1951; Tuchmann-Duplessis, 1975; Roubertoux et al., 1990, 1992). Of course, false significant differences due to random or to undetected biases cannot be completely ruled out but, in our study, it was very unlikely that all the effects found in ANOVA were due to random variations. Moreover, the experimental cautions taken, and the fact that clear differences were observed between sexes or strains made it difficult to identify the influence of an uncontrolled factor. Conversely, it is conceivable that both the primary cellular effects of cryopreservation and their later phenotypic expression could vary according to the genetic background, including sex.

Size of the differences
As we first stated in discussing our results, cryopreservation did not induce major anomalies, even in old animals. When observed, the differences between cryopreserved and control animals were similar in magnitude to other differences related to genotype or sex. Is this fact by itself sufficient to think that these differences were not due to cryopreservation but to sampling variations? In our opinion, given the hypotheses about the possible cellular effects of cryopreservation, finding differences that were equivalent or sometimes larger (e.g. body weight at 67 weeks) than genotype-related ones deserves attention. Variations of multifactorial quantitative traits like those we evaluated, whether spontaneous or experimental, are often moderate (Ramel, 1983; Vogel and Motulski, 1997). Thus, the pattern of the cryopreservation-related differences was compatible with the hypothesis of slight and probably heterogenous alterations of intrinsic developmental determinants. Of course, identifying these alterations by cellular and molecular investigations in cryopreserved embryos would be necessary to confirm a causal relationship between cryopreservation and later phenotypic changes.

Selective bias
Some embryos are destroyed by the freeze–thaw process, or fail to implant and proceed to further development. Therefore, cryopreservation operates a selection among the initial population of embryos. Testart proposes that such a selection might have caused the differences observed between the cryopreserved mice and the controls, which were not exposed to selection. Even if it supposes a relationship between tolerance to freezing–thawing (which may involve accidental features, like for instance the stage of cellular cycle at which the embryo is frozen) and later expressed phenotypic traits, this explanation could be pertinent when the embryos are genetically heterogeneous, as in humans. However, in our experiment, all the embryos from one strain were genetically identical, since they were F1 hybrids derived from inbred parents. There is no solid reason to suppose that some unknown factor had caused, before cryopreservation, a genetic heterogeneity of the embryos inside each strain.

Evaluation of embryo cryopreservation and other assisted reproductive technologies, today and future

In our paper, we concluded that this long-term study confirmed in the mouse that embryo cryopreservation is not severely detrimental, but also indicated that it may not be absolutely free of long-term effects. What could this imply about the safety of embryo freezing in man? Of course, directly extrapolating from mice to humans was not conceivable. In humans, moreover, phenotypic changes like those we observed in highly controlled experimental conditions could be shadowed by the combined influence of genetic heterogeneity and highly diverse environmental conditions. Nevertheless, our results implied a possible susceptibility of development and post-natal phenotype to preimplantation manipulations or environmental factors. Such a notion had already been proposed (Reik et al., 1993). By itself, it justifies a more careful evaluation of embryo cryopreservation and other assisted reproductive technologies (ART).

Since our report, other studies on children born from cryopreserved embryos have been published (Sutcliffe et al., 1995a,b; Olivennes et al., 1996; Wennerholm et al., 1997, 1998). They all concluded that cryopreservation induced no major pathological features. Some differences were found with children born after either in-vitro fertilization (IVF) without cryopreservation or natural conception, e.g. frequencies of major and minor congenital anomalies, parameters evaluating mental age (Sutcliffe et al., 1995a,b) and weight of girls (Wennerholm et al., 1997, 1998), but they were either not significant or significant but isolated and rather small. Obviously, they remained difficult to interpret in the context of these studies where, despite methodological precautions, several confounding factors could not be controlled.

In other mammalian species, it is generally considered that cryopreservation of the embryo does not affect its development after implantation. Most experiments have been done in the mouse and, as said in introduction, have shown that embryo cryopreservation is not strongly teratogenic or mutagenic in this species. However, several studies have suggested the possibility of detrimental effects beyond implantation, as evidenced by increased rates of post-implantation losses (Rall et al., 1987; Kono and Tsunoda, 1988; Trounson et al., 1988; Shaw and Trounson, 1989; Wilson and Quinn, 1989; Liu et al., 1993) or by reduced fetal weight (Shaw and Trounson, 1989). A lower post-implantation viability has also been reported after mouse oocyte cryopreservation (Van der Elst et al., 1993; Wood et al., 1993; George et al., 1994), and although the induction of aneuploidies due to spindle disorganization has been proposed as a cause of fetal loss, this remains controversial. Some years ago, we showed ourselves, in mouse embryos derived from frozen–thawed oocytes, an increased frequency of sister chromatid exchanges, suggesting a mutagenic effect of cryopreservation (Bouquet et al., 1993). To our knowledge, no recent study has focused on post-natal development of animals cryopreserved as embryos.

Interestingly, however, other experiments have evidenced an influence of preimplantation in-vitro culture conditions or embryo manipulations on post-implantation development. For example, lamb birth weight has been found to be affected by the medium in which the embryos were cultivated from the zygote stage to compaction (Thompson et al., 1995). Retarded fetal development and neural tube defects have been observed in mouse fetuses after pre-implantation exposure to ammonium ions (Lane and Gardner, 1994). More generally, it seems that IVF and embryo culture or manipulations can affect post-implantation viability, gestation length and developmental features (Wright and Ellington, 1995; Walker et al., 1996; Thompson, 1997). In humans, the results from different studies about the outcome of IVF pregnancies and the children's health status are contradictory about the possibility of moderate differences with non-IVF pregnancies. Recently, the follow-up of children conceived by intracytoplasmic sperm injection (ICSI) has raised a similar debate about the frequency of malformations (Bonduelle et al., 1997; Kurinczuk and Bower, 1997) and the occurrence of functional disorders (Bonduelle et al., 1998; Bowen et al., 1998). In this case however, paternally inherited factors may be involved.

Thus, numerous observations indicate that post-implantation development and phenotypic characteristics at birth can be modified by diverse manipulations or even by exposure of the embryo, before implantation, to transitory environmental changes. It is noteworthy that in many cases, the effects were observed in only some of the animals, the other being apparently not affected. All these observations highlight the need for improving knowledge about the early embryonic stages' susceptibility to environmental hazards especially (but not only) in the context of assisted procreation. If rather mild changes, such as variations in culture medium composition, can have delayed effects, then observing similar phenomena after cryopreservation, which induces much more dramatic disturbances in the embryo and its microenvironment should not be very surprising. In this respect, the recent finding of formaldehyde, a cytotoxic and mutagenic chemical, in cryoprotectant solutions (Karran and Legge, 1996; Mahadevan et al., 1998), might be a serious matter of concern. A recent meeting at the Jackson Laboratory (Maine, USA, 1997), which celebrated the 25th anniversary of the first birth of a mouse derived from a cryopreserved embryo, came to the similar conclusions. A consensus emerged, stressing the need for a long-term screening including detection of subtle modifications, in order to verify the innocuity of the technique.

Transmission of information to the couples
It is now generally recognized that ART have often been introduced in clinical practice `without sufficient prior animal experimentation' (ISLAT Working Group, 1998). Increasing attention is being given to their potential unexpected consequences. The next years will probably bring new insights about this issue but, at the present time, there are still more uncertainties than certitudes. Should not the physicians explain these uncertainties to the infertile couples? It is quite feasible, given time and care, to provide full information covering the different aspects of ART, including the possibility of unknown risks, without being unduly alarmist. This attitude has been recommended recently by Van Steirteghem (Van Steirteghem, 1998) and for a long time by one of us (Auroux, 1987). The couples themselves are, almost always, firmly in demand of objective and comprehensive information. A young woman said to one of us `we are aware of the tendency of covering our eyes to truth and we demand that doctors help us to act with responsibility, even if this means not acting at all'. With respect to the child, future parents and physicians share a responsibility which obliges them to face

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Friday, June 29, 2007

Autism Can Be Prevented In Some Cases By Fathering All Babies by 33 and Knowing the Other Risk Factors, So Can Alzheimer's Disease and Diabetes

'What can I do?' - SiCKO

Read about paternal age and genetic disorders and breakthrough the brainwashing about the lack of the male biological clock!

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Having Lupus or Lupus in the Family is Connected to a Much Higher Risk of Having Autistic Children and So Is Having a Family History of Diabetes

My question ----Is it the treatments alone or is it the fact of having Lupus which is caused by genetic abnormalities that originated in sperm DNA in one generation or another plus the treatments. Autoimmune genetic disorders in one generation are a risk factor for autism and schizophrenia. The older the father the more DNA mutations in sperm stem cell and sperm DNA. The ALL IMPORTANT MALE BIOLOGICAL CLOCK IS RESPONSIBLE FOR MOST NON-FAMILIAL GENETIC ILLNESS IN OFFSPRING! Age of the father is ideally less that 33.



Lupus Treatments Increase Risk of Infertility in Men

By Peggy Peck, Managing Editor, MedPage Today
Reviewed by Zalman S. Agus, MD; Emeritus Professor at the University of Pennsylvania School of Medicine.
June 28, 2007



SÃO PAULO, Brazil, June 28 -- Men with systemic lupus erythematosus, especially those who begin treatment with intravenous cyclophosphamide after puberty, are at risk for sperm abnormalities associated with infertility. Action Points

Discuss with interested patients the finding that systemic lupus erythematosus or treatments used to manage SLE may be a risk factor for infertility in men.


Discuss the mechanisms and costs of cryopreservation of sperm with affected interested patients.
Compared with healthy males, lupus patients had significantly lower sperm volume (P=0.015), a lower sperm count (P=0.002) and less motile sperm (P=0.004), according to findings reported in the July issue of Arthritis & Rheumatism.


Pollyanna Maria F. Soares, M.D., of the University of Sâo Paulo, and colleagues, said it is not possible to predict which patients will become infertile but, they said, abnormal testicular function appears to be persistent after five or more years of IV cyclophosphamide therapy.


Moreover only 20% of the lupus patients versus 80% of the controls had fathered children (P=0.0001).


The study findings, they wrote, "support the notion of an irreversible lesion and reinforces the need for sperm cryopreservation for male SLE patients who undergo CYC therapy."


They added that "cryopreservation should be discussed early in the disease course to assure an optimal condition to preserve fertility in all men with lupus, since a causal factor has not been recognized in almost one-third of patients with severe semen alterations."


Dr. Soares and colleagues performed measurements of testicular volume and sperm analysis on 35 consecutive lupus patients. The results were compared with 35 age-matched healthy controls.


The mean age of patients and controls was 29.


All lupus patients had evidence of sperm alterations; 18 --group one -- had morphologic changes characteristic of teratozoospermia and 17 -- group two -- had mixed alterations including no evidence of sperm (azoospermia), low sperm count, low sperm motility, or a combination of low sperm count or low motility with abnormal sperm.


More patients who started IV cyclophosphamide after puberty were in group two and testicular volume measured by ultrasound was lower in group two than in group one. Follicle-stimulated hormone levels were higher in group two than group one.


Among the findings:

The lupus patients had a lower median total sperm count (70 X 106 versus 172 X 106, P=0.002).
Lupus patients had a lower median motile sperm count (32 X 106 versus 119 X 106, P=0.004).
Assessment of sperm morphology by World Health Organization guidelines (P=0.011) demonstrated a significantly lower rate of normally formed sperm but by the stricter Kruger criteria the difference was not statistically significant (2.5% versus 5.0% P=0.075).

The authors conclude that because "this disease occurs mainly during reproductive age, a multidisciplinary approach is essential to identify the potential risk factors for infertility and to offer preventive measures for these patients."


Dr. Soares disclosed no financial conflicts.




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Thursday, June 28, 2007

Women Are the Carriers of the Fragile X Gene Which Orginated With A Carrier Mother or An Older Father, Women Should Be Tested For Fragile X

A woman with a brother with Fragile X should be tested because she has a 50% chance of carrying the Fragile X gene. Older fathers carry mutations in their DNA and pass them on to their Daughters and Their Sons. There is a Male Biological Clock and autism could be prevented by understanding the risk factors.

The research showing treatment for Fragile X is very deceptive and the public needs to educate itself because 50 years have gone by and all the massive evidence of the robust role that DNA mutations in sperm stem cells/sperm and most genetic disorders is not reported to the public and spun in the direction of promoting older dads as virile and glamorous.

Examples of X-linked conditions associated with increased maternal grandfather's age include fragile X, hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), Duchenne muscular dystrophy, incontinentia pigmenti, Hunter syndrome, Bruton-type agammaglobulinemia, and retinitis pigmentosa.

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Wednesday, June 27, 2007

Generation Rescue Commissions A Survey That Finds That Vaccinated Boys have 155% More Neurological Disorders like ADHD and Autism than Unvaccinated

Cal-Oregon Unvaccinated Survey

"We surveyed over 9,000 boys in California and Oregon and found that vaccinated boys had a 155% greater chance of having a neurological disorder like ADHD or autism than unvaccinated boys." -Generation Rescue, June 26, 2007

Methodology

Generation Rescue commissioned an independent opinion research firm, SurveyUSA of Verona NJ, to conduct a telephone survey in nine counties in California and Oregon. Counties were selected by Generation Rescue. Interviews were successfully completed in 11,817 households with one or more children age 4 to 17. From those 11,817 households, data on 17,674 children was gathered. Of the 17,674 children inventoried, 991 were described as being completely unvaccinated. For each unvaccinated child, a heath battery was administered.

Generation Rescue chose to use telephone interviews with parents to gather data on children, so as to closely mirror the methodology the CDC uses to establish national prevalence for NDs such as ADHD and autism through their national phone survey of parent responses. Generation Rescue chose to focus on children ages 4-17 to match the age range used by CDC.

Are parent responses a reliable indicator of a child's diagnostic status? According to Dr. Laura Schieve, co-author of the CDC's national phone survey study, in discussing the CDC's two phone surveys on autism prevalence, "the consistency of prevalence estimates across the two surveys supports high reliability or reproducibility of parental report of autism and reliability is one important component of validity."

SurveyUSA is a well-known national opinion research firm with unique expertise in canvassing local communities. SurveyUSA has no vested interest in any outcome this or any survey might produce. You can see a copy of the questionnaire used in the survey here. The data the survey intended to capture included:

- Households with a child or children aged 4-17
- Whether or not that child had been vaccinated
- Whether or not that child had any one (or more) of the following diagnosis: ADD, ADHD, Asperger's, PDD-NOS, Autism, Asthma, or Juvenile Diabetes (the final two of which were added to consider other health outcomes).


The results of the survey allowed us to compare the prevalence (what percentage of children have a particular diagnosis) to see if there was any meaningful difference between unvaccinated and vaccinated children.

The most common way to measure prevalence differences is through a calculation known as relative risk or the Risk Ratio, where we compared prevalence amongst unvaccinated children to prevalence amongst vaccinated children. So, if 5% of unvaccinated children have asthma, and 10% of vaccinated children have asthma, that represents an "RR" of 2.0 (10%/5%), or a difference of 100%. We were also able to look at the data by gender, age, and county.

Results

SurveyUSA gathered data on 9,175 boys and 8,499 girls. Counties surveyed in California included:

San Diego
Sonoma
Orange
Sacramento
Marin


Counties surveyed in Oregon included:

Multnomah
Marion
Jackson
Lane


The results of the survey can be accessed as a pdf file here. This is the primary data we received from SurveyUSA and it can be used for anyone to independently analyze our results.

Generation Rescue analyzed the data provided by SurveyUSA, and a copy of our analysis can be found here. The most notable results of our survey are with the boys, which is not surprising considering boys represent approximately 80% of total cases of NDs. Namely:

All vaccinated boys, compared to unvaccinated boys:
- Vaccinated boys were 155% more likely to have a neurological disorder (RR 2.55)
- Vaccinated boys were 224% more likely to have ADHD (RR 3.24)
- Vaccinated boys were 61% more likely to have autism (RR 1.61)


Older vaccinated boys, ages 11-17 (about half the boys surveyed), compared to older unvaccinated boys:
- Vaccinated boys were 158% more likely to have a neurological disorder (RR 2.58)
- Vaccinated boys were 317% more likely to have ADHD (RR 4.17)
- Vaccinated boys were 112% more likely to have autism (RR 2.12)

(Note: older children may be a more reliable indicator because many children are not diagnosed until they are 6-8 years old, and we captured data beginning at age 4.)


All vaccinated boys, removing one county with unusual results (Multnomah, OR), compared to unvaccinated boys:
- Vaccinated boys were 185% more likely to have a neurological disorder (RR 2.85)
- Vaccinated boys were 279% more likely to have ADHD (RR 3.79)
- Vaccinated boys were 146% more likely to have autism (RR 2.46)


All vaccinated boys and girls, compared to unvaccinated boys and girls:
- Vaccinated boys and girls were 120% more likely to have asthma (RR 2.20)
- No correlation established for juvenile diabetes


All vaccinated girls, compared to unvaccinated girls:
- No meaningful differences in prevalence were noted for NDs (which may be due to the smaller sample size of the study because girls represent about 20% of cases.)

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High Paternal Age is Causing More Type 1 Diabetes in non-Hispanic White Children and Other Children in my Opinion As Well as More Autism etc.

: Diabetes Care. 2007 Mar;30(3):503-9. Links
Increasing incidence of type 1 diabetes in 0- to 17-year-old Colorado youth.Vehik K, Hamman RF, Lezotte D, Norris JM, Klingensmith G, Bloch C, Rewers M, Dabelea D.
University of Colorado School of Medicine, Denver, Colorado, USA.

OBJECTIVE: We sought to assess the long-term trends in the incidence of type 1 diabetes among non-Hispanic white and Hispanic youth aged 0-17 years from Colorado using data from the Colorado IDDM Study Registry (1978-1988) and SEARCH for Diabetes in Youth (2002-2004). RESEARCH DESIGN AND METHODS: Cases of diabetes were ascertained through physician reporting and hospital databases. Type 1 diabetes was defined as use of insulin within 2 weeks from diagnosis. Completeness of ascertainment was estimated as 97%. Annual average incidence rates (per 100,000/year) and 95% CIs for the time periods were computed. Trends in incidence were assessed by Poisson regression. RESULTS: The incidence of type 1 diabetes was 14.8 (95% CI 14.0-15.6) in 1978-1988 and 23.9 (22.2-25.6) in 2002-2004 for the state of Colorado (P < 0.0001). From 1978 to 2004, the incidence of type 1 diabetes increased by 2.3% (1.6-3.1) per year (P < 0.0001). The increase in incidence was significant for both non-Hispanic white (2.7% [95% CI 1.9-3.6] per year, P < 0.0001) and Hispanic youth (1.6% [0.2-3.1] per year, P = 0.013). CONCLUSIONS: The incidence of type 1 diabetes has increased 1.6-fold among Colorado youth from 1978-1988 to 2002-2004, and both non-Hispanic white and Hispanic youth are affected by this trend.

PMID: 17327312 [PubMed - indexed for MEDLINE]





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Posted : Wed, 27 Jun 2007 09:14:00GMT
Author : Anne Roberts




According to a study, the results of which were published in the June 27 issue of JAMA, Type 1 diabetes which is the most common type of diabetes in children is found to be most prevalent in non Hispanic white youth.

These findings were presented at a JAMA media briefing in New York by Colorado University's Health Sciences Center's Dana Dabelea, M.D., Ph.D.

The study was conducted by Dabelea, who, along with her team members in the SEARCH for Diabetes in Youth Study Group, assessed incidences of diabetes mellitus (DM) in Americans even younger than twenty years of age.

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Monday, June 25, 2007

"I am aware of the paternal age effect in many disorders and in the case of autism..."








Professor Angus Clarke
Principal Investigator and Professor in Clinical Genetics





Angus Clarke was born in 1954. He studied Medical and Natural Sciences in Cambridge, taking his Part II in Genetics, and then qualified in Medicine from Oxford University in 1979. After registration, he worked in general medicine and then paediatrics. As a research registrar in the Department of Medical Genetics in Cardiff, he studied the clinical and molecular genetic aspects of ectodermal dysplasia. Subsequently, he worked in clinical genetics and paediatric neurology in Newcastle upon Tyne, developing an interest in Rett syndrome and neuromuscular disorders.

He returned to Cardiff in 1989 as Senior Lecturer in Clinical Genetics. He is now Professor in Clinical Genetics. As well as teaching he also works as a clinician. With his colleague, Peter Harper, he wrote the book, Genetics, Society and Clinical Practice. He directs the Cardiff MSc course in Genetic Counselling.

Research interests:
social and ethical issues raised by advances in human genetics
the genetic counselling process




"I am aware of the paternal age effect in many disorders - and clearly in the case of autism, as with this one family. I am not aware of it in relation to autism in general - but there are cerainly a number of grounds for discouraging the deferral of child bearing to older ages (for men and women) including gene mutations, chromosome anomalies and reduced fertility. Education about the disbenefits of deferring child bearing is important but it is unclear how to achieve this as education is probably a weak force when it is asked to effect major change in a powerful social force.

Don't think that the problems of later child bearing are unrecognised - but if you have useful ways of addressing this then of course do share these"


Best wishes,

Angus Clarke

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At Last the Truth Comes Out Again This Has Been Known Since 1955 Birth Defects and Autism Higher Among Children of Older Fathers


Irish Health Headlines

Birth Defects Higher Among Children with Older Fathers

Older men have an increased risk of having a child with abnormalities, new research suggests.

The common belief is that there is no age limit for men when it comes to fathering a child. Unlike women who undergo menopause, men do not have a fixed “andropause”. However, this view is being challenged as new evidence shows that the rates of birth defects such as achondroplasia (short stature) and autism is higher among children with older fathers.
A recent study carried out at a large Israeli army database found that children of men over 40 were 5.75 times more likely to have an autism disorder than those who had fathers under 30. Another Israeli study suggested that the risk of schizophrenia in children is almost double if the father is in his late 40s.

Prof Sheena Lewis, a consultant in reproductive medicine at Queen's University Belfast, said that as men get older their sperm DNA becomes more fragmented. By the time a man is 50, the cells that create a man’s sperm have replicated up to 800 times, creating many possibilities for error.


According to Prof Lewis:

The impact of the father smoking is even worse than the mother smoking (you can't repair damage caused in sperm DNA)
Viagra can affect fertility by causing the sperm to travel too fast
Cannabis us slows sperm function, resulting in a reduction in fertility
She also warns about the damaging impact of modern lifestyle and environmental factors.

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Saturday, June 23, 2007

Autism immature immune system-families with autoimmune disorders older fathers older maternal grandfathers


The speakers also agreed that autism happens more often in families
suffering diseases of the immune system such as rheumatoid arthritis, lupus,
inflammatory bowel disease and even asthma and eczema. The incidence of all
such diseases has markedly increased in recent decades, they note.

All these disoders and diabetes, MS, Crohn's increase with the age of the fathers at the conception of the child. Many, many genetics disorders are caused by mutations in sperm stem cell DNA which increases with the age of the fathers. Cancers also increase with the age of the father and even Huntington chorea can be created de novo in older father's children. How many men are fathering over 30? A vastly increased number since 1980. Combine this with generations of older fathers and you get diabetes, lupus, autism schizophrenia, MS, hemophilia, Duchenne's, ALL, Alzheimer's, prostate cancer, breast cancer, neurofibromatosis, RETTS, fragile X. Men do have a biological clock! FEAT DAILY NEWSLETTER Sacramento, California http://www.feat.org
"Healing Autism: No Finer a Cause on the Planet"
______________________________________________________
July 28, 2001 Search www.feat.org/search/news.asp

Experts: Redefine Autism as Systemic Illness
Condition thought to be triggered by assault to immature immune system


[By Susannah Benady. Thanks to autismnet.]
http://www.medicalpost.com/mdlink/english/members/medpost/data/3718/21B.HTM

Quebec City - Researchers are calling for a radical new definition of
autism in the wake of evidence presented here that autism is in fact an
autoimmune disease, rather than a mental handicap.
This was the consensus among doctors at the forefront of research into
the physiological complications that affect many children with autism and
autism spectrum problems. They presented their findings at the second
International Medical Conference on Autism held here in April.
No longer can the condition just be considered a psychiatric or
neurological disorder, they argued. Autism had to be seen as a systemic
illness that has gastrointestinal, immunological, endocrinological,
psychological and neurological complications.
Dr. Jeff Bradstreet, a pediatrician and medical director of the
International Autism Research Centre in Palm Bay, Fla., said virtually all
children diagnosed with autism also have some other significant abnormal
function.
He said that is why the term "autism" is misleading and should be
replaced with a phrase that better describes the child's physical condition.
"Autism is a psychiatric term," he said. "I consider 'toxic
encephalopathy' a better description because it implies that there is
something we can do if we detoxify the individuals."
Dr. Bradstreet's research centre specializes in treating children with
autism spectrum disorders by investigating their underlying or coexisting
physiological condition and treating that with a combination of conventional
drug therapy and nutritional supplementation.
The aim is to treat the underlying condition, and also to detoxify and
strengthen the immune system.
In cases where the immunological vulnerability or toxicity can be
identified, and then responds to treatment, children show a marked
improvement in their ability to relate to others, as well as in their
academic performance, he said.
Evidence presented at the conference by physicians researching the
physical symptoms of autism should change the way doctors understand and
treat children suffering from the disorder.
They now believe that autism is triggered by an environmental insult
or toxicity that damages the immature and fragile immune system of a fetus,
infant or very young child. This causes the immune system to react against
body organs.
The result is a condition that has a multisystem effect, not just on a
patient's neurological system. Most frequently, it is the gastrointestinal
system or "second brain" that shows symptoms.
Many of the children also have a long history of susceptibility to
infections and experience hormonal imbalance, such as hyperthyroidism and
early puberty. Some children even display coagulation and circulatory
disorders.
Research presented at the conference showed that tests on blood and
tissue samples from autistic children have detected autoantibodies to
proteins in the brain, gastrointestinal system and other organs.
As Dr. Bradstreet puts it: "The child becomes the victim of his immune
system."
Dr. Andrew Wakefield of London's Royal Free and University College
medical school, who has investigated the gastrointestinal symptoms of more
than 150 autistic children, said these children "show an aberration of the
immune system in some ways similar to people with AIDS."
The speakers also agreed that autism happens more often in families
suffering diseases of the immune system such as rheumatoid arthritis, lupus,
inflammatory bowel disease and even asthma and eczema. The incidence of all
such diseases has markedly increased in recent decades, they note.
According to research by Dr. Anne Comi and colleagues at Johns Hopkins
Hospital division of pediatric neurology in Baltimore that was cited at the
conference, there is a nine-fold increase in the incidence of autism in
children born to mothers with immune illnesses.
Dr. Ed Yazbak, a pediatric infectious disease specialist from Boston,
said research will not find a chromosome responsible for autism. He is a
former professor at Brown University now studying the medical histories of
children with autism in an effort to determine what triggered their
condition.
"Research will show there is a genetic predisposition to autism. What
we have to find is the environmental insult," he said.
Physicians treating children diagnosed with autism must recognize the
children are suffering a medical illness.
This is particularly noticeable in the more recently identified
"regressive autism" that many parents have linked to their children's
immunization with the mumps-measles-rubella vaccine, Dr. Yazbak said.
He called on pediatricians to reclaim care of the child with autism.
"It is a pediatric illness that affects the whole child and it needs a
pediatrician to take care of the whole child," he said.
"The pediatrician needs to co-ordinate consultations with the
psychiatrist, gastroenterologist and occupational therapists.
"If pediatricians do not adopt the new thinking on autism, it will be
left to crooks and charlatans to exploit desperate parents," Dr. Yazbak
warned.

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This Blog is Rated PG 13 because

This rating was determined based on the presence of the following words:

semen (4x) dangerous (3x) drugs (2x) sex (1x)

Online Dating

Mingle2 - Online Dating

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Thursday, June 21, 2007

The use of ejaculated immotile sperm for in vitro reproduction is debatable due to sperm DNA degradation.

Among ICSI children de novo structural chromosome aberrations of male descent are increased.


Hum Reprod. 2007 Jun 18; [Epub ahead of print]Motile human normozoospermic and oligozoospermic semen samples show a difference in double-strand DNA break incidence.Derijck AA, van der Heijden GW, Ramos L, Giele M, Kremer JA, de Boer P.
Department of Obstetrics and Gynaecology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.

BACKGROUND Among ICSI children de novo structural chromosome aberrations of male descent are increased. Misrepair of double-strand DNA breaks (DSBs) is a prerequisite for such aberrations to occur. To date, no absolute assessment of the number of DSBs in human sperm nuclei after gamete fusion has been described. METHODS Using man-mouse heterologous ICSI and gammaH2AX immunofluorescent staining, capable of detecting a single DSB, the number of lesions in ICSI selected sperm from normozoospermic men (n = 2) and oligozoospermic patients (n = 3) was quantified. A comparison with a subfertile male mouse model (n = 5) has been made. In addition, the fate of morphologically normal ejaculated immotile sperm after ICSI was examined. RESULTS A significant increase in the fraction of sperm cells bearing DSBs was found in oligozoospermic semen compared with that from normozoospermic men (P < 0.01). The majority of morphologically normal immotile human sperm showed excess gammaH2AX staining and nuclear disintegration. However, some had a non-deviant DSB pattern. CONCLUSIONS The increased fraction of DSB-positive sperm in both human and mouse oligozoospermic semen is adding to the surmise that semen from oligozoospermic patients has a reduced chromatin quality, causally related to reduced preimplantation embryo development. The use of ejaculated immotile sperm for in vitro reproduction is debatable due to sperm DNA degradation.
PMID: 17580297 [PubMed - as supplied by publisher]

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Wednesday, June 20, 2007

Study Recruiting Parents of children with Autism Spectrum Disorder for On-line Survey

Advanced Grandparental Age as a Risk Factor for Autism
This study is currently recruiting patients.
Verified by University of Mississippi Medical Center June 2007

Sponsored by: University of Mississippi Medical Center
Information provided by: University of Mississippi Medical Center
ClinicalTrials.gov Identifier: NCT00464477


Purpose

The Division of Medical Genetics at the University of Mississippi Medical Center is recruiting parents of children with a pervasive developmental disorder (including autism, autistic spectrum disorder, PDD-NOS, Asperger syndrome, childhood disintegrative disorder, and Rett syndrome) to participate in a study to help determine potential causes of the increasing prevalence of these disorders. The study is being conducted using an anonymous on-line survey available to parents through a secure link.

The study consists of approximately 90 questions about the affected child, siblings, parents, and grandparents, which will take roughly 10-15 minutes to complete. Several families will also be invited to participate in a phone interview. Both the survey and the phone interview are conducted using a self-designated code to protect anonymity and patient privacy. No identifying information such as name, date of birth, address, or phone number will be asked. Only questions regarding the year of birth of family members will be asked.

Condition
Autistic Disorder
Pervasive Developmental Disorder
Asperger Syndrome
Childhood Disintegrative Disorder
Rett Syndrome


MedlinePlus related topics: Asperger's Syndrome; Autism; Mental Health; Rett Syndrome
Genetics Home Reference related topics: Rett syndrome

Study Type: Observational
Study Design: Natural History, Cross-Sectional, Random Sample, Retrospective Study

Official Title: Advanced Grandparental Age as a Risk Factor for Autism and Other Pervasive Developmental Disorders

Further study details as provided by University of Mississippi Medical Center:

Total Enrollment: 100
Study start: June 2007; Expected completion: December 2007


Autism is a genetically heterogeneous entity. Although numerous studies have demonstrated a strong genetic basis, no clear etiology has been identified to date. Recently, two studies have demonstrated an increased risk of autism in children born to fathers over the age of 40. However, given the large male-to-female predominance of autism, it is likely that new mutations on the X chromosome account for a significant number of affected cases. Due to the maternal origin of the X chromosome in males, we hypothesize that advanced maternal-grandpaternal age may also be a risk factor for autism. Precedence for this theory exists with other X-linked disorders such as Duchenne muscular dystrophy and Rett syndrome. Additionally, it has been demonstrated that maternal psychiatric illness, but not paternal psychiatric illness, is more prevalent among parents of children with autism. Using anonymous surveys of families with autistic children, we seek to identify the ages of grandparents at the time the parents were born in order to determine if advanced maternal-grandpaternal age is associated with an increased risk for autism when adjusted for advanced maternal and paternal age. Additionally, we will seek out sister-pairs in order to identify any statistical significance between the ages of the maternal grandfather at delivery of each sister. If advanced maternal-grandpaternal age is, in fact, a risk factor, it would help direct molecular researchers towards genes on the X chromosome as potential etiologies for autism. Also, further study of potential mutagenic exposures in the environment of grandparents may help elucidate the reason for the increasing incidence of autism in recent decades.
Eligibility

Genders Eligible for Study: Both
Criteria
Inclusion Criteria:

Individuals of any age with autism, autistic disorder, autistic spectrum disorder, Asperger syndrome, pervasive developmental disorder, PDD-NOS, Rett syndrome, or Childhood disintegrative disorder
Location and Contact Information

Please refer to this study by ClinicalTrials.gov identifier NCT00464477

Omar Abdul-Rahman, MD 601-984-1900 OAbdulrahman@prevmed.umsmed.edu


United States, Mississippi
University of Mississippi Medical Center, Jackson, Mississippi, 39216, United States; Recruiting
Omar Abdul-Rahman, MD 601-984-1900 OAbdulrahman@prevmed.umsmed.edu



Study chairs or principal investigators

Omar Abdul-Rahman, MD, Principal Investigator, University of Mississippi Medical Center
More Information

If you would like to participate in this anonymous on-line survey, please go to NCT site

Study ID Numbers: 2007-0023
Last Updated: June 18, 2007
Record first received: April 20, 2007
ClinicalTrials.gov Identifier: NCT00464477
Health Authority: United States: Institutional Review Board
ClinicalTrials.gov processed this record on June 20, 2007

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Sunday, June 17, 2007

Vaccination and Autoimmune Disorders




Here is information from the saftety insert of a vaccine for rabies 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.






This is one person's work on the subject of how the vaccines themselves can be very detrimental to some children.
Overview


Introduction
How Could Vaccines Cause Damage?
Early Studies on Vaccine Complications


The DPT Vaccine


DPT and Brain Damage


DPT and Autism


DPT and Vaccine-Induced Neuropathies


Diagnosis of Post-Vaccinal CNS Pathology


Vaccine-Induced Demyelination


Auto-Immunity, Vaccines and Autism '


Database of Vaccine Injury


Vaccines and Mercury


Origins of the Mercury Controversy
Mercury Neurotoxicity
Thimerosal and Neurotoxicity
Is There a Link betwen Mercury Exposure and Autism?
Ethylmercury and the DPT Vaccine
Testing for Mercury Toxicity


The MMR Vaccine


MMR Vaccine and Autism
MMR Vaccine and Other Complications


Other Vaccination Concerns


Concern About Vaccine Adjuvants
Immunological Consequence of Vaccines
Vaccination During Pregancy and Risks for Autism


The Rubeola (Measles) Vaccine


The Rubeola Vaccine, Measles and Autism
The Risks of Not Vaccinating for Measles


Conflict of Interest and Vaccine Development


The Hepatitis B Vaccine


Hepatitis B Vaccine: The Risks
Hepatitis B: The Disease
Available Data on the Safety of Hepatitis B Vaccines


Information on Other Vaccines


Polio Vaccine
Pneumococcal Pneumonia Vaccine
Hemophilus Meningitis Vaccine


Appendix 1: Schedule for Routine Immunizations


Appendix 2: Standards for Pediatric Immunization Practices


Appendix 3: Decline of Number of Vaccine-Preventable Cases over Time


Appendix 4: Childhood Immunizations


The Burden of Suffering
Description of Preventive Measures
Evidence of Effectiveness
Public Policy Considerations
Recommendations of Other Groups
Rationale Statement
Recommendations of the American College of Preventive Medicine






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

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Thomas Wassink and Joseph Piven Know Very Well That the Rise In Cases of Autism is Due To Older Guys Fathering Babies, But Will They Focus On That, No

Of course there are many other causes of autism. Some is familial, some due to a mother having had an older father at her birth. A family history of autoimmune disorders is a strong risk factor for having an autistic child in the next generation.



Thomas H. Wassink1 and Joseph Piven2

(1) Psychiatry Research, MEB, Department of Psychiatry, University of Iowa Hospitals and Clinics, 52242 Iowa City, IA, USA
(2) Department of Psychiatry, University of North Carolina, Chapel Hill, CB 7160, 27599-7160 Chapel Hill, NC, USA


Abstract Autism is a severe neurodevelopmental disorder characterized by communication and social deficits and by stereotyped, repetitive behaviors. The syndrome of autism is highly heritable, is considered to be etiologically heterogeneous and is thought to be the result of multiple, interacting genes. It is more common than previously thought, and has a complex pattern of genetic transmission. From four recently completed genome-wide linkage screens of autism, distal 7q has emerged as the most prominent chromosomal region of interest. Additional support for 7q comes from autistic individuals with gross 7q cytologic abnormalities, and from linkage and association data in families with language and speech disorders. Chromosome 15q11-13 is also of interest because of numerous reports of macroscopic and molecular abnormalities in the region associated with Prader-Willi and Angelman syndromes. In this review, molecular aspects of these data, as well as future avenues of investigation, are discussed.

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Thursday, June 14, 2007

The Causes of Autism Are Known But Prevention Is Not Profitable, CMEs Brainwash Doctors There is a male biological clock and it is responsible for

autism, diabetes, cancers, ALS, Alzheimer's, hemophilia, Crohn's, and other de novo genetic disorders.

-------------------------------------------------------------------------------------

Op-Ed Contributor
Diagnosis: Conflict of Interest
By DANIEL CARLAT
Published: June 13, 2007

Boston

THE revelation that the diabetes drug Avandia can potentially cause heart disease is the latest in a string of pharmaceutical disappointments. Vioxx was pulled from the market in 2004 because it doubled the risks for heart attacks and strokes. Eli Lilly recently paid $750 million to settle lawsuits alleging that Zyprexa causes diabetes. Many have criticized the Food and Drug Administration as being too lax about monitoring drug safety.

While those criticisms have merit, there is another culprit: the transformation of continuing medical education into an enterprise for drug marketing. The chore of teaching doctors how to practice medicine has been handed to the pharmaceutical industry. As a result, dangerous side effects are rarely on the curriculum.

Most states require that doctors obtain a minimum number of credit hours of continuing medical education each year to maintain their medical licenses. Not so long ago, most of these courses were produced and paid for by universities and medical associations. But this has changed drastically over the past decade.

According to the most recent data available from the national organization in charge of accrediting the courses, drug-industry financing of continuing medical education has nearly quadrupled since 1998, from $302 million to $1.12 billion. Half of all continuing medical education courses in the United States are now paid for by drug companies, up from a third a decade ago. Because pharmaceutical companies now set much of the agenda for what doctors learn about drugs, crucial information about potential drug dangers is played down, to the detriment of patient care.

For example, GlaxoSmithKline footed the bill for dozens of educational courses intended to emphasize the benefits of Avandia over other drugs. An influential Internet-based educational program paid for by the company focused on specific studies that highlighted Avandia’s advantages without discussing one of the drug’s most worrisome side effects, increased levels of the lipids implicated in heart disease.

Avandia’s chief competitor, a drug from Takeda Pharmaceuticals called Actos, improves lipid levels but was hardly mentioned. When GlaxoSmithKline’s program did cite Actos, it did so tepidly. The information in the course was presented by noted diabetes academics paid by GlaxoSmithKline and other drug companies.

GlaxoSmithKline is not the only offender. The major organizations in diabetes education, like the National Diabetes Education Initiative, offer dozens of continuing medical education courses on diabetes that are free to doctors and paid for by drug companies. Predictably, each course focuses on the advantages of the sponsor’s product and minimizes discussion of dangerous side effects.

Education that doubles as advertising for drug companies occurs in all branches of medicine. Merck promoted Vioxx for arthritis by using programs for continuing medical education, which helped contribute to the more than 100 million prescriptions of the drug before it was pulled from the market.

According to Dr. David Graham, a safety researcher for the Food and Drug Administration, Vioxx was responsible for up to 140,000 cases of serious heart disease from 1999 until 2004, when it was withdrawn. But the potential cardiac dangers of Vioxx were played down in the courses paid for by Merck. In one instance, the company canceled lectures it had sponsored by a Stanford researcher who had mentioned, in talks to doctors, the cardiac risks from taking Vioxx.........

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Wednesday, June 13, 2007

Hindustan Times Thursday June 14, 2007




"It is curious that although sperm have been around since the beginning of time, we know so little about what is in them, and what makes them tick, er, swim. So scientists spend a lot of their waking hours trying to compare the structure and content of the proteins of sperm in various species, in order to understand their evolution and origin. For instance, the mutated DNA in the genes of the sperm of older fathers is believed to cause many genetic diseases. It is almost as if a man’s biological clock accelerates mutation in sperm cells in his early ’30s."

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How about a News Release on the Risk Factors For Autism, Headed By Older Paternal Age, Older Maternal Grandfather's Age, Family History of Autoimmune




Disorders, Family history of Asperger's, Family history of autism, Family history of Schizophrenia, family history of OCD disorders. By the age of 35 it is advanced paternal age. Some sperm banks cut off donations of sperm at the 35th birthday, some in Africa and Israel cut off sperm donors at the 30th birthday. There definetly is a male biological clock and advanced paternal age 32++++++ equals genetic disorders. Cancers, heart defects, Alzheimer's, Duchennes, hemophilia, diabetes, MS, Crohn's, etc. etc. increase with increasing paternal age and increasing maternal grandfather's age at the mother's birth.


© Newswise.
All Rights Reserved.

Researchers Reveal Structure of Protein Altered in Autism


Source: University of California, San Diego Health Sciences Released: Wed 06-Jun-2007, 19:15 ET
Embargo expired: Tue 12-Jun-2007, 12:00 ET Printer-friendly Version



As a result of mapping the structure of the protein complex implicated in autism spectrum disorders, a research team led by scientists at theUCSD Skaggs School of Pharmacy and Pharmaceutical Sciences has discovered how particular genetic mutations affect this complex and contribute to the developmental abnormalities found in children with autism.




Newswise — As a result of mapping the structure of the protein complex implicated in autism spectrum disorders, a research team led by scientists at the University of California, San Diego (UCSD) Skaggs School of Pharmacy and Pharmaceutical Sciences has discovered how particular genetic mutations affect this complex and contribute to the developmental abnormalities found in children with autism. Their work, published as the cover article in the June issue of the journal Structure, should help scientists pinpoint the consequences of other genetic abnormalities associated with the disorder.

“By understanding the three-dimensional structure of the normal protein, researchers can now make predictions about how mutations in the gene affect the structure of the gene product,” said first author Davide Comoletti, Ph.D., UCSD research associate at the Skaggs School of Pharmacy.

Autism spectrum disorders are developmental disabilities that cause impairments in social interaction and communication. Both children and adults with autism typically show difficulties in verbal and non-verbal communication, interpersonal relationships, and leisure or play activities.

Comoletti and colleagues studied the neuroligin family of proteins that are encoded by genes known to be mutated in certain patients with autism. The neuroligins, and their partner proteins, the neurexins, are involved in the junctions, or synapses, through which cells of the nervous system signal to one another and to non-neuronal tissues such as muscle. These structural studies on neuroligins and neurexins represent a major step toward defining the synaptic organization at the molecular level.

“Normally, individual neuroligins are encoded to interact with specific neurexin partners. The two partners are members of distinct families of proteins involved in synaptic adhesions, imparting ‘stickiness’ that enables them to associate so that synapses form and have the capacity for neurotransmission,” said Palmer Taylor, Ph.D., Dean of the Skaggs School, Sandra & Monroe Trout Professor of Pharmacology, and co-principal investigator of the study, along with Jill Trewhella, Ph.D., of the University of Sydney, Australia and University of Utah.

Incorrect partnering that results when a mutant neuroligin fails to properly align at synapses helps explain why the autism spectrum disorders are manifested in subtle behavioral abnormalities that are seen at an early age.

“Abnormal synaptic development in nerve connections is likely to lead to cognitive deficits seen in patients with autism,” said Taylor. He added that synapse formation and maintenance occurs early in development when the infant brain is still plastic and formative. Therefore, by understanding the structural mutations that affect neurotransmission during development, new leads into drug therapies may emerge.

“We really don’t know what causes autism, but this research represents a solid starting point,” said Sarah Dunsmore, Ph.D., program director with the National Institute of General Medical Sciences, part of the National Institutes of Health, which partly supported the study. “The work suggests that genetic mutations that alter the shape or folding of adhesion proteins in the nervous system influence their interactions. This is another example of how research on basic biological questions, such as the three-dimensional structures of proteins in the brain, can yield valuable medical insights.”

Taylor and colleagues have been studying the structure and function of acetylcholinesterase – a structurally related protein that mediates neurotransmission between nerves and between nerve and muscle – for the past 30 years. They began studying the neuroligins because of the similarity in structure and amino acid sequence with acetylcholinesterase.

The study was a multi-national collaboration, employing synchrotrons at two national laboratories to collect the X-ray and neutron scattering data necessary for resolving the structure. Additional contributors to this study include Alexander Grishaev, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD; Andrew E. Whitten, Bragg Institute, Australian Nuclear Science and Technology Organization; and Igor Tsigelny, UCSD Department of Pharmacology, Skaggs School of Pharmacy and Pharmaceutical Sciences.

This work was supported in part by grants from the National Institutes of Health, the U.S. Department of Energy, and the Cure Autism Now Foundation.

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Tuesday, June 12, 2007

The Rise in Autism is Not a Mystery, but There is a PR Campaign to Make You Think it is, Older Fathers and Older Maternal Grandfathers Cause Mutations

Advanced Grandparental Age and Autism Survey


Many other lesser genetic disorders are also caused by genetic changes in sperm DNA that increase with a man's age. The Center for Disease Control will never inform the public, nor will the NIH, or NIMH, or NARSAD or NAMI. It is the inability of the child's immune system to handle the antigens that causes the problems when the children are vaccinated. Risk factors for autism and schizophrenia should be made public and new vaccinations schedules made if men insist on having babies past the age of 32. Also the mother's father's age should be noted and if higher than early 30s a special schedule should be used. Any family history of autoimmune disorders should put the baby in the high risk category as well as a family history of autism, schizophrenia or OCD.


If you want to do something to prevent autism get informed by reading about it. No one is going to tell the public that older paternal age is past 31 32 and it is that increasing genetic disorders in offspring is a result of the male biological clock caused by mutations in sperm DNA. Sperm come from somehere, they are not made fresh out of nothing. Everyone in the field of autism/schizophrenia research knows that the incidence increases with paternal age and maternal grandfather's age at the mother's birth. Most researchers are happy to keep this secret from the public and get funded to do research that does nothing postitive but make more money for themselves, pharmaceutical companies and genomic studies institutes. They will take your genes to make money for themselves and not help your child.


With the number of men fathering over 35, when over 33 is old and dangerous, there has to be more autism./schizophrenia, diabetes, MS, Lupus, fibromyalgia, endometriosis, Alzheimer's disease, heart disease, Crohn's disease, IBD, Duchenne's, hemophilia, prostate cancer, breast cancer, colon cancer, ovarian cancer, etc. etc. etc.


Some industries are very happy about the rise in autism/schizophrenia think pharmaceuticals, academia,psychiatric researchers on the whole special ed field etc. The March of Dimes is set up to distract from Paternal Age as the major cause of birth defects. Many researchers with big research departments know that their whole professional life revolves around the fact that no one informed the public in the 1950s that older paternal age causes birth defects and damaged children. Any researcher who tries or tried to inform of the connection was called crazy and not allowed to publish in any reputable journal. It is a bit like the connection between smoking and cancer, we have been taught that older fathers are wonderful and to be admired. This is pure PR.


For a good discussion on the paternal age roots of non-familial schizophrenia including childhood schizophrenia/autism, its name since 1994 read through the following paper by Dr. Dolores Malaspina, Chair of the Department of Psychiatry at NYU School of Medicine.




Schizophrenia Risk and the Paternal Germ LineBy Dolores Malaspina
Dolores Malaspina

Paternal age at conception is a robust risk factor for schizophrenia. Possible mechanisms include de novo point mutations or defective epigenetic regulation of paternal genes. The predisposing genetic events appear to occur probabilistically (stochastically) in proportion to advancing paternal age, but might also be induced by toxic exposures, nutritional deficiencies, suboptimal DNA repair enzymes, or other factors that influence the fidelity of genetic information in the constantly replicating male germ line. We propose that de novo genetic alterations in the paternal germ line cause an independent and common variant of schizophrenia.
Seminal findingsWe initially examined the relationship between paternal age and the risk for schizophrenia because it is well established that paternal age is the major source of de novo mutations in the human population, and most schizophrenia cases have no family history of psychosis. In 2001, we demonstrated a monotonic increase in the risk of schizophrenia as paternal age advanced in the rich database of the Jerusalem Perinatal Cohort. Compared with the offspring of fathers aged 20-24 years, in well-controlled analyses, each decade of paternal age multiplied the risk for schizophrenia by 1.4 (95 percent confidence interval: 1.2-1.7), so that the relative risk (RR) for offspring of fathers aged 45+ was 3.0 (1.6-5.5), with 1/46 of these offspring developing schizophrenia. There were no comparable maternal age effects (Malaspina et al., 2001).
Epidemiological evidenceThis finding has now been replicated in numerous cohorts from diverse populations (Sipos et al., 2004; El-Saadi et al., 2004; Zammit et al., 2003; Byrne et al., 2003; Dalman and Allenbeck, 2002; Brown et al., 2002; Tsuchiya et al., 2005). By and large, each study shows a tripling of the risk for schizophrenia for the offspring of the oldest group of fathers, in comparison to the risk in a reference group of younger fathers. There is also a "dosage effect" of increasing paternal age; risk is roughly doubled for the offspring of men in their forties and is tripled for paternal age >50 years. These studies are methodologically sound, and most of them have employed prospective exposure data and validated psychiatric diagnoses. Together they demonstrate that the paternal age effect is not explained by other factors, including family history, maternal age, parental education and social ability, family social integration, social class, birth order, birth weight, and birth complications. Furthermore, the paternal age effect is specific for schizophrenia versus other adult onset psychiatric disorders. This is not the case for any other known schizophrenia risk factor, including many of the putative susceptibility genes (Craddock et al., 2006).
There have been no failures to replicate the paternal age effect, nor its approximate magnitude, in any adequately powered study. The data support the hypothesis that paternal age increases schizophrenia risk through a de novo genetic mechanism. The remarkable uniformity of the results across different cultures lends further coherence to the conclusion that this robust relationship is likely to reflect an innate human biological phenomenon that progresses over aging in the male germ line, which is independent of regional environmental, infectious, or other routes.
Indeed, the consistency of these data is unparalleled in schizophrenia research, with the exception of the increase in risk to the relatives of schizophrenia probands (i.e., 10 percent for a sibling). Yet, while having an affected first-degree relative confers a relatively higher risk for illness than having a father >50 years (~10 percent versus ~2 percent), paternal age explains a far greater portion of the population attributable risk for schizophrenia. This is because a family history is infrequent among schizophrenia cases, whereas paternal age explained 26.6 percent of the schizophrenia cases in our Jerusalem cohort. If we had only considered the risk in the cases with paternal age >30 years, our risk would be equivalent to that reported by Sipos et al. (2004) in the Swedish study (15.5 percent). When paternal ages >25 years are considered, the calculated risk is much higher. Although the increment in risk for fathers age 26 through 30 years is small (~14 percent), this group is very large, which accounts for the magnitude of their contribution to the overall risk. 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.
Biological plausibilityWe used several approaches to examine the biological plausibility of paternal age as a risk factor for schizophrenia. First, we established a translational animal model using inbred mice. Previously it had been reported that the offspring of aged male rodents had less spontaneous activity and worse learning capacity than those of mature rodents, despite having no noticeable physical anomalies (Auroux et al., 1983). Our model carefully compared behavioral performance between the progeny of 18-24-month-old sires with that of 4-month-old sires. We replicated Auroux's findings, demonstrating significantly decreased learning in an active avoidance test, less exploration in the open field, and a number of other behavioral decrements in the offspring of older sires (Bradley-Moore et al., 2002).
Next, we examined if parental age was related to intelligence in healthy adolescents. We reasoned that if de novo genetic changes can cause schizophrenia, there might be effects of later paternal age on cognitive function, since cognitive problems are intertwined with core aspects of schizophrenia. For this study, we cross-linked data from the Jerusalem birth cohort with the neuropsychological data from the Israeli draft board (Malaspina et al., 2005a). We found that maternal and paternal age had independent effects on IQ scores, each accounting for ~2 percent of the total variance. Older paternal age was exclusively associated with a decrement in nonverbal (performance) intelligence IQ, without effects on verbal ability, suggestive of a specific effect on cognitive processing. In controlled analyses, maternal age showed an inverted U-shaped association with both verbal and performance IQ, suggestive of a generalized effect.
Finally, we examined if paternal age was related to the risk for autism in our cohort. We found very strong effects of advancing paternal age on the risk for autism and related pervasive developmental disorders (Reichenberg et al., in press). Compared to the offspring of fathers aged 30 years or younger, the risk was tripled for offspring of fathers in their forties and was increased fivefold when paternal age was >50 years. Together, these studies provide strong and convergent support for the hypothesis that later paternal age can influence neural functioning. The translational animal model offers the opportunity to identify candidate genes and epigenetic mechanisms that may explain the association of cognitive functioning with advancing paternal age.
A variant of schizophreniaA persistent question is whether the association of paternal age and schizophrenia could be explained by psychiatric problems in the parents that could both hinder their childbearing and be inherited by their offspring. If this were so, then cases with affected parents would have older paternal ages. This has not been demonstrated. To the contrary, we found that paternal age was 4.7 years older for sporadic than familial cases from our research unit at New York State Psychiatric Institute (Malaspina et al., 2002). In addition, epidemiological studies show that advancing paternal age is unrelated to the risk for familial schizophrenia (Byrne et al., 2003; Sipos et al., 2004). For example, Sipos found that each subsequent decade of paternal age increased the RR for sporadic schizophrenia by 1.60 (1.32 to 1.92), with no significant effect for familial cases (RR = 0.91, 0.44 to 1.89). The effect of late paternal age in sporadic cases was impressive. The offspring of the oldest fathers had a 5.85-fold risk for sporadic schizophrenia (Sipos et al., 2004); relative risks over 5.0 are very likely to reflect a true causal relationship (Breslow and Day, 1980).
It is possible that the genetic events that occur in the paternal germ line are affecting the same genes that influence the risk in familial cases. However, there is evidence that this is not the case. First, a number of the loci linked to familial schizophrenia are also associated with bipolar disorder (Craddock et al., 2006), ), whereas advancing paternal age is specific for schizophrenia (Malaspina et al., 2001). Next, a few genetic studies that separately examined familial and sporadic cases found that the "at-risk haplotypes" linked to familial schizophrenia were unassociated with sporadic cases, including dystrobrevin-binding protein (Van Den Bogaert et al., 2003) and neuregulin (Williams et al., 2003). Segregating sporadic cases from the analyses actually strengthened the magnitude of the genetic association in the familial cases, consistent with etiological heterogeneity between familial and sporadic groups.

Read Dr. Malaspina's whole paper and its sources.

See the following post for autism as an extreme autoimmune disorder related to a family history of autoimmune disorders caused by older paternal age in one generation or another.


Pediatrics. 2003 Nov;112(5):e420. Links
Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders.Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM, McDougle CJ.
Department of Psychiatry, Indiana University School of Medicine, and James Whitcomb Riley Hospital for Children Indianapolis 46202-4800, USA.

OBJECTIVES: Increased prevalence of familial autoimmune disease is a common finding among probands with various autoimmune disorders. Autistic disorder (autism) is a highly genetic disorder with known immune and immunogenetic abnormalities. Previous research has found an increased frequency of autoimmune disorders in families with autistic probands. We further investigated this association by determining the frequency of autoimmune disorders in families that have probands with pervasive developmental disorders (PDDs), including autism, compared with 2 control groups. METHODS: Three well-defined study groups, including 1) families that have a child with a PDD, 2) families that have a child with an autoimmune disorder, and 3) families with a healthy control child, constituted the sample. A questionnaire inquiring about which first- and second-degree family members had received a diagnosis of having specific autoimmune disorders was completed by 101 families in each group. RESULTS: The frequency of autoimmune disorders was significantly higher in families of the PDD probands compared with families of both the autoimmune and healthy control probands. Autoimmunity was highest among the parents of PDD probands compared with parents of the healthy control subjects. Hypothyroidism/Hashimoto's thyroiditis and rheumatic fever were significantly more common in families with PDD probands than in the healthy control families. CONCLUSIONS: Autoimmunity was increased significantly in families with PDD compared with those of healthy and autoimmune control subjects. These preliminary findings warrant additional investigation into immune and autoimmune mechanisms in autism.

PMID: 14595086 [PubMed - indexed for MEDLINE]


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Thanks to Ginger's blog Adventures in Autism

Since Autism Speaks is coming under such close examination, I thought I would bring to you the keen observation of an anonymous poster on the Evidence of Harm List.
Labels: autism prevention?, Autism Speaks, causes of autism, charities, follow the cash


posted by concerned heart at 12:13 PM 0 Comments Links to this post

Friday, June 8, 2007
I Found The Post Below the Picture This Morning on Adventures in Autism
The $2,000,000 for Mark Rothmeyer doesn't surprise me at all. Neither do the other expenses and salaries. If anyone is interested in the causes of autism and the history of its creation as a mysterious disorder go to the autism prevention blogspot. Autism, until 1994 used to be a diagnosis given for a very specific set of symptoms and it was sometimes considered the severest example of early childhood schizophrenia. The paper by Kanner on classical autism can be linked to on the site.


Autism Speaks never does anything to help anyone with autism, or prevent even one case of autism. The causes of autism are known, the way to prevent more autism is known in a percentage of cases. How to take a tragic disorder and turn it into a lucretive business venture is demonstrated again by Autism Speaks and the Institutions it funds.

.....................................................................................


GINGER's Blog: ADVENTURES IN AUTISM

Thursday, June 07, 2007
I Take Back Every Nice Thing I Have Ever Said About Autism Speaks

"I read this today and it just made me sick. I don't even have the words to comment on it."~Ginger
....................................................................................
I am a professional that has reviewed many non profit organization's IRS Form 990s. Autism Speaks Form 990 raises serious red flags. Serious. This is all from the official filing for 2006.





1. Three members of the Board of Directors received $2.5 million for their own organizations.

2. The President Mark Rothmeyer, just received a 5 year contract for about $2,000,000 including bonuses with no prior background with autism.

3. The grants are primarily going to those representing institutions that are reviewing the grants. There is no indication that these conflicts are independently reviewed

4. The location of this small and new foundation is in very expensive downtown New York facilities rented for $200,000 by the institution that is run by the Chairman of Autism Speaks.

5. A expense of a Private Jet plane for $57,000 was noted. This is very unusual for a new non profit groups.

6. The head of the scientific review received the majority of the funds for 2005 for his institution for a data base - almost $3 million

Since the funding is now from the public - and the advertising and promotion tugs at the publics heart strings with images of families in need - the funds collected MUST be about those it raises the money for.

The following are all taken from the Form 990 filing

Web Site $830,000
Software for the computer $514,000
Lawyers $440,000
Computers $337,000
Public relations $285,000
Office annual rent $200,000
HR consultant $110,000
Editorial Consultant $76,000
Private Jet Plane for someone that entertained $57,000


Mark Rothmeyer* $360,000
Peter Bell [$240,000?]
Alison Singer $168,000
Mr Ringall $150,000
Andy Shik $110,000

Remember all the above also gets significant fring benefits that
probably add.

Mark Rothmayer also can get $50,000 more with a bonus a year benefits

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Monday, June 11, 2007

Vaccines and Autism Connection Controversy Heats Up, The Real Connection Between Autism and Vaccines Is Known, Kept Secret Read Below to Discover It





















Many many different combinations of mutations in DNA cause autism/schizophrenia but one cause is certain and that is older paternal age in one generation or another.



Autism Prevention- father your children 23-33 Autism today's term for various neurodevelopmental disorders.MOST AUTISM DUE TO AN OLDER FATHER IN ONE GENERATION OR ANOTHER The Autism Spectrum Disorders, have been devised to confuse any serious discussion of why there is an epidemic. Risk factors for non-familial autism are an older father over 32, autoimmune disorders in family, mother had old dad. Some autism is X-linked and some autosomal recessive. Childhood schizophrenia is now called autism. Older paternal age a major risk factor.


Increased prevalence of familial autoimmunity in probands with pervasive developmental disorders.Sweeten TL, Bowyer SL, Posey DJ, Halberstadt GM, McDougle Department of Psychiatry, Indiana University School of Medicine, and James Whitcomb Riley Hospital for Children Indianapolis 46202-4800, USA.OBJECTIVES: Increased prevalence of familial autoimmune disease is a common finding among probands with various autoimmune disorders. Autistic disorder (autism) is a highly genetic disorder with known immune and immunogenetic abnormalities. Previous research has found an increased frequency of autoimmune disorders in families with autistic probands. We further investigated this association by determining the frequency of autoimmune disorders in families that have probands with pervasive developmental disorders (PDDs), including autism, compared with 2 control groups. METHODS: Three well-defined study groups, including 1) families that have a child with a PDD, 2) families that have a child with an autoimmune disorder, and 3) families with a healthy control child, constituted the sample. A questionnaire inquiring about which first- and second-degree family members had received a diagnosis of having specific autoimmune disorders was completed by 101 families in each group. RESULTS: The frequency of autoimmune disorders was significantly higher in families of the PDD probands compared with families of both the autoimmune and healthy control probands. Autoimmunity was highest among the parents of PDD probands compared with parents of the healthy control subjects. Hypothyroidism/Hashimoto's thyroiditis and rheumatic fever were significantly more common in families with PDD probands than in the healthy control families. CONCLUSIONS: Autoimmunity was increased significantly in families with PDD compared with those of healthy and autoimmune control subjects. These preliminary findings warrant additional investigation into immune and autoimmune mechanisms in autism.







"The issue is that the older man will have sperm that has undergone more divisions and therefore had more chances to have mutations. The COMPLEXITY of the myelination process makes it more vulnerable to mutations. I am not talking of one specific mutation. Many things could MANIFEST in the myelination or myelin breakdown process because it is so vulnerable - something going slightly wrong will impact it while it will not impact bone growth or the heart. A good example is ApoE4 - whatever else it may affect, it manifests in the reduced capacity of myelin repair and earlier onset of AD." Prenatal and Perinatal Risk Factors for AutismA Review and Integration of Findings Alexander Kolevzon, MD; Raz Gross, MD, MPH; Abraham Reichenberg, PhD Arch Pediatr Adolesc Med. 2007;161:326-333. Objective To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders. Data Sources Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic. ....The results of this review show that 3 of the 4 population-based studies28-29,32 to examine paternal age reported a significant association with risk of autism and ASDs. The fourth study31 also found that paternal age was older in fathers of case patients with autism compared with fathers of controls, although this relationship was statistically weaker in the adjusted analysis. Thus, advancing paternal age is consistently associated with increased risk of autism and ASDs.Advanced paternal age has been associated with several congenital disorders, including Apert syndrome,40 craniosynostosis,41 situs inversus,42 syndactyly,43 cleft lip and/or palate,44-45 hydrocephalus,44 neural tube defects,46 and Down syndrome.47 In addition, advanced paternal age has been associated with schizophrenia15 and decreased intellectual capacities in the offspring.48 The most widely proposed mechanism underlying these congenital anomalies is known as the "copy error" hypothesis, first proposed by Penrose.49 After puberty, spermatocytes divide every 16 days, and by the age of 35 years, approximately 540 cell divisions have occurred. As a result, de novo genetic mutations that result from replication errors and defective DNA repair mechanisms are believed to propagate in successive clones of spermatocytes. These mutations accumulate with advancing paternal age and thus help explain how this disorder, which has a large genetic component, can be maintained in the population despite reduced reproduction in affected individuals.-----------------------------------------------------------------------------------



Thursday, April 12, 2007 AUTISM WAS RARE IN 1988 2-5 PER 10,000 Vol. 45 No. 10, Oct., 1988 Autism and genetics. A decade of research S. L. Smalley, R. F. Asarnow and M. A. Spence Department of Psychiatry, UCLA School of Medicine 90024. The last ten years of research on the genetics of infantile autism were critically reviewed. Epidemiologic findings have shown that autism is a rare disorder with a prevalence of two to five per 10,000, a male-female ratio of 3:1, and an association with mental retardation (66% to 75% of autistic subjects have full-scale IQ scores [70]). Autism is familial, as reflected in an empiric sibling recurrence risk of 3% and pooled monozygotic and dizygotic concordance rates of 64% and 9%, respectively, which are much greater than the population prevalence of 0.02% to 0.05%. Genetic heterogeneity is pronounced with potential genetic subgroups, including autosomal recessive inheritance, X-linked inheritance, and sporadic chromosomal anomalies. Studies of subclinical markers in autism have elucidated potential markers at various levels of phenotypic expression from the DNA to the behavioral level. Linkage and cytogenetic studies point to two chromosome regions as putative markers, 9q34 and Xq27. Results of family studies support a putative biochemical marker, low levels of plasma dopamine-beta-hydroxylase, and a putative cognitive marker, ie, normal visuospatial but low verbal functioning, in autism. The frequency of minor physical anomalies and presence or absence of mental retardation are two dimensions of the physical and behavioral phenotype that may demark etiologically distinct subgroups. Genetic heterogeneity is offered as one explanation of the observed sex difference in the prevalence of autism. Directions for potentially fruitful research should

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