An NT in aspie shell?

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It is really interesting to learn that in the 50-s the programs were more effective then now. And, somehow, its not surprising. I guess I always thought of modern generation as being overly-medicated and overly-sheltered, neither of which are conductive things to more healthy type of learning. And, speaking of medicated, both myself and my parents are against them, so, gladly, I wasn't taking any. But maybe the broader aspects of todays mindset affected how much people were trying to help me.

Thats interesting. I guess my problem is that NT-s look at the aspies in the way that I look at ice creams as opposed to the way you look at ice creams. And I disagree with them: I would prefer if they used your way of looking at ice creams, but they just don't.

A brief summary of this collected body of information. Twin concordance studies showed an estimated 70% concordance among monozygotic twins (reported ranges 36%–95%). In contrast, concordance among dizygotic twins was around 3% (range 0%–31%) or 30% if a broader phenotypic definition was used. Heritability estimates were noted to be 0.8 to 0.9. [Heritability Estimates tell us what proportion of variation in a given behavior or a disorder is due to genes versus the environment. These estimates range from 0.0 to 1.0, with 0.0 indicating that genetics are not a contributing factor at all and 1.0 indicating that genetics are the only factor.] The estimated relative (sibling) risk ratio is reported to be about 150 for monozygotic twins and 8–10 for dizygotic twins and full siblings. In the realm of the discipline of population genetics this is overwhelming support of a genetic basis to ASDs. This data have been replicated and validated in more recent and larger studies. With a broader design and larger sample size, these more recent studies have also added another population parameter not previously noted. A 2–3-fold increased recurrence risk of ASD has been documented in half-siblings (both maternal and paternal) of probands with an ASD. The increased occurrence in even less closely related individuals lends very strong support for the genetic basis of autism.

Considering the above definitions, ASDs clearly fall into the category of multi-factorial inheritance. The recurrence risk pattern of multi-factorial traits typically demonstrate:
* An increased recurrence risk in close relatives as compared to the general population frequency,
* A non-linear decrease in frequency with increasing distance of relationship—typically no increased recurrence rates are seen beyond 3rd degree relatives,
* The recurrence risk increases with the number of affected individuals,
* There is an increased risk with increased severity of the condition,
* There is an increased risk if person(s) affected are of the “rarer” gender. (In ASD a distinct gender bias of a 3- to 4-fold rate of affected males has been noted.)

Recurrence risk data that had accumulated up until about 2008 matched well with this model. The overall recurrence risk for a sibling of a single proband with ASD was reported as 3%–10%. Further refinement of these risks noted that the estimated recurrence risk for a sibling of an affected person with an ASD was established as 4% if the affected individual was male and 7% if female. If there were more than one affected sibling with an ASD, the recurrence risk for future siblings increased to a remarkable 30%–50%. These numbers have been verified in multiple studies.

The established heritability rates of around 0.8 or more implies that the majority of the ASD phenotype is determined by genetic factors.