Study: Autism Is Half Genetic, Half Environmental
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AnonymousAnonymous
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Joined: 23 Nov 2006
Age: 34
Gender: Male
Posts: 70,124
Location: Portland, Oregon
06 May 2014, 1:48 pm
Hmmm...I'm not sure what to make of this. If the environment is more of a cause of Autism than genetics, then anti-vaccine groups should stop targeting Auties/Aspies ASAP!
http://www.rawstory.com/rs/2014/05/04/s ... ronmental/
_________________
Silly NTs, I have Aspergers, and having Aspergers is gr-r-reat!
06 May 2014, 4:35 pm
Here is a link to the abstract of the actual study. You need JAMA access (which I don't have) to get the methods/results etc., but at least it's more than you get from the news media interpretations.
http://jama.jamanetwork.com/article.asp ... 00#Methods
Quote:
Importance Autism spectrum disorder (ASD) aggregates in families, but the individual risk and to what extent this is caused by genetic factors or shared or nonshared environmental factors remains unresolved.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
No details on what they are suspecting as environmental factors. It may be that if something isn't attributed to genetics, the default is environment. There are probably multiple environmental factors. The state of the pregnant woman- including her age and health status- may be factors, as well as actual external substances (pollution, environmental chemicals, yes possibly even vaccines).
Even without a list of environmental suspects, the study is not meaningless. Its' meaning is that it challenges previously held beliefs ( held by scientists, not Jenny McCarthy) that it is 80-90% genetic and 10-20% environmental.
07 May 2014, 2:49 pm
smenon3 wrote:
Would stuff like McDonalds, Burger King, Sonic, Arby's, etc. and vaccines be an environmental factor. Everybody tells my I have Aspergers and ADHD because of my unhealthy eating habits which I am making progress on impoving.
Aspergers, and ADHD, are presumably present at birth.
So how could the way you eat today have retroactively caused you to have been born with aspergers, and ADHD?
07 May 2014, 3:21 pm
Janissy wrote:
Here is a link to the abstract of the actual study. You need JAMA access (which I don't have) to get the methods/results etc., but at least it's more than you get from the news media interpretations.
http://jama.jamanetwork.com/article.asp ... 00#Methods
No details on what they are suspecting as environmental factors. It may be that if something isn't attributed to genetics, the default is environment. There are probably multiple environmental factors. The state of the pregnant woman- including her age and health status- may be factors, as well as actual external substances (pollution, environmental chemicals, yes possibly even vaccines).
Even without a list of environmental suspects, the study is not meaningless. Its' meaning is that it challenges previously held beliefs ( held by scientists, not Jenny McCarthy) that it is 80-90% genetic and 10-20% environmental.
http://jama.jamanetwork.com/article.asp ... 00#Methods
Quote:
Importance Autism spectrum disorder (ASD) aggregates in families, but the individual risk and to what extent this is caused by genetic factors or shared or nonshared environmental factors remains unresolved.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
No details on what they are suspecting as environmental factors. It may be that if something isn't attributed to genetics, the default is environment. There are probably multiple environmental factors. The state of the pregnant woman- including her age and health status- may be factors, as well as actual external substances (pollution, environmental chemicals, yes possibly even vaccines).
Even without a list of environmental suspects, the study is not meaningless. Its' meaning is that it challenges previously held beliefs ( held by scientists, not Jenny McCarthy) that it is 80-90% genetic and 10-20% environmental.
I wonder what they mean by environmental? If this is the perinatal environment or environment of early fetal development, then some of this may come down to epigenetic effects. "Environment" does not necessarily mean the same thing in the study as it does in the vernacular. I would be interested in seeing more on this.
07 May 2014, 4:53 pm
Adamantium wrote:
Janissy wrote:
Here is a link to the abstract of the actual study. You need JAMA access (which I don't have) to get the methods/results etc., but at least it's more than you get from the news media interpretations.
http://jama.jamanetwork.com/article.asp ... 00#Methods
No details on what they are suspecting as environmental factors. It may be that if something isn't attributed to genetics, the default is environment. There are probably multiple environmental factors. The state of the pregnant woman- including her age and health status- may be factors, as well as actual external substances (pollution, environmental chemicals, yes possibly even vaccines).
Even without a list of environmental suspects, the study is not meaningless. Its' meaning is that it challenges previously held beliefs ( held by scientists, not Jenny McCarthy) that it is 80-90% genetic and 10-20% environmental.
http://jama.jamanetwork.com/article.asp ... 00#Methods
Quote:
Importance Autism spectrum disorder (ASD) aggregates in families, but the individual risk and to what extent this is caused by genetic factors or shared or nonshared environmental factors remains unresolved.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
Objective To provide estimates of familial aggregation and heritability of ASD.
Design, Setting, and Participants A population-based cohort including 2 049 973 Swedish children born 1982 through 2006. We identified 37 570 twin pairs, 2 642 064 full sibling pairs, 432 281 maternal and 445 531 paternal half sibling pairs, and 5 799 875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.
Main Outcomes and Measures The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.
Results In the sample, 14 516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100 000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).
Conclusions and Relevance Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
No details on what they are suspecting as environmental factors. It may be that if something isn't attributed to genetics, the default is environment. There are probably multiple environmental factors. The state of the pregnant woman- including her age and health status- may be factors, as well as actual external substances (pollution, environmental chemicals, yes possibly even vaccines).
Even without a list of environmental suspects, the study is not meaningless. Its' meaning is that it challenges previously held beliefs ( held by scientists, not Jenny McCarthy) that it is 80-90% genetic and 10-20% environmental.
I wonder what they mean by environmental? If this is the perinatal environment or environment of early fetal development, then some of this may come down to epigenetic effects. "Environment" does not necessarily mean the same thing in the study as it does in the vernacular. I would be interested in seeing more on this.
I agree. When People say environmental causes it is usually understood like the way your parents treated you or what you ate.
07 May 2014, 8:22 pm
This is the problem with psychology. Its all just guesswork based on observation.
Autism IS genetic.
That being said, are there times when life-events (particularly when young) and toxins can create similar symptoms to autism? Yes.
The problem with psychology at this point is they are bunching the genetic group and the environmental group as one to treat them. The treatment one group receives is not going to be of much use to the other...for the environmental group is for the most part (meaning all those whose condition is caused by brain damage inflicted by toxins), NT's which do respond better to NT-designed procedures/medication/therapy.
For example, a genetic AS and a childhood trauma induced AS symptomatic NT person undergo cognitive therapy. Said therapy literally tries to teach them how to act normal by pretending to be what they aren't. The genetic AS person will only learn how to fake, the NT on the other hand actually gets 'healing' from it.
Until there is a 'brain scan' or genetic test for autism that can be performed as routine for diagnosis, psychologists will simply keep guessing and playing the alchemist card.
Frankly I'd prefer a system where people that diagnose should have degrees in neuroscience and psychology otherwise they won't have a freaking clue how to do their job.
08 May 2014, 1:59 pm
Dantac wrote:
Until there is a 'brain scan' or genetic test for autism that can be performed as routine for diagnosis, psychologists will simply keep guessing and playing the alchemist card.
Frankly I'd prefer a system where people that diagnose should have degrees in neuroscience and psychology otherwise they won't have a freaking clue how to do their job.
Requiring a degree in neuroscience and psychology before somebody could diagnose would create quite a high bar and would make diagnosis even harder to get than it already is.
09 May 2014, 12:14 pm
Dantac wrote:
For example, a genetic AS and a childhood trauma induced AS symptomatic NT person undergo cognitive therapy. Said therapy literally tries to teach them how to act normal by pretending to be what they aren't. The genetic AS person will only learn how to fake, the NT on the other hand actually gets 'healing' from it.
.
.
In effect that is what I did. I learned the queues and clues Normals use empirically and eventually I learned to pass for human. I am well adapted to the Neuro Typical world without be an NT myself. My wife is NT and 3 out of my 4 kids are NT. One of my grandson's may be on the spectrum. He was diagnosed young with NLVD (non-verbal learning disorder) which is a fancy terms for "I do not know what is wrong with this kid". He has outgrown it mostly. He is learning to adapt. My grand daughters are completely normal.
ruveyn
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