New Autism Twin Study Demolishes Decades-Long Belief in Genetic Causation
By Mark Blaxill
For over two decades now, so-called “autism experts” have been claiming that autism is more than 90% caused by genes. The influence of these claims on autism policy and research funding is hard to overstate. But few realize that the basis of these claims hangs on a fragile evidence base: two small twin studies--one from Great Britain, the other from Scandinavia--that reported high rates of concordance for autism among identical twins and no concordance at all among fraternal twins. Last week, the largest and most rigorous twin study ever conducted, the California Autism Twin Study (CATS) reported contradictory new evidence that struck a devastating blow to these claims. The CATS identical twins had lower and the fraternal twins higher concordance rates than past studies, a striking finding that suggests that instead of being highly heritable, the vast majority of autism cases stem from environmental causes.
It’s hard to overstate the importance of the CATS findings. They mean that everything leading “autism experts” have been saying for decades is wrong. And everything leading autism parent advocates have been saying for years is right.
The foundations of autism orthodoxy
As the reality of the autism epidemic began settling in over the last decade, an odd drumbeat in the writing of autism geneticists became more insistent. The more obvious it had become that something new and terrible was happening to a generation of children, the more extreme the statements of the genetics researchers became. It’s as if repeating the orthodox statements as frequently as possible would give them more weight. And the more their extreme claims went unchallenged, the more a spurious “scientific consensus” could be claimed. Here’s a small sample: (1) “Autism is clearly among the most heritable of all psychiatric disorders“(2003); (2) “Autism is one of the most heritable complex disorders, with compelling evidence for genetic factors and little or no support for environmental influence” (2004); (3) “Autism spectrum disorders are considered to be among the most heritable of all mental disorders…. recent reviews estimate the heritability of autistic disorder to be more than 90%.” (2010); (4) “ASDs are known to be highly heritable (~90%)” (2010).
Despite the fact that an explosion in autism rates rendered illogical any ongoing belief in the genetic inheritance of autism, the influence of this orthodox position on autism’s research funding remained profound. Hundreds of millions of research dollars were spent over the last decade in a vain hunt for autism genes; a spending binge that has continued unabated, with over $100 million spent at NIH on genetics-only research during the latest two years of the Combating Autism Act alone.
In the meantime, a mini-industry of epidemic denial has emerged among academics willing to posit a newfound popularity among physicians and parents for the autism label, one that has produced increasingly bizarre claims of diagnostic excess in many forms: substitution, oversight, expansion and accretion among them. These claims have been retracted, disavowed and falsified multiple times, yet because of the overriding need to feed “the hungry lie” these claims keep cropping up in novel forms. Meanwhile, the research funding to support them continues, including active support from NIH. And sadly, anyone in the scientific community with the courage to stick their necks out and suggest that autism rates might be going up because, well, there were more cases of autism, found themselves facing reactions ranging from polite ostracism to ruthless censorship.
The basis for this orthodox belief in autism’s heritability rests on a very specific body of autism research: the investigation of concordance rates within twin pairs. These studies take advantage of a seemingly simple test--the presence or absence of similar outcomes in twins--to estimate the relative contribution of nature (i.e., genes) and nurture (i.e., the environment) to a given disease. To the extent that identical twins have the identical outcomes and fraternal twins have different ones, the cause can reasonably be assigned to genes. To the extent that identical twins have different outcomes and fraternal twins have the same outcome, the cause lies in the environment.
In the case of autism, this test has been applied to twins with increasing frequency, but the orthodox belief in heritability hangs on a slender thread of evidence: the first, a British study of twin pairs first recruited in 1977 (5) and then expanded in 1995 (6); the second, a Scandinavian study from 1989 (7). The 1977 British study reported on just 21 twin pairs, 11 identical and 10 fraternal. Of these, only 4 of the identical twin pairs were concordant for autism (a remarkably low rate that is frequently forgotten). The 1989 Scandinavian study with the same small sample size, 11 identical pairs and 10 fraternal pairs, found autism in both identical twins in 10 of 11 pairs and again no concordance in any of the fraternal pairs. Subsequently, nearly two decades after their first study, the British team recruited 28 new pairs in 1995 and pooled them together with some of the previous group. These new pairs showed a similar profile: only one twin in each of new fraternal pairs had autism (i.e., a zero concordance rate); and of the new identical pairs, 11 of 16 were concordant, giving a 69% concordance rate that fell between their original calculation and the Scandinavian group.
The British team then added an important new element: a heritability calculation. Using a complex approach (with formulae that defy clear explanation), they took all these concordance rates banged them against two different background rates of autism, ran them through a model and declared, “The estimates of broad heritability were 93% and 91% for the base rates of 1.75 and 10 in 10,000.”
And thus was born the belief that autism was more than 90% genetic.
The orthodoxy in quiet crisis: discordant evidence on twin concordance
Oddly enough, the 1995 date of this publication coincided with the first awareness among public health officials of the autism epidemic, with an inflection point generally assigned to the birth years 1989-90 (8-9) and with awareness of this shift emerging with a lag as these new birth cohorts were being diagnosed 3-5 years later. Because of this confluence of events—the convergence of some “autism experts” around a self-proclaimed “scientific consensus” on autism’s cause and an epidemic rise that directly contradicted that consensus—for over 15 years now, autism research has been hijacked by a bizarre cognitive dissonance between a deeply held belief in autism’s heritability and the impossibility of a genetic epidemic.
Interestingly, there was plenty of evidence available, even as early as 1995, to show that the extravagant conclusions of the British team weren’t true. Most notably, other collections of twin reports found much higher concordance rates in fraternal twins. First among these was a 1985 twin study from Utah (one with a larger sample than either of the initial British and Scandinavian studies) that found a 24% concordance rate among fraternal twins (10). Because this rate was too high for the orthodox scientists to explain (the Utah study authors found such a high autism rate among identical twins they suggested that autism might come from a single recessive gene) the Utah findings were effectively written out of history. The reason? The Scandinavian authors argued that the Utah twin registry began recruiting twins by putting an advertisement in an autism newsletter. And since the evidence from Utah didn’t fit the orthodox story, the evidence was rejected in order to keep the orthodoxy intact.
But just as the 90% heritability mantra was spreading in the years following the 1995 British paper (aptly titled to promote the message “Autism as a strongly genetic disorder: evidence from a British twin study”), more discordant evidence began accumulating. A 2003 Missouri twin study that collected (but didn’t report) autism concordance rates contained an intriguing parenthetical comment (11). Referring to the previously reported differences in the ratio of identical to fraternal autism twin concordance, the authors described these previously reported relationships as “concordance ratios greater than 2 (which we did not observe in our sample).” Another discordant note came from a 2008 twin study from Japan (12), which reported results that were nearly identical to the Utah findings, but with an even higher 31% concordance rate in fraternal twins. Reinforcing the dissonance, a 2009 study using an America registry of autism cases reported results that were nearly identical to the Utah and Japan studies (13).
Alongside all this other discordant evidence came the early rumblings from what eventually became the California Autism Twin Study (CATS). The study of California twins had begun as much as a decade before last week’s CATS publication and hints of their eventual findings have leaked out before. One 2002 abstract (14) on California twins raised the idea that “heritability estimates from previous studies may have overestimated the role of genetics and underestimated the role of environmental factors in the etiology of autism.” The formal launch of the CATS project took place a couple of years later, in July 2004; even so the dimensions of this early suggestion took many more years to come out into the open.
“It was better than CATS”
Orthodox scientists will undoubtedly spin the California results, arguing that the study was flawed in some fatal respect and that other studies were better than CATS. But actually, it’s pretty hard for a twin study to be much better than CATS; certainly none of the previous autism twin investigations come close. The California project is without question the most ambitious study of autism twins ever attempted. First of all, CATS is the largest twin study, enlisted from a registry based on the entire California autism population and including a final sample of 192 twin pairs, more than four times larger than any other previous twin study and nearly an order of magnitude larger than the first British and Scandinavian studies. The registry based approach (identifying twins from a complete roster of California autism cases rather than selective outreach) also makes the CATS sample less vulnerable to recruiting bias.
Perhaps most important at all, it’s hard to argue that the CATS author group is biased against inherited genes and in favor of environmental causation. The author group includes a healthy mix of orthodox autism scientists: Lisa Croen and Judy Grether are among the original “epidemic deniers” in autism (although their early claims of “diagnostic substitution” in California proved incorrect and, to their credit, they retracted them); Claire Lajonchere and Janet Miller are leaders of AGRE, Autism Speaks’ “autism genetic resource exchange”; first author Joachim Hallmayer and Linda Lotspeich of Stanford have been members in good standing of the Autism Genome Project Consortium; and senior author Neil Risch has been active in autism genome scanning work for over a decade.
What did CATS find that turned previous assumptions about nature and nurture in autism upside down? In brief, they found concordance rates in identical twins that were substantially lower than the Utah and Japan studies and rates in fraternal twins that were far higher than those found in Great Britain and Scandinavia. Identical twin concordance rates in CATS were significantly lower than rates of ~95% reported (and criticized) in Utah and Japan: 43% for full syndrome autism and 59% for ASD. At the same time, fraternal twin concordance was higher than the 0% rate reported in the British and Scandinavian studies, at 8% and 13% for autism and ASD respectively.
Using the concordance data, the CATS team went on to perform a number of elaborate calculations (again, using a complex approach with formulae that defy clear explanation) to assign theoretical causality for autism to three sources: inherited genes (A), common or shared twin environment (C) and non-shared (they also called it “random”) twin environment (E).
The calculations resulted in a dramatically lower rate of heritability (A) than anyone expected, 37% and 38% for autism and ASD, respectively. By extension, the shared twin environment estimates of 55-58% were far higher than expected. And of course, the mere concession that the environment took precedence over genetic causation in autism (even if it was only a 40/60 effect), made news. After all, going from 91-93% heritability to 37-38% was nearly a two thirds blow to the autism gene hunt in a single stroke.
But the talking points that made the news don’t do justice to the real weight of the evidence. Crucially, the low 37-38% number for “A” dramatically overstated the role of heritability, a point the authors conceded in the paper’s fine print, where they acknowledged two major biases.
1. The study design explicitly excluded the possibility of an environmental effect being mediated by genetic vulnerability in a subset of children. In other words, their ACE model excluded the possibility of gene-environment interaction. According to the authors, “The ACE model we used has several inherent assumptions. First, it assumes no gene environment interaction. If such a gene environment effect does exist, it would be confounded with the A parameter in our analysis, implying that as an estimate of pure genetic effect, A may actually be an overestimate.”
2. A more subtle bias of the study involved the way their model treated the twins’ environment in the womb. Twins are known to have variable gestational environments but the authors’ model assumed that both identical and fraternal twins faced the same “shared twin environment.” In fact, identical twins share a fetal environment (via a shared placenta or amniotic sac) far more often than fraternal twins (who almost always share neither). To the extent that the ACE model assigned the higher concordance of identical twins to heritability, the authors’ calculations excluded the fact that identical twins not only have identical genes, but a more nearly identical environment as well. The authors point out how this simplifying assumption raises their heritability estimate. “Similarly, a critical assumption in the model is that the shared twin environmental effect is the same for monozygotic [identical] and dizygotic [fraternal] twins. If, in fact, monozygotic twins share the relevant environment to a greater degree than the dizygotic twins, some of the effect included in the parameter A would actually be environmental rather than genetic; again, A may actually overestimate the true genetic heritability.”
It’s hard to guess how much lower the 37-38% heritability estimate would fall if these two biases were removed. But the effects are more likely large than small and full adjustment for these two biases would almost certainly turn the nature/nurture causation estimates on their head: instead of a world in which >90% of autism causes come from inherited genes, it’s more likely that >90% of its causes come from the environment.
Which is exactly what so many autism parent advocates have been saying for years.
Separated at birth
In the enthusiasm over the move from a 90/10 gene-environment split to one that the CATS team conceded was closer to 40/60, there’s one additional subtlety that has gone overlooked. In a crucial oversight, the authors calculated estimates for both A, C and E, but once they dispensed with genes (A) and turned to the environment, the only variable they reported was the “shared twin environment” (C). In the process, they completely ignored E, or the “non-shared twin environment.” For those interested in environmental causation, this non-shared component E is far more intriguing than C. It includes everything in the twin experience that is unique to an individual twin. Inside the womb, for example, there might be differences between two different amniotic sacs or placentas that put one twin more at risk for autism than the other. More to the point, the twins might experience different environmental exposures outside the womb, exposures that could also account for different autism risks. These non-shared exposures are of special interest because they provide the strongest evidence for exposures that can be avoided so that autism, even in a genetically vulnerable child, can be prevented.
In CATS, the amount of causality assigned to the non-shared twin environment was estimated (although never directly reported) at 4-8%. It’s perhaps not surprising that the numbers were that low, since identical twins are often reared in highly similar environments. There environments are more similar than most siblings and even than fraternal twins. It takes a rare set of circumstances to vary the environment of identical twins enough to provide different autism risks.
In an extreme case, however, twins will maximize their non-shared environment if they are separated at birth.
In our book, The Age of Autism: Mercury, Medicine and a Manmade Epidemic, Dan Olmsted and I report on the most extreme cases of non-shared post-natal environment in autism twins ever described. One of these was a pair of non-concordant, identical twin boys, given up for adoption at birth by a woman named Kim Stewart who retained contact with the adoptive families. Both families provided a loving environment for their sons, both children lived in similar parts of the country and developed normally, as “healthy, happy boys,” for the first fifteen months of life. The first joined a family of Christian Scientists, received no vaccinations of any kind and continued to develop normally. The second joined a family that followed more conventional infant vaccination schedules and regressed into autism after receiving his fifteen month shots. The only non-shared twin environmental risk the birth mother could pinpoint was that separating the boys at birth led one to be fully vaccinated and autistic and the other to be unvaccinated and healthy. “I became convinced,” she told us, that “vaccinations played a significant role in his regression.”
* * *
The body of twin evidence in autism as most recently revealed by the CATS study demonstrates the power of scientific orthodoxy to sustain itself in the face of overwhelming evidence when its believers have strong research interests and the power to perpetuate a hungry lie. In situations like this, putative claims of “scientific consensus” can become a pernicious influence when that consensus favors a convenient lie.
My friend JB Handley has made this point before and pointed the readers of Age of Autism to a compelling quote by the late Michael Crichton MD, author of The Andromeda Strain and Jurassic Park, who had this to say about scientific consensus.
"I want to pause here and talk about this notion of consensus, and the rise of what has been called consensus science. I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you're being had."
--
Mark Blaxill is Editor at Large of Age of Autism.
--
References:
1) Yonan AL et al. A genomewide screen of 345 families for autism-susceptibility loci. Am J Hum Genet. 2003;73(4):886-97.
2) Veenstra-Vanderweele J, Christian SL, Cook EH. Autism as a paradigmatic complex genetic disorder. Annu Rev Genomics Hum Genet. 2004;5:379-405.
3) Lichtenstein P et al. The genetics of autism spectrum disorders and related neuropsychiatric disorders in childhood. Am J Psychiatry. 2010;167(11):1357-1363.
4) Pinto D, Pagnamenta AT, Klei L, et al. (Autism Genome Project Consortium) Functional impact of global rare copy number variation in autism spectrum disorders. Nature. 2010;466(7304):368-72.
5) Folstein S and Rutter M. Infantile Autism: A Genetic Study of 21 Twin Pairs. J Child Psychol Psychiatry. 1977;18(4):297– 321.
6) Bailey A, et al. Autism as a strongly genetic disorder: evidence from a British twin study. Psychol Med. 1995;25(1):63– 77.
7) Steffenburg S, et al. A Twin Study of Autism in Denmark, Finland, Iceland, Norway, and Sweden. J Child Psychol Psychiatry. 1989;30(3):405– 16.
8) McDonald ME, Paul JF. Timing of increased autistic disorder cumulative incidence. Environ Sci Technol. 2010;44(6):2112-8.
9) Blaxill MF. What's going on? The question of time trends in autism. Public Health Rep. 2004;119(6):536-51.
10) Ritvo ER et al. Concordance for the syndrome of autism in 40 pairs of afflicted twins. Am J Psychiatry. 1985;142(1):74– 7.
11) Constantino JN, Todd RD. Autistic traits in the general population: a twin study. Arch Gen Psychiatry. 2003;60(5):524-30.
12) Taniai H et al. Influences on the broad spectrum of autism: study of proband-ascertained twins. Am J Med Genet B Neuropsychiatr Genet. 2008; 147B:844– 849.
13) Rosenberg RE et al. Characteristics and concordance of autism spectrum disorders among 277 twin pairs. Arch Pediatr Adolesc Med 2009;163:907–914.
14) Croen LA, Grether JK, Hallmayer J. A population based study of autism among twins in California. IMFAR, Orlando, FL, November 2002:69.
This might be late, but better than never. Just pointing to a wonderful documentary on this topic: "Finding The Words". It is available on "Youtube". t is about "Children Recovering from Autism". Just wonderful.
Posted by: riad awad | November 04, 2012 at 09:29 AM
To correct a misinterpretation here by many, the 'environment' in question is in utero (in the womb), not related to diet, vaccines, toxins or parental care, as is made clearer in better write ups and the original paper.
Studies on twins have shown that the lower birth weight twin 3 times more likely to be the autistic one in discordant pairs. This shows that in utero nutrients and oxygen supply is a fairly critical player in the development of ASD where there is the genetic potential for it in an embryo.
I quote from one twin study:
"for every 100 g increase in birth weight, a 2% decrease in severity of ASD"
"Twins lower in birth weight in ASD-discordant twin pairs (n=34) were more than three times more likely to meet criteria for ASD than heavier twins "
This write up is very misleading: you've lead people tp believe that they mean post birth environment, it did no such thing. Environmental condtions for twins in utero can be significantly different' leading to serious weight difference between them at birth and differeing levels of disability.
Posted by: Heretique | August 11, 2012 at 04:34 PM
Right on Jack,lower birthweight and lower gestational age
will increase the detrimental effects of vaccines.Autism is not genetic and Dr.Wakefield's name will be cleared in the near future.Please look up the study by Vijendra K.Singh,Ph.D. Autism,vaccines and immune reactions.
The truth will stand,only a question of time when all answers will be found.
Posted by: oneVoice | July 26, 2011 at 12:22 AM
I think it may be time for a new full-page ad in, say, USA Today, detailing the CATS study findings for the environment and maybe even some of the current politics. I think the timing may be right.
Posted by: Jen | July 19, 2011 at 11:46 PM
Finally! A "genetics" study that reinforces what my personal study has been showing me for 10 years - its more than genetics. I have identical boys - one ASD and one NT. All the experts try to tell me their not identical then - which I refute they shared one placenta!
It's also very true about multiples being early and smaller - my boys were vaccinated in the NICU - they told me I couldn't take them home until they were (at less than 5 pounds). I wish I had known my rights then! Kick myself everyday. Not to mention the lower immune systems. Oh and my sons 22 antibiotics in one year for ear and other infections - but he'll grow out of it!
I'm convinced that they genetic research is to just develop a marker for in utero - ask the down's syndrome people how that works of them (not!)
Posted by: Diane | July 18, 2011 at 02:49 PM
..."Parents should always do their own research and think for themselves."
Exactly, but more often than not, they don't.
Posted by: Bayareamom | July 16, 2011 at 07:56 PM
Jack, your statement "Twins in general could be at a higher risk because they are often premature and have low birth weight. Which effectively means they are getting a higher dose of vaccine components by weight and are getting that dose at an earlier stage of development than full term babies would be."
Thank you for a brilliant observation! And, it reinforces even greater the insanity of injected vaccine toxins at birth, 2 months, 4 months, 6 months, on and on.
Whereas, if vaccine toxins (everything in a vaccine is toxic) are injected later at 4 or 5 YEARS, instead of day of birth, and at 2 or 4 MONTHS per the Schedule below (please pull it up everybody, and pass it on).
I have for years deemed this Immunization Schedule to be "America's Weapon of Mass Self-Destruction."
http://www.cdc.gov/vaccines/recs/schedules/downloads/child/0-6yrs-schedule-pr.pdf
Posted by: david burd | July 16, 2011 at 05:32 PM
I forgot to mention in my previous comment that other factors that contribute to autism include a child being given multiple vaccines at one time (one doctor's office visit) or a child being vaccinated when the child is unwell--has a cold or fever or diarrhea, etc. (immune system already weakened). Of course, this is just common sense--but our medical system doesn't use common sense. One of the most inexcusable actions is when a child has previously had an adverse reaction to a vaccination, such as high fever or screaming for hours, and the doctor continues with the vaccination schedule, administering subsequent vaccinations which do further damage to the child.
Parents should always do their own research and think for themselves.
Posted by: VMV | July 16, 2011 at 04:17 PM
This is a valuable article--especially the paragraph about the identical twin boys adopted at birth by two different families--only one received vaccinations, and regressed into autism after his 15 month shots. My personal idea is that there MAY BE a genetic predisposition that makes it more likely for some children to become autistic after a vaccination--but the main cause or at least trigger, is without doubt, vaccination. Other possible factors could be whether a child is on antibiotics before or after vaccination or whether the child is given Tylenol (acetaminophen) to reduce fever after a vaccination, especially after the MMR shot. I have read that there was a study of children that showed that children given Tylenol after an MMR shot were more likely to develop autism. Many mothers today give their child Tylenol at the first sign of a fever--they are under the belief that it's something harmless. They are even told by doctors to give Tylenol for a fever. However, a fever is the body's way of fighting disease. It's a different story if it's an extremely high fever--I'm talking about fevers that are not dangerously high.
Posted by: VMV | July 16, 2011 at 04:06 PM
J, Any danger of a real name? I would use it if there was no danger to me.
And perhaps you can logically explain the basis of your sarcasm? You say:
"Knowing the genetics of autism is the same as knowing the blueprints of a building"
Sorry Dave, it was not meant as sarcasm and I can logically explain that I did not see in advance that it would be taken as sarcasm. I have asperger's and we often seem sarcastic when we are not meaning it that way.
Nor was I claiming anything about the completeness of someone or other's knowledge of the genetics of autism. I was making an analogy.
My point is, which you seemed to have missed: "I am autistic and I want safe legal access to my medicine, what has the cause of autism got to do with getting access to treatment?"
Sure, if there was no treatment, then knowing the cause might help find the right treatment but seeing as I already have the right treatment, I'd like to see that $100 million spent on getting FDA Approval for my medicine.
Then when we have our medicine, we can help you to find the cause. Not the other way round, thank you.
Posted by: J | July 16, 2011 at 01:49 PM
No one will ever convince me that anybody ever really believed that autism was genetic. It was clearly a ruse to continue the agenda.
I'm currently reading a book about thalidomide and pharma's tactics have not changed a bit. Pharma distracted away from thalidomide by blaming food additives, tv, a virus, detergents, etc. Sounds familiar. They even went so far as to say the deformities caused by thalidomide were caused by the mothers botched attempts at trying to abort their babies. I don't think they tried this yet with autism, but they probably will. Or even more grotesque, pharma claimed that thalidomide saved deformed babies from being miscarried. Sounds familiar, too - Why it was all over the radio a few months ago that autism was the result of heroic efforts in the NICU and vaccines keeping kids who would have died from dying. Thimerosal SAVES kids not brain damages them. Same playbook different drug. Yuck.
Posted by: Nothing changes | July 16, 2011 at 10:33 AM
I'm waiting.. Waiting for Nancy Snyderman Matt Lauer and the Today show to discuss this important news. Or what about Sanjay Gupta or Anderson Cooper? I'm pretty sure Paul Offit won't be bringing it up and Orac is busy talking about anything other than this. Bullshit! (you can edit out that word of you want).
Posted by: Jen | July 16, 2011 at 10:29 AM
Twins in general could be at a higher risk because they are often premature and have low birth weight. Which effectively means they are getting a higher dose of vaccine components by weight and are getting that dose at an earlier stage of development than full term babies would be.
Posted by: Jack | July 16, 2011 at 07:11 AM
All those who have been "handling" the research results for the last decade belong in prison.
"But there is now the point at which the research results have to be handled, and even if this committee decides that there is no association and that information gets out, the work has been done and through the freedom of information that will be taken by others and will be used in other ways beyond the control of this group. And I am very concerned about that as I suspect that it is already too late to do anything regardless of any professional body and what they say…My mandate as I sit here in this group is to make sure at the end of the day that 100,000,000 are immunized with DTP, Hepatitis B and if possible Hib, this year, next year and for many years to come, and that will have to be with thimerosal containing vaccines unless a miracle occurs and an alternative is found quickly and is tried and found to be safe."
- Dr. John Clements, World Health Organization, Simpsonwood, GA, June 7, 2000
Posted by: Kevin Barry | July 16, 2011 at 01:48 AM
I remember reading research that found a higher risk of autism for twins that in the general population. I'm curious, if there are factors related to being a multiple birth sibling that increase autism risk, if that increased risk among twins might also be falsely attributed to genetics in some of the research?
Posted by: Jeannette Bishop | July 16, 2011 at 01:17 AM
Wow--absolutely loved the content presented in this article. I have a now 4 year-old son who was diagnosed with autism at age 2. Jen and J really hit it on the nail. During labor with my son they gave me Pitocin even though I wasn't overdue (they just wanted to hurry the labor and I agreed I wanted to be out of the pain and I thought it was safe). The nurses really stressed me out when they said I wasn't getting enough oxygen which meant the baby too. Also, when my son was 2 weeks old he choked on his bottle and stopped breathing. As for the vaccine issue, yes we noticed a huge regression the day after his shots (and they were given late at 2 years instead of 18 months). So yet another story supporting some views here. Oh and I just wanted to add that you never heard of as many cases of what might have been autism in the 1950s and so on, so how can the "experts" really say it's almost totally genes when we parents know it's a combination of factors? Sometimes I think some docs get their training and degrees out of a cracker jack box and I just can't understand why they don't have common sense like we do? They rely on the AAP for answers and it is sad because so many children are falling through the cracks as we speak....
Posted by: Kristen | July 16, 2011 at 12:47 AM
This article is superb.Lot of issues came up also.The twin studies have very small numbers to be truly useful.The issue
also that more twins do not get to 37 weeks gestation (full
term)most of them delivered preterm at 34-36 weeks at a less
developed stage.Number two, present delivery managements are very agressive and fast and do not allow for delayed clamping which means the fetal blood stays in the placenta,
rather than move to the newborn and help to make sure that the newborn has satisfactory blood volume,oxygenation and also more stem cells to allow for the "wiring" of the developing brain to complete itself specially in the first year of life.Then comes the HepB vaccine and the (male) circumcision to complete the abuse on the newborn who just delivered.The problem with the experts,they do not listen to the parents.Yes,they are feeding a hungry lie.
Posted by: oneVoice | July 16, 2011 at 12:23 AM
What an interesting study. My triplets...all with autism...are made up of two identical, and one singleton.
Posted by: Betsy | July 15, 2011 at 10:00 PM
I have identical twins. No doubt if someone throws a brick that hits them in the head they both bleed. I'm sure genetics plays a role in how fast their blood clots and I suspect they'd require an equal number of stitches.
Still, I'm pretty mad at the kid that threw the brick and think that maybe I should try make sure no one else throws a brick at my kids' heads.
Posted by: Jack | July 15, 2011 at 10:00 PM
Superb - thank you Mark.
Something I have often wondered - how many parents or grandparents of those 37% apparently inherited autism cases, had in their lifetimes suffered some toxic insult, giving rise to genetic aberrations which could then be passed down?
Posted by: Seonaid | July 15, 2011 at 06:33 PM
My kids went from non-intelligle speech, ignoring everyone, etc. to regular school. It's very treatable. (Of course it also takes a lot of time and money.) I am very upset that anyone over 40 would ever think that autism or ADHD was mostly genetic because they were there when no one had it. They went to school when the kids sat quietly in their seats. They are choosing not to remember.
Posted by: Heidi N | July 15, 2011 at 06:14 PM
Thank you for another very helpful analysis. I'm preoccupied by your closing quote! I'm not sure I can count all the elements of "consensus" that have allowed, facilitated, or caused the injuries in our children: vaccines are safe, of course they are, they are the most thoroughly studied pharmaceutical in use, the benefits vastly outweigh the risks, autism is the result of homicidal parenting, no wait it is actually bad genes, thimerosal is safe--we've been using it for decades, amalgam is safe--we've been using it for centuries, ethylmercury must be at least as "safe" as methylmercury, it's a bigger molecule, oh and we've reduced the amount of antigen in vaccines by the use of more adjuvant, less germs=safer vaccines...
Then there are consensus elements that hinder access to recovery for our children, some of them are the same as above, such as autism is genetic..., but others revolve around a general preference for using pharmaceuticals over other therapies, or viewing autism as a static neurological condition, present at birth...
Similar elements of consensus seem to negatively influence the understanding, healing, and prevention of other conditions, many of which our children also bear. I'm hoping all such will soon fall away together.
Posted by: Jeannette Bishop | July 15, 2011 at 05:50 PM
J, Any danger of a real name? And perhaps you can logically explain the basis of your sarcasm? You say:
"Knowing the genetics of autism is the same as knowing the blueprints of a building"
Well, actually nobody has actually shown any genuine blueprint of the "genetics of autism" as something you surmise has already truly proven. But of course these genetic conjectures and hypotheses elicit $100's of Million for study from our tax dollars. Are you someone who has been receiving a bit of this largesse?
David Burd
Posted by: david burd | July 15, 2011 at 05:48 PM
Excellent article, thank you!
Posted by: Natasa | July 15, 2011 at 05:17 PM
Great job Mark!
I always know that when you do an article it will be wonderful!
Keep the bad guys on the run!
Posted by: Kent Heckenlively | July 15, 2011 at 05:12 PM
Well now that the largest, most rigorous study has shown environment to be in fact more important than genes, I expect this new, updated and incredibly important information to start appearing STAT in anything published (CDC info, web MD, wikipedia, DSM's etc.) Oh, but they'll try and drag their heels, especially if it's anything owned by the Murdochs.
Posted by: Jen | July 15, 2011 at 04:59 PM
Mark, thanks as always for your eloquent outrage. The Folstein & Rutter paper does provide case reports, which are more informative than their conclusion that autism must be genetic. In every case, the twin that developed autism suffered serious compromise at birth.
The great worry about a difficult birth is oxygen insufficiency. The effects of oxygen deficiency should be well known. Nuclei in the brainstem auditory pathway are susceptible to injury. This is because blood flow and metabolism are higher in nuclei of the auditory pathway than in any other area of the brain.
Toxic substances can also injure the auditory system, or add insult to injury from anoxia. It is common practice now to clamp the umbilical cord right at birth, then resuscitate the baby if necessary; then they add toxic substances via vitamin K and hep B injections.
We need something like the National Transportation Safety Board (NTSB) to investigate what is causing the increase in autism.
Posted by: Eileen Nicole Simon | July 15, 2011 at 03:50 PM
Hi
Knowing the genetics of autism is the same as knowing the blueprints of a building. It does not tell us why or how the building got there but it does make it a lot more easy to repair or treat the building
Anyway, cause of autism can wait. I wanted to know what are AoA's thoughts and position of cannabis therapy for autism please?
Thanks
J
Posted by: J | July 15, 2011 at 01:37 PM
I went to the hospital yesterday to visit my niece (we are only 4 yrs' apart in age) and her new baby, her third. I saw him at age 18 hours! Beautiful ,beautiful boy, nursed well, content. Today, after receiving his hepb last night and circumcision, he is screaming, taking paniclike attacks at the breast with difficulty latching on, and runnning a temperature of 100.8. Obviously my suggestion yesterday that he skip hapb fell on deaf ears. If something turns up wrong, will everyone agree, "he was born like that".
Posted by: barbaraj | July 15, 2011 at 12:44 PM
Excellent analysis Mark!
Get ready for the 80,000 ways the search for environmental factors will be derailed.
A new group of researchers are ready to line their pockets while promising the NIH not to rock the boat. The autism community will need to push hard for research looking at the obvious culprits.
The sad thing is that the mothers of today are already in worse shape (more autoimmune diseases, increased drug use during pregnancy, etc.) and it will take fewer and fewer triggers to push future generation of kids over the edge.
Posted by: Cassandra | July 15, 2011 at 11:37 AM
Superb Mark, you are fantastic. I read and like everything from you and I really feel you are pushing the right buttons.
The truth will out.
Posted by: Goran | July 15, 2011 at 11:01 AM
Thanks, Mark, for bringing clarity and perspective to this issue. I can see the forest. Next question: now that the heritibility claim has been credibly challenged, what is the likely effect on autism policy, research funding, and better treatments for our children?
Is it time to break out the champagne?
Posted by: Dan E. Burns - SavingBenBook.com | July 15, 2011 at 11:00 AM
Another possibility is that the genetic role has diminished during the epidemic.
Posted by: GH | July 15, 2011 at 09:53 AM
""'The study design explicitly excluded the possibility of an environmental effect being mediated by genetic vulnerability in a subset of children.""""
Now does this mean that the continued statement I have heard for the past two decades is not true either?
The statement goes something like this:
"Vaccines is not the cause of autism, that not to say, however, that there is a small subset of children who may be particularly vulnerable to vaccines."
SOOOOOOO My family is not a small subset???
I knew it, I knew it, I knew it!
It is more like the sermon given by a German Pastor;
First they came for the communists,
and I didn't speak out because I wasn't a communist.
Then they came for the trade unionists,
and I didn't speak out because I wasn't a trade unionist.
Then they came for the Jews,
and I didn't speak out because I wasn't a Jew.
Then they came for me
and there was no one left to speak out for me.
1983 They came for my duaghter, she had Kawasakis but that was a disease that was common for Japaneses so my aunt by marriage said she guessed my husband had some foreign blood in him. Meanwhile her young six year old duaghter had rheumtoid Artheritis. I bet they came for her too she just did not know it.
Posted by: Benedetta | July 15, 2011 at 08:22 AM
Excellent critique Mark!
When the mainstream media broadcast and printed stories about the CATS Study I distinctly recall their stories reinforced the orthodoxy view that inherited genes were far more responsible than environmental factors -- thus yet another example of the media being in the pocket of Pharma and Fauci.
The fact that Big Pharma pays the media $75 Billion a year for "direct to public" advertising has long completely corrupted any honest reporting.
Posted by: david burd | July 15, 2011 at 07:56 AM