This is a bombshell! Autism genetic causation with millions of dollars
invested in this wrong direction is all but dead when the world reads the
attached in-depth report.
Of course, erroneous ideas hang around in medicine for years, as there is
so much money involved in sticking with out-moded concepts. This destroys
the "expert" standing of so many autism so-called experts so do not expect
overnight acceptance of the environment causation, which to anyone not
involved in genetic research will find is clearly the logical explanation for
not just autism but the fact that in USA one in four in school today are on
drug therapy for some condition, diebetes, asthma, mental issues including
depression adhd, obsessive compulsive and so on.
This latest large study moves the pendulum away from genetic causation
back to environment!! This study is carefully reported here in all detail so
if you are involved in autism please read the attached in its entirety, as
there are important details you will want to express accurately if you are
advising patients or teaching.
I have always known that what Andrew Wakefield reported on, see his
website and book Callous Disregard, had merit (IE MMR triggered autism in what
had seemed to be normal children up until then). I have dealt with many of
these families and attended numerous conferences
However, things are not always simple A + B = C and Thiomersal may not be
acting alone and there are these Epigenetic issues we know are happening
when substances like Bisphenol A impair methylation, as Randy Jirtle at Duke
has documented in Agouti mice. Then the issue becomes one of what are the
contributing environmental toxins and they may well vary from case to case.
Then when you try to study which nutrient deficiencies are contributing to
the autism spectrum, you have issue including D, Magnesium etc and now
issues around the need for methylation support in order to better handle the
load of toxins found in every child's cord blood (see Ten Americans at
www.ewg.org).
Then the bomb shell of cerebral folate deficiency now reported in NEJM
last week where we find that some antigen is blocking the folate receptors in
brain and the only hint of nutrient deficiency was documented only in
cerebral spinal fluid. Now we have many potential culprits for this new
autoimmune disease of the folate receptor - milk protein or whatever you want to
implicate to help explain why the folate receptor in brain are blocked and
cannot take up folic acid unless in the form of Folinic acid or 5'MTHF and
apparently needed by some in significant orthomolecular levels.
Now we have the time line of events and a turning point in the disease was
1988, which we now find is when vaccine manufacturers turned away from egg
and incorporated aborted fetal tissue for vaccine production.
WILL someone ever make sense of all this so that we can stop this
epidemic?
I vote for anyone wanting a healthy baby to start a one or two year
aggressive detox program for prospective mom and dad along the lines I advocate
with oral chelation including my Power Drink with ZeoGold added along with
regular exercise and some sauna exposure to enhance sweating, as a minimum.
Then hopefully start a boycott of all vaccines made on aborted fetal
tissue that includes 24 of them today. That would be nice but since that in some
countries is met with jail terms and a gun pointed at the prospective
recipient of the vaccine, maybe we have to settle for now with trying to
decrease the number of adverse outcomes by at minimum using aggressive Vitamin C
based oral program. That means using a minimum of one gram per 10# of
weight or roughly for year of age, as one program to try to diminish the clear
risk I see in associated with current vaccine use in a world population whose
immune system is compromised from birth with over 220 known toxins
including an average of over 1000 times more lead in tissues than was present 700
years ago (see Cal Tech, Clair Patterson).
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
http://www.ageofautism.com/2011/07/new-autism-twin-study-demolishes-decades-
long-belief-in-genetic-causation.html
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."
References
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