Reviewer reports from
Neurotoxicology journal, with author’s replies
Ref.: Ms. No. NEUTOX-D-13-00253
Robin P Clarke
Autism, adult disability, and 'workshy': Major epidemics being caused
by non-gamma-2 dental amalgams
Reviewer #1:
1. The Abstract is misleading
as to what information this manuscript provides, stating that, "This is
the first-ever study of health consequences of non-gamma‑2." This is not a
"study," as usually defined, as no measurements of non‑gamma-2 were
made, nor were any health consequences assessed except population-level
statistics about prevalence of disability.
Three baseless pseudo-points in
one sentence there – I will chop it up for my replies.
>no measurements of
non-gamma-2 were made,
As my review stated, indeed,
no-one has ever bothered to keep records of the usage or prevalence of
non-gamma-2. Even my own dental
hospital records never recorded the different amalgam types (and I am aware
that I started off with the earlier crumbling “conventional” types and later
had the extremely durable non-gamma-2’s).
That lack of data is not a fault
of this work but rather a scandalous offence by those authorities who didn’t
bother to even keep records. However, a
confident inference can still be made that the overall amount of non-gamma-2 in
people’s mouths would have progressively increased as more and more of their
teeth were fitted with the new materials.
This review thus provides the absolute best quantitative information
currently (and almost certainly ever) available.
>nor were any health
consequences assessed except population-level statistics about prevalence of
disability.
Again, that lack of data is not
a fault of this work but rather a scandalous offence by those authorities who
didn’t bother to even seek reports on possible adverse events from amalgam, but
instead implemented the cover-up measures documented in the paper. Which means those population-level
statistics are about as good as it can get.
It does not follow that they are worthless, else quite a number of other
“not-really-studies” in very prestigious journals would also have to be
dismissed.
>This is not a "study", as usually defined,
as no measurements of non-gamma-2 were made, nor were any health consequences
assessed except population-level statistics about prevalence of disability.
Really? In that case there are numerous other papers
which were “not really a study”, despite being published in the most
prestigious journals and highly promoted as indeed being important “studies”. Their authors likewise didn’t do any
measurements or diagnoses but instead presented existing data as I have. These include for instance:
o
JAMA. 2003 Oct 1;290(13):1763-6. Association
between thimerosal-containing vaccine and autism. Hviid A, Stellfeld M,
Wohlfahrt J, Melbye M.
o
Pediatrics. 2003 Nov;112(5):1039-48. Safety of
thimerosal-containing vaccines: a two-phased study of computerized
health maintenance organization databases. Verstraeten T, Davis RL, DeStefano
F, Lieu TA, Rhodes PH, Black SB, Shinefield H, Chen RT; Vaccine Safety Datalink
Team.
o
N Engl J Med. 2002 Nov 7;347(19):1477-82. A
population-based study of measles, mumps, and rubella vaccination and
autism. Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, Thorsen P,
Olsen J, Melbye M.
o
Pediatrics. 2003 Sep;112(3 Pt
1):604-6.Thimerosal and the occurrence of autism: negative ecological evidence
from Danish population-based data. Madsen KM, Lauritsen MB, Pedersen CB,
Thorsen P, Plesner AM, Andersen PH, Mortensen PB.
o
J Child Psychol Psychiatry. 2005 Jun;46(6):572-9.
No effect of MMR withdrawal on the incidence of autism: a total population study.
Honda H, Shimizu Y, Rutter M.
o
Pediatrics. 2004 Sep;114(3):584-91. Thimerosal
exposure in infants and developmental disorders: a retrospective cohort study
in the United kingdom does not support a causal association. Andrews N, Miller
E, Grant A, Stowe J, Osborne V, Taylor B.
o
Pediatrics. 2006 Jul;118(1):e139-50. Pervasive
developmental disorders in Montreal, Quebec, Canada: prevalence and links with
immunizations. Fombonne E, Zakarian R, Bennett A, Meng L, McLean-Heywood D.
No-one has ever proposed that
any of those were not really studies.
And that’s just a few I’ve come up with this minute. A more reasonable consideration of the
matter is as follows. Journals categorise
papers as either “reviews”, or “studies”, or something else such as
commentaries. But that categorisation
is rather crude, like categorising people as either “black” or “white”. In reality there is a fudging between two
notional ideal types, namely “proper reviews”, of which the input data consists
entirely of pre-existing published studies (of for instance whether walking
causes autism), and “proper studies”, in which the investigators do some
measuring either in a laboratory or out in the wider world. Those seven famous papers listed above fit
into neither of those ideal categories, just like this present one. But so what. There has never before been ANY scientific paper about the health
consequences of non-gamma-2 amalgams.
And no-one has ever compiled any measurements into a published
study. It follows that it cannot be
either of those ideal types, but it does not follow that it cannot be an
excellent scientific paper any more than those seven above are not. In reality it is properly described as both
the first ever study of the known data, and as the first ever review of the
evidence.
2. P.4: Evidence needs to be provided for the
statement that “...Hal Huggings and other dentists were struck off the register
of practitioners.” for issuing warnings about the amount of mercury released
from non-gamma-2 amalgams.
Firstly, that point is far from
a key foundation for any conclusions of this review. I doubt whether it warrants taking up additional space on
documentation merely on the basis that some people might wish to not believe
it. Secondly here are some evidential
details of the matter which I have quickly dragged from the web:
Hal Huggins de-licenced for
challenging amalgam:
“Judges
Block Dental Board Gagging Dentists Who Discuss Risks of Mercury Fillings” http://www.cdchealth.com/judgeblocks.html
“CALIFORNIA'S COMPLIANCE WITH DENTAL AMALGAM DISCLOSURE POLICIES” “the American Dental Association has a gag rule--yes, a gag rule telling dentists not to give warnings about the toxic effects mercury might have”
http://www.gpo.gov/fdsys/pkg/CHRG-108hhrg93640/html/CHRG-108hhrg93640.htm
Details of several more dentists
struck off, and it only takes a handful to scare all the rest into never
telling their victims that “silver” fillings are actually mainly mercury:
3. P.5: The statement that, "Consequently, declining
rates of amalgam installation would conceal an increase of prevalence of the
amalgams in patients' mouths" is a non-sequitur. If fewer amalgams
are being placed, how could their prevalence increase? It might mean that this
trend would conceal an ongoing release of mercury vapor in the mouths of
individuals with such amalgams, but not the number of individuals with them.
Dear Reader, please go to your
kitchen sink, put the plug in firmly and water-tight, and then turn on the tap
to flow fairly fast, till an inch or two of water accumulates. Then turn the tap down so there’s only a
little more coming out per second. And
now you can see that the water level in the sink stops rising but instead
quickly goes down, as it must because the rate of additional input of the water
has decreased, so obviously the total amount in the sink must decrease
correspondingly. Or at least that is
presumably what happens in the kitchen of someone with enough scientific
expertise to judge such things.
For the educationally-deprived
among us I’ll go through that paragraph again, with tutorial hints added:
Dear Reader, please go to your
kitchen sink [analogous to patients’ mouths], put the plug in firmly and
water-tight [analogous to the fact that non-gamma-2s stay in those mouths for
whole lifetimes], and then turn on the tap [analogous to dentists installing
non-gamma-2s] to flow fairly fast, till an inch or two of water
accumulates. Then turn the tap down so
there’s only a little more coming out per second [analogous to “declining rates
of amalgam installation”]. And now you
can see that the water level [analogous to the prevalence of the amalgams in
the mouths] in the sink stops rising [contrary to silly me’s expectations] but
instead quickly goes DOWN [well, highly-qualified expert Reviewer #1 apparently
thinks so, so there], as it must because the rate of additional input of the
water has decreased, so [“]obviously[”] the total amount in the sink must
decrease correspondingly. Or at least
that is presumably what happens in the kitchen of someone with enough
scientific expertise to judge such things.
I did emphasise in my review
that the whole point of non-gamma-2 was that they are far more durable
(indeed can easily last a whole lifetime).
Just like that water which doesn’t suddenly start to rush out of the
sink just because you turned the tap down.
4. P.5: The author states
that information is not available on "usage or total prevalence of
non-gamma-2 in people's mouths." Given this, any statements made about the
health consequences must remain purely conjecture.
Firstly Reviewer #1 here
misrepresents what I wrote. I did not
state that “information is not available…”.
My words were:
“I
have been unable to obtain any numerical data on usage or total prevalence of
non-gamma-2 in people’s mouths. The DH
have told me they have no such records.
And NHS dental records have not recorded the types of amalgam used. It is unlikely that any better information
is available in other countries. But we
can very reasonably assume that the overall prevalence of non-gamma-2 will have
gradually, progressively increased in the decades following its introduction.”
And you can see there that I had
already pre-answered this half-baked objection. It is in the nature of reality that the prevalence of something must
inevitably increase for some period after its introduction as the new standard
product. And it is common knowledge
that people usually have their further tooth fillings put in in dribs and drabs
over the years so their prevalence will correspondingly increase over a period
of years rather than of minutes or millenia.
Which is very much in line with those increase curves of autism, adult
disability, and later age of onset, which also occur over years following the
change to non-gamma-2.
.
5. P.6: The author states that he or she did not
"cherry-pick.. selected data to prove any point," yet that is done in
the last paragraph on this page, when reviews supporting the hypothesis that
mercury is etiologically involved in autism are cited, but reviews that
conclude that it is not are not cited.
But again, Reviewer #1’s
assertions are multiply untrue.
Firstly, reviews are not data.
Secondly, in that very section supposedly at fault here, I did
indeed explicitly cite the entire (supposed) counter-data, namely the three
studies which have been claimed to disprove the mercury-autism link, namely Ip
et al, Soden et al, and Hertz-Picciotto et al.
So that instance asserted by Reviewer #1 shows the exact opposite of what
Reviewer #1 asserts. And thirdly, my statement
about not cherry-picking was only in my section headed “My epidemiological
investigations”, and specifically a comment about my own presentation of data
of the time-trends of autism, adult disability, and amalgams. What great contrary data have I omitted
there? In reality there has been not
the slighest cherry-picking and this is merely yet more nonsense from this
so-called peer reviewer.
6. P.7: The fact that mercury excretion is increased
following administration of DMSA in individuals with autism does not prove
much, as the action of DMSA is nonspecific. Excretion of other metals (lead,
antimony) is also increased.
Yet more cheap muddle from
Reviewer #1. The finding in Bradstreet
et al was not “The fact that mercury excretion is increased following
administration of DMSA in individuals with autism”. Rather it was the finding of a major difference between
autistics and non-autistics, with the autistics outputting three times as much
mercury as the non-autistics (with fluke probability of 1 in 5000). AS
ALREADY CLEARLY STATED RIGHT THERE.
Did this faceless reviewer cheat to get their PhD too?
7. P.7: The conclusions of the Holmes et al. (2003) study
are weak, not because of whatever biases the investigators might or might not
have but because the findings are not credible. In this study, the mean mercury
level in the hair of controls was 3.63 ppm, which is much higher than would be
expected in a representative sample of infants. By comparison,
measurements of mercury in children's hair in an NHANES survey conducted about
the same time (1999-2000) (McDowell et al., Environ Health Perspect
2004;112(11):1165-1171) reported a mean of 0.12 ppm (and 0.16 among
fish-consuming children). This suggests that the controls included in the
Holmes et al. study were biased with regard to their mercury status and that an
8-fold reduction reported in the hair mercury level of "autistic
cases" is likely an artifact.
Here Reviewer #1 shows a bit
less incompetence, and stumbles only in terms of a rather more subtle
fallacy. We could call it “the fallacy
of the assumed all other things being equal”.
A good other example of it is found in various comments about the
Hallmayer et al 2011 twin study finding of autism being mainly
environmental. Commenters on Hallmayer
et al have concluded that it shows that the earlier twin studies were
“wrong”. But well, they “must be wrong”
mustn’t they?, because Hallmayer et al is a big powerful new study and so it
must trump those little old ones into the wastebin of “wrong” results.
The
fallacy here is the unfounded assumption that all other things are equal
(constant). In respect of those twin
studies, please have a look at my still-unchallenged paper “A theory of
general impairment of gene-expression manifesting as autism”, which appeared in
print in 1993 and is still essential reading for anyone who wants to have a
clue about the subject. Therein I
specified the conditions under which autism would change from a mainly genetic
condition to mainly environmental: “If a rare perinatal
adversity were to become somewhat more common, then obviously, autism of the
environmental category would become more prevalent.” And now with the huge impact of
non-gamma-2 in parents’ and carers’ mouths, exactly such a condition has indeed
occurred, and so hardly surprisingly the causation of autism has indeed CHANGED
from mainly genetic to mainly environmental.
There is no real conflict between Hallmayer and the earlier twin
studies, merely differences of the underlying and unexamined variables. Likewise, in respect of mercury and autism
we know that there is a lot we do not know.
You can see in my own review section there how the various studies of
autistic hair give divergent results and that there is nevertheless good reason
to find them all valid and true.
Likewise, to dismiss the Holmes et al result as “not credible” just
because of those non-standard levels entails an unwarranted gross presumption
that there are no important unknowns going on between the different
studies. And so the finding of Holmes
et al should not be dismissed unless there is a more substantial basis for
doing so. And on the contrary, later
studies have supported their ‘perverse’ data of lower hair mercury levels in
autism. This Reviewer #1 is here categorising
the careful work of Holmes et al as {either grossly incompetent or grossly
fraudulent}, on a basis of no real evidence but merely because he/she does not
find their results in accordance with the required
commercially/professionally-convenient dogma.
> I don't think it is appropriate to state that a
pattern of findings provides any evidence as to whether an investigator was
"acting competently and honestly."
Whereas I do think it
appropriate. And that is because
fraudsters or incompetents are extremely unlikely to come out with a whopping
strong result that is:
(1) markedly contrary to what
they would have expected;
(2) markedly contrary to what
they would have found convenient to report; and
(3) only subsequently supported
by the collection of results of later other-people’s studies of autistic
hair mercury.
And in the context that many
have presumed to shallowly discredit Holmes et al as either incompetent or
fraudulent (as Reviewer #1 here does him/herself), that consideration is
outstandingly eminently appropriate to be stated.
8. P.7: The author multiplies
the P-values from 6 studies to calculate the probability that the findings are
due to chance. This is a meaningless calculation. First, the studies included
reached different conclusions about the hair mercury levels of children with
and without autism (although the author argues that age needs to be taken into
account). Second, given that all P-values are less than 1, multiplying them
necessarily results in a smaller and smaller number the more studies one
includes. If each of the 6 studies yielded a P-value of 0.5 (indicating
no statistically significant relationship), then using the author's method, the
combined P-value would be 0.0156, which would suggest that, in aggregate, the
studies provide significant evidence of an association. Third, even if the
author's method was valid, it would be necessary to include in the calculation
all of the studies ever conducted of a particular hypothesis, not just those
selected because they purport to show an association (just as it is necessary,
in a meta-analysis, to include all available evidence).
(It is absolutely standard
probability maths to multiply together probabilities to get the compound
probability of them all happening merely by fluke, as any betting shop can
confirm, but we must continue here with Reviewer #1’s further exposition on
this point…...)
>Firstly, the studies
included reached different conclusions about the hair mercury levels of
children with and without autism (although the author argues that age needs to
be taken into account).
This misrepresents the
situation. I don’t “argue” that age
needs to be taken into account, rather I observe that age needs to be
taken into account, in that the earlier ages always give lower mercury in
autistics, while the later ages always give higher mercury. Thus none of those studies are in any
conflict with the reasonable hypothesis mentioned by Majewska et al that the
adrenarche plays a role in the hair mercury levels. There is therefore not any real conflict between these studies
but rather voices declaring in common that mercury is involved in autism in
some way. (And Reviewer #1 is here
again employing that fallacy of the presumed all other things being equal – age
in this case.) And so there is no valid
ground there for not multiplying together those probabilities.
>Secondly, given that all
P-values are less than 1, multiplying them necessarily results in a smaller and
smaller number the more studies one includes.
That is of course true. [Note
for non-expert readers: smaller P-values indicate the results are less likely
to be mere flukes and so are more “significant”.]
>If each of the 6 studies
yielded a P-value of 0.5 (indicating no statistically significant
relationship), then using the author's method, the combined P-value would be
0.0156, which would suggest that, in aggregate, the studies provide significant
evidence of an association.
And that is also indeed
true. But so what. It is indeed the reality that several bits
of weak evidence can add up to strong evidence. Indeed that is the whole point of making a (for instance
clinical) study large enough to give a significant result. Any such study can be conceived of as being
a combining together of lots of smaller sub-studies, any one of which could
give non-significant results, but when all put together would enable a highly
significant result. And that high
significance is not some specious false result, rather it is the entirely sound
statistical inference. And that’s what
I’ve done there, except that my p values were all highly significant
already. And the fact that the
evidence there is of diverse types adds all the more to its methodological
robustness, as it is not wholly founded on any one premise.
>Thirdly, even if the
author's method were valid, it would be necessary to include in the calculation
all of the studies ever conducted of a particular hypothesis, not just those
selected because they purport to show an association (just as it is necessary,
in a meta-analysis, to include all available evidence).
Again, not so. Firstly, there IS no contrary evidence on
the mercury-autism question such as could make any meaningful reduction of my
combined calculation. I’ve pointed out that
even the three supposedly counter results were actually pro in reality. Secondly, I made the point that that is the
probability only from those few studies combined. It logically follows that if there were more studies, and
continuing on the same 100% positive connection trend, then that would simply make
my big fluke number even bigger (smaller).
So there is still no sound objection to my probability calculation.
9. P.8: The argument about the evidentiary value of never
having seen the Queen is a little ridiculous and, in my view, has things
completely backwards. It is by means of the falsification of hypotheses that
science advances. A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias (all it takes is the observation of one black swan to refute the
statement that, "all swans are white"), but no number of positive
observations is sufficient to demonstrate the universality of a statement.
Again I will need to chop this
up for my replies.
>9. P.8: The argument about the evidentiary value of
never having seen the Queen is a little ridiculous and, in my view, has things
completely backwards.
As we’ll see in the next
few lines…(?)
.
>It is by means of the falsification of hypotheses that science
advances.
Partly so, but also there cannot be any advance at
all if hypotheses are prevented from being properly raised in the first place.
And Reviewer #1 is doing a great job of preventing some very important
hypotheses being raised, via these unflattering would-be-critiques right here.
>A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias (all it takes is the observation of one black swan to refute the
statement that, "all swans are white"), but no number of positive
observations is sufficient to demonstrate the universality of a statement.
Reviewer #1 here uses
some extremely incompetent language to confuse the matter. Namely the notion of a “negative
result”. For example an investigation
of whether or not the Queen actually exists could come up with two very
different types of results, both of which Reviewer #1 would have us class as
“negative results”. On the one hand,
there could be a failure to see the Queen on peeping over the palace wall; on
the other hand there could be a finding of the absence of the Queen anywhere in
the UK following an insanely.detailed mega-search from South to North and
back. The difference between a
“negative” failure to find something and a (positive) finding that that
something is actually absent, is complete and absolute, and not to be confused
by conflating into a false notion of “negative results”.
>A single negative result is enough to call into
question a positive result that has repeatedly been observed and might be the
result of bias
I shall here now correct
Reviewer #1’s grossly incompetent language.
“A single FINDING OF
POSITIVELY CONTRARY evidence is enough to call into question THE UNIVERSALITY
OF [an earlier] result that has repeatedly been observed and might be the
result of bias.”
“A billion mere
FAILURE-TO-FIND results CAN BE STILL NOT enough to call into question [an
earlier] result that has repeatedly been observed and might be the result of
bias.”
When I used the words
”negative results” it was self-evident from the context that I could only mean
the latter, more common meaning of the term, and not the “positively contrary”
meaning. But Reviewer #1 still managed
to muddle it as ever.
>a little ridiculous and, in my view, has things
completely backwards.
Indeed.
10. P.8: The discussion of
the validity of the three studies sometimes described as refuting an
autism-mercury link requires fleshing out. It is necessary to tell the
reader the arithmetic error Ip et al. made and to demonstrate the extent to
which it altered the study conclusions. The reader is told that DeSoto and
Hitlan (2010) concluded that Soden's study "actually proved the
opposite," but no information is provided that would enable the reader to
evaluate this statement. The conclusions of Hertz-Piccioto et al. are
misstated. The second-to-last sentence of this paper actually states,
"This report did not address the role of prenatal or early-life Hg
exposure in the etiology of autism." The major finding was that
total Hg in blood was not elevated or reduced in preschool children with
autism/ASD compared with unaffected controls and resembled those of a
nationally representative sample. The reason for the authors'
qualification is that only concurrent measures of blood Hg were available,
meaning that they could draw no conclusions from their data about the role of
prenatal or early-life mercury exposure. To say that the authors
concluded that their data, ".constituted no evidence whatsoever against
causation of autism by mercury" is simply wrong.
Again, I need to chop this up
for my replies.
>10. P.8: The discussion of the validity of the three
studies sometimes described as refuting an autism-mercury link requires
fleshing out.
….because…..
>It is necessary to tell the reader the arithmetic
error Ip et al. made and to demonstrate the extent to which it altered the
study conclusions.
Really? I cited the conclusion of DeSoto and Hitlan
(2010) that the study actually proved the opposite. (Ip et al was retracted due to their major but elementary
error.) On this question this reviewer
should either explain why D&H were wrong or else shut up. Here’s what they said:
>The reader is told that DeSoto and Hitlan (2010)
concluded that Soden's study "actually proved the opposite," but no
information is provided that would enable the reader to evaluate this
statement.
Not so. I provided the citation of D&H along
with the citation of the original Soden, which is all the information that is
needed for that evaluation. If Reviewer
#1 reckons there is something wrong with D&H’s conclusions then he/she
should state what it is, or else shut up.
Here’s what D&H said:
“In
the end, the statistical test conducted by Soden and coworkers is meaningless
and distracting from the essentials of what was done. The authors measured
metal levels, then (based on the lab definition of toxicity) all values were
defined as zero, then – they tested this actual zero statistically and found
that one could not rule out zero. “
“But
let readers be clear about this central point: if one is willing to consider
the actual numbers reported and test those numbers, the results are clear - a
larger proportion of autistics had heavy metals excreted as the result of
chelation.”
It is not the business of
authors of papers to have to recite the details of all the prior papers they
cite in support; if they did there would be even more that everyone had to
read. Any half-proper peer reviewer
would check out the background references themselves (where required), and
indeed in this case ought to be an expert familiar with these important key
papers (on Neurotoxicology of autism) already anyway. What a timewasting pseudo-expert charlatan.
>The conclusions of
Hertz-Piccioto et al. are misstated.
Not so. They are not in the slightest mis-stated in
my own report.
>The second-to-last sentence of [their] paper actually
states, "This report did not address the role of prenatal or early-life Hg
exposure in the etiology of autism."
Indeed that is the case. But so
what? That is exactly my point about
it. [Note to non-expert readers: “Hg”
means mercury and “etiology” means causation.
You may wish to guess whether they used that unnecessarily abstruse
language there for the same reason that they hid that absolutely crucial sentence
right at the end, second last, of their paper which supposedly did indeed dis-evidence
a mercury-autism connection.]
>The major finding was that total Hg in blood was not
elevated or reduced in preschool children with autism/ASD compared with unaffected
controls and resembled those of a nationally representative sample.
Indeed that is the case. But so what? I never said otherwise.
>The reason for the authors' qualification is that
only concurrent measures of blood Hg were available, meaning that they could
draw no conclusions from their data about the role of prenatal or early-life
mercury exposure.
Indeed that is the case. But so
what? That is exactly my point about
it.
>To say that the authors
concluded that their data, ".constituted no evidence whatsoever against
causation of autism by mercury" is simply wrong.
No it isn’t. Their words quoted above
indicate PRECISELY that. As Reviewer #1
appears to be having some peculiar difficulty with either language or logic I
will try to parse this for them as follows.
( I apologise that I have to assume the reader is an idiot here.)
We begin with their paper’s
second-last sentence that:
"This report did not
address the role of prenatal or early-life Hg exposure in the etiology of
autism."
That means effectively the same
as:
"This report was not
capable of providing any information about the role of prenatal or
early-life Hg exposure in the etiology of autism."
Which means that it is also the
case that:
"This report did not
provide any information about the role of prenatal or early-life Hg
exposure in the etiology of autism."
And hence:
"This report did not
provide any evidence about the role of prenatal or early-life Hg
exposure in the etiology of autism."
And hence:
"This report did not provide
any evidence about the role of prenatal or early-life Hg exposure in the causation
of autism."
And hence:
"This report did not
provide any evidence about the role of prenatal or early-life mercury
exposure in the causation of autism."
And hence:
"This report did not
provide any evidence about the causation of autism by prenatal or early-life
mercury exposure."
And hence:
"This report did not
provide any evidence against the causation of autism by prenatal or
early-life mercury exposure."
And hence:
"This report constituted
no evidence against the causation of autism by prenatal or early-life
mercury exposure."
And hence on merely removing a
redundant word:
"This report constituted no
evidence against [the] causation of autism by prenatal or
early-life mercury."
….which would be identical to my
own statement except that there is that extra bit about “prenatal or
early-life”.
So I was wrong there. I overlooked that autism could still be not
caused by exposure to mercury later in life, after that person has already
become autistic. So we’d best not
publish my non-gamma-2 rubbish after all.
And whatever it takes to become
a reviewer for Neurotoxicology, it’s all too clear I don’t have it
myself.
Reviewer
#2:
Dental amalgams are a
continual source of controversy. The current review attempts to survey the
adverse health consequences of the amalgam formulation known as non-gamma-2. It
asserts that these restorations "are currently by far the main cause
of chronic disability in the UK, US, and other such countries, with about 10%
of the UK working-age population disabled thereby." It also claims that
its introduction led to a 10-fold increase in the incidence of autism.
Indeed. But no faults are there providing basis for
non-publication so far.
As a contribution to this specialized journal, the
manuscript lacks any clear connection. It offers no neuro-mechanistic
foundation for such a correlation, especially for autism, which is a product
of disordered early development.
Not so. In respect of autism, my
review(/study/rant/) ties in the newer mercury factual data with the prior
unchallenged theory and the related fact of how the mercury binds with DNA to
reduce gene-expression and hence [as my 1993 had predicted] cause autism. And meanwhile in respect of adult mercury
poisoning there is quite a developed understanding of how the symptoms are
caused. The details of that causality
are in the cited literature or secondarily-cited.
It doesn't attempt to demonstrate any kind of
dose-response relationship.
No data is available that would
enable that. But it doesn’t follow that
there is no other useful evidence presented.
Its definition of autism lacks specificity.
It doesn’t need to. It just uses the definitions that are used
as standard by others. As is common practice.
In addition, the claim that this amalgam formulation
accounts for 10% of chronic disability requires advanced statistical modeling
of exposure-consequence relationships in which other kinds of exposures are
concurrently evaluated.
Firstly, I did not claim that it
accounts for 10% of chronic disability.
I reckoned from the data that it now actually accounts for MOST chronic
disability (something like 70-90%).
That 10% figure was my estimate that wholly 10% of the UK workforce has
been disabled by non-gamma-2 (4 million victims out of a 40 million
workforce).
That 10% is not a “claim” but
rather was expressly only a rough estimate, from looking at figure 5. You can see that it shows an increase of
about 2 million accepted claimants, easily all attributable to
non-gamma-2. And you can see that it
peculiarly levels off about year 2000 as would be expected from the stated
political agenda of “claimant count now controlled”. And you can see that otherwise it would most likely have
continued upward to something like 4 million – hence 10% of the working-age
population.
And no fancy statistical
modelling is required to understand what these graphs are showing us. Of course they are not absolute proof, but
neither are they any lack of evidence, else we’d have to retract an amazing lot
of highly-acclaimed “studies” from the most prestigious journals.
In the absence of these kinds of information, it is
difficult to see how this manuscript is compatible with the aims and audience
of this journal. Perhaps the author should consider another kind of journal and
audience.
Or perhaps instead the so-called
Neurotoxicology journal should consider changing those aims and
audience, or perhaps change its name to reflect its “specialised” nature, for
instance to Specialised Neurotoxicology, Pedantic Neurotoxicology,
or best of all to Die Zeitschrift der Lysenkoischen
MeisterNeuroToxikologisten von Nurnberg (The Journal of the Lysenkoist
MasterNeurotoxicologists of Nuremburg).
Reviewer #3: This is an opinion piece on the possible role of mercury
exposure in the causation of autism.
Not so. It is not “an opinion piece”. Like all scientific papers it does include
proposed conclusions which are necessarily of an opinion nature. But for the most part it consists of
presentation of data and reasoning thereon, which is entirely in line with any
normal scientific paper and not “an opinion piece”.
The author makes a very impassioned case for non-gamma-2
amalgam fillings being the major cause for the rise in incidence of autism
using ecological data from UK, US and few other countries.
Not so. It is not at all “very impassioned” but
rather “very filled with as much useful factual evidence as can be found”.
No primary research has been undertaken by the author to
test this hypothesis.
So what. Exactly the same could be said about all
those seven highly-rated studies listed on the first page here. Has anyone ever called for their retraction
yet?
My main concern with this work is that it is not an
objective assessment of the evidence available at present.
….because / for instance…..
Key statements that form the basis for the author's
argument are unsupported by high-quality evidence.
…such as….
For example, the exposure of children to mercury from
their parents' amalgam restorations needs to be confirmed before the author can
make such a far-reaching conclusion.
Indeed, no one has bothered to
do any measurement studies of this question to date. But that is not the fault of this author or this review. Rather it highlights the urgent need to make
a start by publishing this first study of the subject, which can be then
followed up by testing studies. But I
did already explain why we can be confident that there is enhanced
exposure. That is because there is very
low background atmospheric mercury vapor, and it is known to constantly emit
from parents’ and carers’ amalgams, and they commonly spend much time together
with babies in enclosed spaces, even talking at them through their amalgam-filled
mouths, and so it logically follows that many babies are going to breathe in an
increased amount of mercury vapor at least on average. [Studies have also shown prenatal
transmission.]
Randomized clinical trials of dental amalgam (Bellinger
et al 2006; DeRouen et al. 2006) showed no significant neurodevelopmental
deficits in the children receiving amalgam restorations compared to non-mercury
fillings.
Those two studies have already
been solidly debunked as evidence, as I pointed out via my first page citation
of Muttter 2010 (and others). Not least
they started too old to relate to causation of autism, and they stopped too
young to relate to causation of adult disability. In fact (as in my earlier journal replies) if I myself had been
in those studies I would have been recorded as evidence of harmlessness,
because my life only became chronically ruined (by the amalgam scam) AFTER the
age at which those propaganda studies stopped.
And an editorial in the very same issue of the journal stated that those
two studies did not constitute evidence of amalgam safety. Why didn’t Reviewer
#3 mention that counter-point in their “unbiased” commentary here?
In fact, Maserejian et al. 2012 have reported that
compared to amalgam restorations, children receiving composite (non-mercury)
fillings showed impaired psychosocial function. There are several other such
instances in the manuscript where important data have been ignored.
Maserejian et al had not been
published when I first sent this review to a journal in July 2012, else I might
have mentioned it. But exactly the same
methodological problems arise as with the two others cited above. I myself was doing fantastically well at school
before the effects of the amalgam scam imposed themselves so devastatingly on
my life. And perhaps bisphenol-A might
well have injurious effects but that is a separate matter out of the range of
my own documents.
In my opinion, this
manuscript does not add unbiased scientific knowledge to the topic of mercury
and autism, and I cannot support it being published.
But rather it is this Reviewer who is biased, and has raised only bogus reasons
for suppressing the publication of this outstandingly important cautionary
information.
IN CONCLUSION:
These three reviewers have failed
to raise even a single sound reason for preventing the publication of this very
important information. And they have
meanwhile deployed a whole load of shallow pseudo-objections, which raises
considerable questions about both their supposedly expert competence and their
honesty.
And that comes in the context of
ten previous journals likewise raising only specious excuses for refusing
publication.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Further reply from PseudoNeurotoxicology (23rd October 2013).
“…. Thank you for
your email. I forwarded it to the editor of the journal. After
review it was concluded that your manuscript was handled appropriately and the
original decision stands…..”
Notably there was an
absence of any rebuttal of any of my rejoinders.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
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