In my previous post on this subject I tackled the shortcomings in the Porph study and Professor Lathe’s reliance on extremely haphazard science. I also touched on his strange reluctance to publish _all_ associated data relating to that study and his peculiar relationship with co-author and DAN! doctor Lorene Amet. I also reported on how Lathe conceded that several key aspects of his theory relied on unverified science – notably the Holmes et al paper.
In this post I’ll be discussing key aspects of Lathe’s book ‘Autism, Brain and Environment’ and how they do not hold up to scrutiny.
The central theory of the book is that we are experiencing something Lathe calls ‘New Phase Autism’ which is a new type of genetically based, environmentally triggered autism – notably via metals such as tin, lead and mercury. His hypothesis states that some people have a genetic predisposition which, when exposed to environmental insults, reveals occult phenotypes.
There are two main supporting arguments that Lathe attempts to marshal to support this hypothesis.
1) Prevalence.
2) Limbic system ‘damage’. Lathe makes strong use of the Limbic system because a) it governs socialisation and b) its (to some degree)
repairable.
Lets be clear, without these arguments, Lathe’s entire hypothesis falls. Without an ‘epidemic’ there is no reason to suspect a new type of metal influenced autism and without strong science to support the autism/limbic system hypothesis there is no reason to _assume_ a connection here either.
We know from Mike’s sterling work that the prevalence issue was very selectively presented and only utilised data that supported Lathe’s hypothesis. The much more valid and pertinent data that did _not_ support Lathe’s hypothesis was ignored.
What I intend to do in this post is address the issue of limbic system involvement. Why Lathe argues for it and why his hypothesis rests on very shaky foundations.
On page 64, Lathe states:
….it is the limbic system which is believed to be centrally involved in the problems associated with ASD.
No paper is cited to support this opinion. No evidence is offered to show support for this belief.
Lathe discusses a number of papers that clearly establish a connection of some kind between the limbic regions of the brain and autism but none of these studies refer to the limbic _system_ being _central_ to ASD. Lathe himself points out the many issues with the techniques used to gain data in this area, noting that histological study of the post-mortem brain is restricted to those very few samples available. Imaging studies are also skewed towards the older and Asperger end of the spectrum and thus cannot be representative of the whole spectrum.
Nevertheless this does not stop Lathe from pronouncing that limbic damage is central to ASD. He attempts to prove this by seeing if:
ASD features are consistent with limbic dysfunction.
Lathe states that anxiety is closely associated with limbic dysfunction (p76) and then goes on to say that anxiety is often an accompaniment to ASD. But lets not forget that Lathe is centring the role of limbic damage around his hypothesis of ‘new phase autism’ – a new type of chemically and metal caused autism that results in ‘severe/kanners/classic’ autism. It’s interesting to note that as far as anxiety is concerned that:
ASD children are significantly more anxious than controls, but the severity of anxiety varied according to ASD subtype with *Asperger disorder exceeding PDD-NOS, and both exceeding autism proper* […] on the anxiety rating scale.
This does not shed any light on Lathe’s ‘new phase’ autism. Rather it shows that if we look at anxiety as a correlator of limbic damage and ASD, then AS and PDD-NOS are more closely related than ‘autism proper’.
Lathe next examines ‘desire for sameness’ (p76) saying that it is:
[characteristic of autism]…as noted in the clinical behavioral rating _”obsessive desire for sameness”_ employed by several researchers.
And yet once again, Lathe fails to cite these researchers or the work that showed them employing this rating, or in what context it was used. It should be noted that ‘desire for sameness’ forms no part of the DSM(IV) and there are no cites showing how common a desire for sameness actually is amongst autistic children, particularly children Lathe might judge to be part of his ‘new phase’ subgroup.
In fact the only clinical studies Lathe cites in this section are two studies on rats from 1964 and 1965 respectively. And yet when discussing a later study Lathe states (p100):
…it is perhaps unsafe to extrapolate too freely from rodents to humans.
Quite.
In an odd contradiction, Lathe later goes on to describe sameness as the inverse of novelty which Lathe claims can be attributed to the hippocampus and amygdala – both components of the limbic system – and that lack of appreciation of novelty can be attributed to amygdala damage. He then cites an example he knows of where an autistic child (p77):
…seemingly failed to react to the presence of a film crew in the bath.
This seems a rather bizarre contradiction. On one hand Lathe claims that ASD can be characterised by an ‘obsessive desire for sameness’ and on the other hand that ASD kids are unfazed by large scale changes in routine. Both, surely, cannot be true.
Lathe next states that ‘deficit in recognition of facial emotions’ (p77) is a key component of ASD and limbic system damage. The evidence he cites is:
This is shared by *some* patients with frontotemporal dementia, *associated* with limbic atrophy and by *some* patients with schizophrenia where involvement of the…[components of the limbic system]…has long been *suspected*
In other words, its an educated guess. Might be right but might equally be wrong.
Social interaction is next on Lathe’s list which is one of the very few items on Lathe’s list which genuinely _is_ a defining feature of ASD. Lathe makes his case valiantly but freely admits that (p77):
Few satisfactory studies have been performed on humans
and once more falls back on rodent studies which (as we know) Lathe has strong reservations about. He also makes of use a study using monkeys and yet, as with rodents, Lathe later states (p82):
….it may not be easy to extrapolate from monkey to man.
Which begs the question of why this chapter relies so heavily on rodent and monkey studies?
Lathe next makes a central and common error regarding autism, stating that (p78):
Language delay is a central diagnostic feature of ASD.
This is not correct. Language delay is merely one of four possibilities encompassed under a criteria heading of ‘Impaired *communication*’. This is _not_ a trivial distinction. Especially when we recall that this must all fit within the umbrella on Lathe’s ‘new phase autism’.
Lathe next tackles seizures, stating that seizures are recorded in up to 30% of autistic people (p79). However, we must again remember that Lathe is attempting to tie this in to his ‘new phase autism’ and his subsequent discussion of how autistic adults have a continued level of seizure (around 25%) this would indicate that seizures are not new to autism and hence cannot be part of Lathe’s ‘new phase autism’.
Sensory deficits is next on Lathe’s list. He starts off by stating what may well be uncontested fact – that hearing deficits (using Lathe’s words) are present in less than 9% of the autistic population, visual impairments in less than 24% and a lack of response to painful stimuli ‘has been noted’ in a 1999 study and given at rates of 7 in 18 in a study from the 1970’s.
However, Lathe freely admits that there is little to no research to tie in sensory processing and the limbic system, limply noting one study on monkeys. A subject group we will remember Lathe has reservations about.
Lathe next looks at stereotypy and repetitive/compulsive behaviours, correctly noting that this is a diagnostic feature of ASD. However, Lathe then goes on to state:
To this one must add alteration between a restricted range of activities…..This behavior is consistent with limbic damage.
As before when Lathe makes this bold assertion he does so without any evidence. No cites are made in support of this apparently imperative addition and it does not appear anywhere in the DSM(IV). It seems that this imperative addition is only imperative to establishing a link between a hypothetical ‘new phase’ type of ASD and limbic damage.
Lathe devotes a whole chapter to GI disturbances which is outside the scope of this particular post suffice it to say that that chapter contains frankly embarrassing references to unpublished work from Krigsman and cites altcorp.com as a valid reference of science.
In this chapters concluding pages, Lathe cites a study that he says (p83):
Causally link limbic damage to autistic behaviour.
In fact, he says there are seven but he only references one so its hard to place much faith in the others. The one referenced paper is over thirty years old.
Lathe then attempts to wrap up his case (p85 – 86):
behaviors associated with limbic damage resemble autism in a long list of different categories.
Thats a possibility but as we’ve seen, Lathe’s supporting evidence is flawed on numerous levels.
1) Over reliance on animal studies. A flaw Lathe makes note of himself.
2) Reliance on very old science.
3) Misrepresentation of the ASD diagnostic criteria. Theories should fit the known facts. The known facts should not need to be twisted to make a theory work.
4) Lathe is attempting to make a case for a new metal/chemically caused type of autism. A lot of his cited science relies on adult subjects born well before the time period Lathe needs to concentrate on.
Second, the limbic brain is consistently abnormal (in ASD)
.
Definitely interesting but yet again argues _against_ new phase autism, not in support of it. If limbic damage is _consistently_ abnormal in ASD then why the insistence on limbic damage being supportive of ‘new phase autism’? Remember that a lot of Lathe’s cites references adult autistic people born and diagnosed long before the time frame Lathe targets as the birth epoch of his ‘new phase autism’.
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