Neuropsychiatry and Immunology/Oncology

Mike Clark mrc7 at
Mon Jun 14 09:22:35 EST 1999

In article <376168C3.4B66B7E at>, Alan J. Robinson
<URL:mailto:robin073 at> wrote:
> Just after I posted a couple of messages concerning paradigms (or
> the lack of them) in immunology - to expressions of extreme incredulity
> -
> there was a most extraordinary coincidence.
> CNN carried a report of an article in this week's New England Journal
> of Medicine about brain damage/dysregulation in cancer and autoimmune
> diseases including multiple sclerosis.  Several studies were quoted
> and a variety of experimental findings and interpretations were
> mentioned.  (This news item may still be available in the CNN WEB
> archives.
> Alan J. Robinson
> robin073 at

I'm not sure what you mean by expressions of 'extreme incredulity'?
Certainly I have looked at all the public postings in the thread 'The
danger of ''Danger'' and as far as I can see most of the arguments seem to
be about the lack of definitive evidence for the ideas you discuss rather
than the impossibility of the ideas. Certainly I believe that at present
there are reasons to remain sceptical but surely this is a good basis for
scientific investigation? A good scientific hypothesis is one which makes
predictions which can be easily tested by well controlled scientific
experiments or observations. It could be argued that it is usually the
sceptical viewpoint which advances science because this promotes the
sceptic to design experiments which provide the evidence to reject the
accepted hypothesis. I tend to reserve 'my own expressions of extreme
incredulity' for those biological scientists who come up with observations
in defiance of well trusted and tested laws of physics, for example the
ability to dilute a molecule to less than one per tube, yet still show it's
biological effect!

Now to get back to your specific statements, the problem I have with your
arguments is that you lump too many ideas together in one basket and try to
put a single label on them. I would prefer to have more specific claims
made one at a time in such a way that each claim could be tested on the
basis of scientific observation.

For example in one of your postings you say

>> 'Much disease results from these survival mechanisms becoming
>> dysregulated. e.g. the autoimmune diseases.  The dysregulation occurs at
>> least initially in the brain, rendering invalid the current sharp
>> distinction between psychiatric and medical disease.'

To me the problem is the implication in your statement that 'all'
autoimmune diseases start with dysregulation in the brain. I would be
mildly surprised if this were indeed true. It probably wouldn't defy any
laws of physics but it would seem biologically unlikely. One of your
examples you quote is multiple sclerosis, a disease of the nervous system
which would appear to have a major autoimmune component. Clearly it would
not be biologically very surprising to find your arguments being valid for
this example however it might equally also turn out that both the
autoimmunity and changes in neurophysiology were secondary to an infection
of the nervous system ie they are both secondary correlates of an infection
rather than one being the cause of the other. 

But do you really wish to lump all autoimmune diseases together? Do you
honestly believe that it is as likely for autoimmune diabetes to be caused
by a change in neurophysiology as say multiple sclerosis? Equally I would
suggest that bringing 'cancer' into the argument merely weakens your case
further. Genetics is starting to provide strong data to support the
classification of cancers into many different disorders based on the
cellular mechanisms of regulation of cell division and differentiation.

One of the ideas that Polly Matzinger likes to use is the idea that every
cell in the body actually should be considered as having a role in the
immune system ie the 'immune system' is not an easily identifiable 
separate organ, tissue  or collection of tissues. This idea could easily
encompass 'a role' for the nervous system in regulating 'some' immune
reactions and indeed 'a role' in 'some' autoimmune conditions. The question
is then can any of these roles be easily identified and tested in
experimental situations?

Mike Clark,                        <URL:>
 o/ \\    //            ||  ,_ o   M.R. Clark, PhD. Division of Immunology
<\__,\\  //   __o       || /  /\,  Cambridge University, Dept. Pathology
 ">    ||   _`\<,_    //  \\ \> |  Tennis Court Rd., Cambridge CB2 1QP
  `    ||  (_)/ (_)  //    \\ \_   Tel.+44 1223 333705  Fax.+44 1223 333875

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