The danger of "Danger"

Mike Clark mrc7 at
Fri Jun 11 05:16:24 EST 1999

In article <376039FB.80F3DE83 at>, Alan J. Robinson
<URL:mailto:robin073 at> wrote:
> >Subject:     Re: The danger of "Danger"
> >Date:        1999/06/10
> >Author:      Mike Clark <mrc7 at>
> >In article <375FD401.DFBFA790 at>, Alan J. Robinson
> >>[snip]
> >>...
> >>
> >> 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.
> >>
> >>[snip]
>> It may be that there are neurological effects on autoimmune diseases but
>> I would beg to suggest that there is far more evidence for involvement
>> of easily identifiable immunological factors. ...  
>> In your example of acute trauma above it would be very hard to
>> distinguish effects which might be due to neurological changes from
>> those due to simple physical damage and infection. In the absence of a
>> simple experimental approach which could be used to distinguish the two
>> types of effect it seems best to me to adopt the hypothesis  for which
>> there is the most experimental evidence.
> >Mike Clark,                        <URL:>
> >M.R. Clark, PhD. Division of Immunology
> >Cambridge University, Dept. Pathology
> Care to place a small wager? <g>
> In fact, there is overwhelming evidence of many different sorts for the
> primacy of brain dysregulation in the pathogenesis of HUMAN autoimmune
> disease.  Indeed, in the case of multiple sclerosis the striking
> similarities with Chronic Fatigue Syndrome have been noted by several
> observers, implying a common pathogenesis and shared pathophysiological
> pathways.  It's just in the final pathway that the difference between
> the two diseases becomes evident.
> That's not to say of course that all these other factors you mention
> don't play a role too.  One of the complicating factors is that neurons
> share a lot of the same molecular signaling mechanisms with blood cells,
> so that genetic polymorphisms in neurons which cause brain dysregulation
> could also cause similar dysregulation directly in the blood cells of the
> immune system.

To place a small wager on what?

It is quite clear that most autoimmune conditions are under polygenic
control. It is also true that, as you state above, that there are shared
dependencies between neurons and haemopoetic cells. Thus polymorphisms in
some genes including hormones, cytokines, neurotransmitters etc might have
effects on both systems. This however is not evidence for a direct cause
and effect.

However it is a highly misleading and unscientific way of thinking to say
that because two proceses are similar in 'appearance' that this is strong
evidence for a 'common pathogenesis'.

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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