From: Bostrom,N (pg) (N.Bostrom@lse.ac.uk)
Date: Tue Oct 12 1999 - 09:51:09 MDT
I have been too busy to post anything recently -- to the point where I got
an email today asking if I was dead. So I thought that I should give a life
sign. Here are some ruminations on whether we can expect there to be
smartdrugs. Comments?
Are there smartdrugs?
One theoretical argument against the possibility of smartdrugs is that if
there were a simple way of boosting intelligence, evolution would already
have discovered it.
Some things might still be possible. For example, if a higher brain
metabolism would increase cognitive performance, it might still not have
evolved because of the energy cost. So theoretically, there might be a drug
(caffeine?) that would make us think better by boosting mental energy. Other
examples might be if a drugs that facilitate some aspects of cognition at
the expense of others. Say, it facilitates memory consolidation but inhibits
ability to notice patterns and generalities (ampakines?). Or it promotes
abstract thinking and reflection but at the cost of making us slightly
absent-minded and less aware of our what we are not currently focusing on
(nicotine??). Such effects might not have benefited our evolutionary
ancestors, but they could nonetheless be useful for people living in today's
society.
What one wouldn't expect if the above theoretical argument is correct is to
find some drug that makes cognition more efficient without any downsides.
But I think the argument might be flawed. Consider the following model:
there are many different variables that influence cognition (release-rates
of neurotransmitters, density of certain types of synapses, concentrations
of enzymes that break down the neurotransmitters etc.). Let's assume that
each of these variables are normal distributed around some mean m in the
population. Evolution predicts that m should be close to optimal - but for
the population as whole, not necessarily for most individuals. For what is
the optimal value of a variable in one individual might not be optimal in
another individual. How much monoamideoxidase of type B you should have, for
instance, presumably depends on how efficient your dopamine-reuptake
channels are and how many dopaminergic neurons you have etc. etc., and this
will be different in different individuals. So evolution might have a
difficult time providing you with the optimum levels (for you) of MAO-b.
If this is correct, what one would predict is the following: We will not
find smartdrugs that improve cognition in the population as a whole (except
those that have some downside - like energy expenditure or shift of focus,
as discussed above). What we may find, however, are drugs that improve
cognition in some subjects and worsens it in others. Testing on a large
group of people, we would not find any effect.
Such drugs could still be very useful, but they would require some
individual experimentation. You have to try many things to see what works
for you. A proper clinical trial for a proposed smartdrug could thus have
two stages: the first stage identifies the people who seem to react most
favorably, and the second stage tests the overall effect on this special
population. My impression is that this is not usually done today, with the
possible consequence that many smartdrugs have gone unnoticed. Thus one
would predict that the smartdrugs that are discovered with today's methods
are found in the context of treatment of some special disease. Maybe having
that disease is correlated with having one of your brain variables displaced
in a certain direction from its optimum. Maybe people with some kinds of
brain damage typically benefit from higher levels of acetylcholine, for
example, and this could lead to a drug like Piracetam being identified as a
smartdrug. (The reality is more complicated, but it illustrates the idea.)
This reasoning only shows the theoretical possibility of smartdrugs. Whether
any useful ones can actually be developed is of course an empirical
question. Still, it makes the search look much more hopeful. And it suggests
that measuring the average effect on a representative sample of the
population is a flawed method of testing the efficacy of smartdrugs. These
observations generalize to other chemical interventions designed to enhance
normal human functioning.
Nick Bostrom
Dept. Philosophy, Logic & Scientific Method
London School of Economics
http://www.analytic.org <http://www.analytic.org>
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