From: mccla_d@aelle.cs.odu.edu (dennis mcclain-furmanski)
Subject: RE: Instant Addiction
Organization: Old Dominion University, Norfolk, VA, USA
Distribution: sci.psychology
Date: Thu, 23 Jul 1992 14:31:51 GMT

jpk@Ingres.COM says:

> ... tolerance, withdrawal, change of the organism's physiology and chemistry
> from the normal state, as well as behaviors that seek the substance.
> If you change neurotransmitters and get none of these, you don't have
> addiciton.

And if you change them, and get those, then you do. Except tolerance. I won't
continue to beat that horse. All the others, yes. They've been observed and 
reproduced.

> don't see how this [THIQ] applies to the neurotransmitter explaination of 
> addiction.

THIQ as a byproduct of serotonin is radically and permanently increased as
a result of interation with high levels of acetaldehyde. In the organisms
which show this increased THIQ level, all the sympotoms of addicition are
present. In organisms in which addicition to alcohol is present, abnormal
levels of THIQ are also. Direct application of THIQ creates all the symptoms
of addiction, except physiological tolerance. Due to interaction with 
acetaldehyde, some of the breakdown prodcts of serotonin are diverted to THIQ
production, and a depletion of serotonin begins. I've read that high THIQ is
also present in barbiturate addiction, though I didn't read far enough to 
learn what the mechanism is. To my knowledge, every organism which shows this 
level of THIQ also shows addiction symptoms. Serotonin depletion continues
with continued drug administration. It reverts to normal levels during
abstinance, though THIQ remains high.

> Rats' with "innate aversion to alcohol" are not comparable to rats that
> can take it or leave it.

Definitely not. It would not be as significant to induce addiction behaviors
in organisms which could become addicted on their own. The control group
would refuse to drink alcohol even when it was the only thing they had. The
experimental group also refused alcohol until THIQ was administered. Then,
they couldn't get enough. The effect could not occur naturally. I find
the results all the more significant for that, not less. If I'm missing a 
point of logic there, please let me know.

> It's also hard to say that addicition is severe during abstinence, what's
> the state of something that can't be measured right now.

True. The claim is typically made due to the rapid, even immediate, onset of
symptoms of the addiction (excluding tolerance at first, but it catches up 
soon). The progression in severity of withdrawal and drug seeking behaviors
shows over all straight line advance throguh pre-, during, and post-
abstinance, although the symptoms aren't seen in the middle. Although it
can't be measured at the time without negating the state being studied, the
constant progression of symptom severity in the absence of the symptoms
themselves is taken as evidence that the addiction is still present and 
increasing in severity. This evidence is all due to self-report by second-go-
round patients. It's pretty consistent. I've never heard one say it was easier
the second time around, nor have I heard reports of such from others. This
*is* the type of thing I would expect to be stifled by the admin and marketing
types, but we rarely go through them when we talk to each other, and they
don't control the literature.