[From Hank Folson (920616)]

Some anecdotal information on addiction from a conversation on a bicycle ride
with a fellow who evaluates drug programs: 1. Crack babies can fully recover,
but they need a great deal of touching, holding, and hugging. 2. There are
drug programs that work. We didnUt discuss success rates. They are cost
effective, mainly because avoiding one crack baby saves $350,000. 3.
Detoxification of addicts is only the beginning of treatment. Long term
addicts have no experience making decisions, and may be taking drugs to avoid
making decisions. Recovering addicts need a lot of counseling time to train
and support them in making decisions about their lives. 4. Conservative
Republicans are against even cost effective programs as they perceive
addiction as the result of a lack of will power.

I do not use drugs and my knowledge is limited to a TV special on PBS, so I am
not controlling for approval of my PCT thoughts on cocaine/heroin addiction:

The mind functions by chemical action, so our reality is chemically based.
When we are sober, we have one reality, call it a sober reality. When mind
altering drugs are in the brain, they interact with the chemical action of the
brain to create a second d rug based reality. One anecdote I recall from a PBS
special is that researchers were surprised at how many returning Viet Nam War
veterans dropped heroin habits. In war, the sober reality can not compete with
the drug reality. But once these soldiers left the Viet Nam reality, wouldn't
the sober reality at home be preferred over the drug reality in Viet Nam? The
addiction would disappear for those who came home to a happier environment.

Our reality is a running average of the daily experiences in our lives,
weighted by the impact of various experiences. My guess is the drug reality
neither adds onto nor overwrites the sober reality, but exists along side of
it. The person can connect the drug reality to instances of drug use, and so
keep the two realities separate. The next step in my supposition is that we
compare the two realities. If the drug reality produces lower error signals
than the sober reality, the user would, I think, control for the drug
reality. The behavior that results is more drug use, as the user controls for
what he perceives as a better reality.

The drug reality is completely inside the user's head, insulated from the
outside world, so it stays much the same no matter what happens to the sober
reality. The financial and social costs of supporting the habit degrade the
quality of the sober reality , so the sober reality relatively looks worse and
worse. The increased error signals will lead to controlling for the drug
reality. The addicted behavior becomes stronger, and harder to break.

Soberly, Hank Folson
Henry James Bicycles, Inc. 704 Elvira Avenue, Redondo Beach, CA 90277
310-540-1552 (Day & Evening) MCI MAIL: 509-6370 Internet: 5096370@MCIMAIL.COM

[From Bruce Abbott (980703.0745 EST)]

Bob C.(980701.2249 PT) --

Bob, are you familiar with Solomon and Corbit's (1973) "opponent process"
view of addiction? According to this view, the brain/body acts so as to
maintain certain physiological variables near internally-specified reference
values. Disturbances to those variables result in the appearance of an
action which opposes the effects of the disturbances. (Hmmm . . . something
familiar about that . . .) For variables in some systems the opposing
action must be "recruited" (my term, not theirs) in that the response to
disturbance is at first absent or weak but becomes stronger with repeated
exposure to episodes of disturbance. The action is also sluggish in another
sense in that it persists for a time after the disturbance ceases. Because
the recruited action opposes the effect of the disturbance on the variable
in question, Solomon and Corbit refer to it as the "opponent process."

Solomon and Corbit have applied this model to a variety of phenomena,
including drug addiction. In the latter case, the drug (e.g., heroin)
artificially disturbs a biochemical system in the brain, resulting in the
experienced pleasurable effects of the drug. Because the effects are highly
pleasurable, the person desires to experience those effects again, which
requires taking more of the drug. However, repeated experience with the
drug begins to recruit the opponent process, which more and more effectively
opposes the effect of the drug and the result is that the pleasurable
experiences resulting from the drug's actions on the brain diminish; this
effect is described as "drug tolerance." The person acts to oppose this
disturbance by increasing the dosage of the drug.

As drug administration increases, the increasingly large disturbances to the
biochemical system in question are opposed by an increasingly strong
opponent process. However, as the drug actions wear off following
administration, the aroused opponent action, which is slow to terminate once
activated, now is acting to compensate for a disturbance which is no longer
present. As a result the person experiences the psychological correlates of
activity in the opponent system, which tend to be opposite those produced by
the primary system which the opponent system was recruited to oppose. These
"withdrawal symptoms" are experienced as decidedly unpleasant. The person
now is taking the drug as much to avoid experiencing the withdrawal symptoms
as to experience the pleasurable effects of the drug, and _must_ take the
drug to avoid the former. The person is now addicted.

The mechanism accomplishing all this need not be complex. For example, the
neurons involved may limit the level of activity at their synapses; when
activity is enhanced beyond this limit by the drug, the neurons may act to
oppose this excess by reducing the amount of neurotransmitter released with
each neural impulse or by reducing the number of receptors for the
neurotransmitter in the postsynaptic membrane. However, as this adjustment
develops, the system would become less responsive to its normal inputs
(reduced synaptic activity for a given level of input), creating an
imbalance between affective systems having opposing experiential properties
(e.g., depression begins to dominate over elation). The person begins to
feel "bad" under normal levels of input and can restore a neutral state only
by taking more of the drug. Of course, other models are possible and there
is a need for empirical work to provide support for one model or another. I
present this one here to illustrate how one might go about accounting for
addiction phenomena within a regulatory or control system framework.


Bruce A.

[From Bruce Nevin (980703.1030 EDT)]

Bob C.(980701.2249 PT) --
Bruce Abbott (980703.0745 EST)--

It sounds like addictive substances alleviate unpleasant feelings that
accompany chronic error. Addicts' accounts suggest this. "When I'm high I
don't feel bad any more." "I drink to forget my troubles."

For addictions relating to blood sugar homeostasis, there are physiological
changes in the pancreas that account for requiring larger doses to
experience the same effect. Alcohol is assimilated very quickly, so the
blood sugar rises quite rapidly. To counter such rapid change, the isles of
Langerhans in the pancreas become larger and produce more insulin. However,
this increases not only the rate but also the amount by which blood sugar
is lowered. The person becomes dependant upon alcohol (or candy, or coffee,
or rage/adrenalin, etc., or some combination) to counter the unpleasantness
of low blood sugar, which I should think would be intrinsic error. The
swings become more extreme as the addiction progresses. This sounds like an
example of an "opponent process" per Solomon and Corbit. If so, it shows
that it need not be a neurological or neurochemical process in the brain.
Since we're dealing with intrinsic error, isn't the push-back likely to
come from more primitive parts of the organism (in evolutionary terms)?

Blood sugar homeostasis is clearly a negative feedback control process.
Half of it is easy to identify. Sensors respond to changes in blood sugar
level. When the blood sugar level goes up, the pancreas releases insulin to
bring it back down, storing the sugar as fat. When blood sugar goes down,
one obvious counter-mechanism is experienced as hunger, and if that goes on
long enough the ATP/Adenosin stuff kicks in to convert stored fat and raise
blood sugar. However, that mechanism is very conservative (don't know when
the next wooly mammoth might come along). You usually have to exercise
about 40 minutes before you start burning fat.

If the organism doesn't raise the blood sugar by eating, the consequences
vary a lot. Everything in the body from the brain to the flexing of the
toes runs on blood sugar. Hyperactivity looks to me a lot like what I'd
expect reorganization to look like. The reason ritalin works on hyperactive
kids, I've been told, is that it raises their blood sugar; fixing their
diet works better. The enormously varied symptomology of hypoglycemia
sounds to me like the effects of intrinsic error becoming evident through
whatever part of the organism is in most trouble, and using whatever means
the organism has learned by reorganization, by example of others, and maybe
by instruction.

  Bruce Nevin.