Is Alcoholism A Disease?
Presented by Jill Pinkerton
About the Speaker
About the Event
Announcements
Dennis M. discussed the particulars of the Adopt-A-Highway
gathering of FAOWM members with the group. He also handed
out surveys he had put together for our group, to provide a
“snapshot” of our membership in order to help guide future
meeting topics, format and discern interests. These are
anonymous and not to be used for stands on political issues or
for publicizing FAOWM positions on any issues, but to give an
idea of our makeup. These will be passed out again at the next
couple of meetings to give those who hadn’t had an opportunity
before, to fill them out.
Correction to our bulletin: The Annual FAOWM Picnic will be June
16; approx. 10AM-5PM, at Fallasburg Park in Lowell, MI.
Upcoming topics and events are as follows:
Ø APRIL 25, 7PM: “Are There Objective Human Values?”
Presented by Dr. Joseph Ellin.
Ø APRIL 28, 10AM: Adopt-A-Highway Cleanup. Organized by
Dennis Murphy. Meet at Citgo gas station between 5 Mile and E.
Beltline on Plainfield.
Ø MAY 9, 7PM: “Determinism vs. Free Will.” Presented by
William Merriman.
Ø MAY 23, 7PM: “Gun Control.” Presented by Dennis Murphy.
Ø MAY 24-26: Design, Self-Organization and the Integrity of
Creation Conference at Calvin College. See
http://www.calvin.edu/fss/dembschd.htm.
Check our website for more information, links to sites of interest
and more: http://www.cfimichigan.org.
Presentation
Our topic for this meeting was “Is Alcoholism A Disease?”
presented by Jill Pinkerton. Jill began by focusing on what
constitutes a disease. Magill’s Medical Companion relates
disease to lesions, which it considers to be the “essential
expression of disease.” This is further defined as “any
pathological or traumatic discontinuity of tissue or loss of
function of a body part.” As to mental illness, it predicts that it “is
likely that future research will reveal the presence of ‘biochemical
lesions’ in these cases.” In the DSM-IV (Diagnostic & Statistical
Manual of Mental Disorders), mental conditions are always
referred to as “disorders” rather than “diseases.” The patterns or
syndromes reflect distress, disability or any significantly
increased risk of death or important loss of freedom. It also pairs
mental disorders clearly with individual dysfunctions more than
societal responses, unless those deviant responses are
symptomatic of the individual dysfunction.
In her hand-out, Jill had 11 examples of conditions that have
been termed “diseases” ranging from less controversial ones
such as arteriosclerosis and hypertension, to the highly dubious
ones, including rageaholism (inability to control one’s rage) and
workaholism. We also looked at how Americans have in the past
and present viewed alcoholism. In the late ‘40s, 58% saw no
difference between an alcoholic and a habitual drunkard, while
this same statistic became the one for those who saw
alcoholics as suffering from an illness in the late ‘50s; with 38%
considering these individuals “morally weak.” By 1987, the
Gallup Poll found that 90% of respondents believed that
alcoholism was a disease, with 60% considering it to be a
congenital condition.
Next we examined the physiology of alcohol/drug dependence,
taking a look at the neuronal structures; dendrites, synaptic
gaps, the sites of neurotransmitters and the location of neural
pathways and the route that pleasure- inducing dopamine takes
in the brain and how this is triggered. We discussed the phases
of drinking, and how this relates to relapse following detox, the
build up of tolerance, and personality changes.
Following on this last item, we considered whether alcohol
addiction is symptomatic of an underlying personality disorder or
if the classic behaviors of paranoia, depression, aggression and
lower self-esteem result from the disorder/ disease.
Jill, in her paper and oral presentation, cited the Vaillant
Longitudinal Study that researched what factors best predicted
who would become an alcoholic. Alcoholic relatives and ethnicity
were strong determinants. Interestingly, the study showed that
while several other factors were not significantly predictive of
which examinees were to become future alcoholics, they did
tend to predict an earlier onset for symptomatic drinking in those
who would become alcoholics. Another interesting aspect of this
research was that addicts tended to create myths about the
causes (traumas, upbringing, etc.) of their addiction. When
investigated, these experiences post-dated their addiction! Other
events perhaps influenced, but did not ultimately decide their
alcoholism.
Going back to the physiology of alcoholism that Jill presented, it
was noted that alcohol consumption releases dopamine and
that this system of receptors and pathways goes right through
the most primitive brain regions; the most hard-wired responses
for basic survival functions, the reactions of which are triggered
by pleasure, pain, aggression, fear, etc. The course of the
dopamine pathway travels through the pleasure centers and
emotional parts of the brain and ends up in the behavioral
option-sorting parts. In effect, making the choice to drink is
rewarded in the same way as an organism is rewarded (via
well-being/pleasure inducing dopamine) for choices that
enhance its reproductive success. It is not clearly understood
why alcohol (and cocaine and other drugs of abuse) are so well
mated with these internal brain structures and feedback loops.
However, drinking does tend to make the one imbibing more
expansive, self- confident, verbal; attracting more attention-
potentially with a member of the opposite sex.
As more alcohol is consumed, more reward circuits are
stimulated via dopamine-but this heavier flow can have negative
effects on the neurology of the drinker, resulting in tics and
psychosis. The response is a pruning back of receptors,
generating a higher tolerance for the substance as well as a
need for higher quantities to achieve the same dopamine
reward. This also causes smaller, more everyday pleasures to
be enjoyed less. After detox programs, the substance abuser is
still in the same boat-not enough receptors to replace
drug/alcohol abuse with other pleasure-giving behavior and
finding the only way to re-ignite those remaining receptors is with
the drug that got them there in the first place.
As to the phases of drinking, it was explained during the
presentation that the brain takes steps, during a single night of
drinking, to quiet things down, releasing an inhibitor GABA which
acts as an anesthetic, to counteract a cascade effect that would,
if unchecked by this response, result in a grand mal seizure. The
outward effects of this quieting down, is the slurred speech and
lack of coordination one sees after sufficient alcohol is
consumed. Unlike with surgical applications, this anesthetic
response is not carefully monitored when induced by drinking,
which is why a person can actually die as a result of this. As time
goes on, the brain becomes less capable of quieting itself down
and tremors can be seen in the individual. They can have
seizures when coming off drinking, presenting them with a
“double whammy” where the drinking behavior creates neuronal
problems but going off it hits them as well.
Another interesting point Jill made is how dopamine is integral
in the learning process. It was shown in studies that brains “light
up” merely at the presentations of images of the paraphernalia
of their habit. They get a “high” just in anticipation of its use, so
strong are the associations in the brain. Physiological
responses for craving have been seen in three- year post-abuse
individuals when presented with the stimulus of items related to
their substance of abuse. Many see alcoholism as a series of
choices that over time become habituated with the tendencies
for abuse increasing as the tolerance heightens.
As to ethnicity, as mentioned in the Vaillant study, there appear to
be styles of drinking that are impacted by one’s culture. Some
cultures see the drinking- to- black-out style positively, while
others deem it in strongly negative terms. We explored the
contribution of behaviors to physiological disease. In studies by
Blum & Noble, it was shown that different individuals have
different alleles as to dopamine receptor quantities. Therefore
some people derive their response to the environment and/or
substances faster than others with the same quality/quantity
stimuli. The question was posed whether this has any
connection with the cortisol levels that are responses to
stimulation from excitement. Thrill-seekers seem to have a
higher threshold than non-thrill-seekers for cortisol saturation,
for instance.
We closed by talking about societal influences on behavior and
how changes in behavior reflect different attitudes by society.
Religion’s role in beliefs concerning behavior and substance
use and abuse was discussed as well. And we talked about
how the possible over diagnosing of some conditions as
“diseases” can limit the proper response to perhaps more
legitimate diseases. The differing behaviors seen in different
conditions labeled diseases also mitigate our responses to
them. As one person said, we don’t blame the sufferer of
coronary artery disease (even though he may well have brought
the condition on himself), but then he isn’t necessarily as likely to
be involved in spouse abuse, highway deaths, and so on.
Secretary: Charles LaRue
