Subjective Knowledge, Mental Disorders, and Meds How to Parse

the Equation
Mark D. Rego
Philosophy, Psychiatry, & Psychology, Volume 17, Number 1,
March 2010, pp. 57-60 (Article)
Published by The Johns Hopkins University Press
DOI: 10.1353/ppp.0.0275

For additional information about this article

http://muse.jhu.edu/journals/ppp/summary/v017/17.1.rego.html

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Subjective
Knowledge, Mental
Disorders, and Meds:
How to Parse the
Equation
Mark D. Rego

Keywords: psychopathology, antidepressants, suicidality, subjective experience, pre-reflective

few weeks, ago I was walking down

the hall to my office when I spotted my
brother-in-law coming the other way.
This was odd on two accounts. First, he lives in
Kentucky (I am in Connecticut) and second, he is
at least a foot taller than the man in my hallway.
Nonetheless, I struggled to figure out why he was
there. The resemblance was so striking it took
me a minute or two to convince myself it was not
him. Even after such convincing, the feeling that
it was him remained.
Later, I imagined that had I just returned from a
crack cocaine den I would have been hypervigilant,
if not paranoid, and consequently would be certain
that my brother-in-law had arrived unannounced.
Furthermore, I would probably assume that he
was up to no good.
How did I retain a strong feeling of recognition,
the feeling that maybe it was really him, when I
already concluded otherwise? And why, were I on
crack cocaine, would the obvious facts be useless
in rendering a decision about the identity of the

2010 by The Johns Hopkins University Press

man in the hall? Last, why would the post-cocaine

man in the hall become a nefarious brother-in-law
rather than a benign one?
If I just computed some symbols to figure this
out, wouldnt the feeling have gone away? If I activated a brother-in-law neural network, how did I
come to acquire an evil brother-in-law neural network? And why wouldnt that go away either?
In his article in this issue of Philosophy, Psychiatry, & Psychology, Hadreas looks at questions
like these through the prism of before and after
effects of people treated with selective serotonin
reuptake inhibitors (SSRIs). Hadreas investigates
the implications of a straightforward recomputation of self-awareness when treated with these
medicines and finds such approaches unsatisfying
and incomplete in their explanatory power. (My
example looks at a type of awareness, but not
specifically self-awareness, as does Hadreas. Furthermore, my paradigm asks about computational
conclusions using language more common in psychiatric literature, whereas Hadreas uses standard
philosophical terms. Although not isomorphic, I
believe the interchange of the two remains true to
the issues Hadreas is addressing).

58 PPP / Vol. 17, No. 1 / March 2010

In my example, there is clearly something else

going on than the incorrect arrangement of symbols or the misfiring of nodes in a network that
influences how I feel and what I think. Neither
reason nor empiricism seem to serve me well here.
Hadreas utilizes Husserl to begin to unpeel the layers of self-awareness and self-states that intermix
to form the shifts and contradictions which are so
common in psychiatric treatment (and in common
experience as I describe).
This is a welcome reckoning; the psychiatric literature is overflowing with unquestioned
premises about the neuropsychiatric correlates
of reason and empirical approaches (described
more as computation and neural networks in
the literatureagain, not strictly analogous, but
the same criticisms apply) Hadreas is critical of.
Unfortunately, Hadreas has navigated through a
sea of highly questionable assumptions about the
psychopharmacology of depression to illustrate his
points. This is due in large part to the common
practice of consulting literary narratives and critics
rather than one of immersion in the literature as
a whole and the daily life of patients and active
clinicians. He arrived at his destination despite
this, because many of these details did not affect
his particular analysis. However, to look forward
to a continuation of this work and clarify some
important issues I devote most of my commentary to these issues. The points I raise are more
extensively discussed in a previous edition of this
journal (Rego 2005).

Affect to Reason Shift

Lets begin with the idea that SSRIs work by
dampening emotions. An extension of this idea is
that they dampen negative emotions and strengthen positive ones like assertiveness, confidence, and
optimism. An even further development in this
direction is that, by dampening strong emotions,
cognitive enhancement takes place with SSRI treatment. A summary observation then is that SSRIs
facilitate a shift from an affective state to a more
reasoned one.
There is much to say about each of these points
(particularly about affective blunting and personality improvement which are taken up below).
Much of this description is based on Kramers early

work in Listening to Prozac. Although Kramer

describes many of these changes in his patients,
he concludes that there is no personality-altering
property of SSRIs. Subsequent research and years
of experience have found him to be correct.
More to the point here is the change from an
affective to a cognitive state of mind. There is nothing unique to SSRIs, antidepressants, or anything
psychiatric about this type of mental shift. When
under stress, very worried, extremely fatigued,
traumatized, overjoyed, intoxicated, and so on,
the affective position predominates. When relieved
from these, a more volitional state can take over.
The relief can come in a pill, a nap, a friend, or
the passing of time. Even the noted improvement
in memory in SSRI subjects versus desipramine
subjects can be a misleading paradigm. It is easier
to be treated for depression by SSRIs than by
tricyclics like desipramine (the side effects and
toxicities of tricyclics make SSRIs much more
attractive). If degree of depression and burden of
side effects were taken into account, there would
be no difference between the two groups (in fact,
the anticholinergic effects of desipramine cause
memory impairment by themselves).

Affective Dampening
Rather than a mechanism of action of SSRIs,
this particular symptom is a well-known side
effect. It is known to be related to serotonergic
stimulation, but is not related to antidepressant
response. Patients may have more or less of this
effect and the complete opposite degree of antidepressant response. It is dose dependent and occurs
in a small minority of individuals. Interestingly, it
tends to occur in the same people with any SSRI
treatment, although a change of SSRI occasionally
remedies the problem.
In the office, this is an uncommon but problematic adverse effect of SSRIs. I mention it here
specifically to take it out of the analysis of SSRI
qua antidepressants. In addition to misunderstanding antidepressant effects, the affect dampening
assumption may lead to an over-attribution of
psychodynamic changes in patients as is made
by Healy and some of the authors quoted in the
paper.

Rego / Subjective Knowledge, Mental Disorders, and Meds 59

Effects in Normals
Another area of contention about SSRI treatment has been that they are mood elevators and
thus could produce improved moods in anyone.
The papers cited here are old and not in agreement
with more current studies (Furlan et al. 2004;
Gorenstein et al. 1998; Gelfin et al. 1998; Harmer
2003). I have made a more extensive argument the
mood elevator effect in a past issue of PPP. In fact,
many of the points made here are reviewed in this
paper (Rego 2005). For the purposes of this short
commentary, suffice it to say that there is little
to no evidence that SSRIs improve the moods of
people unafflicted by depression.

Suicidality and SSRIs

It was noted by the U.S. Food and Drug Administration (FDA) that SSRIs could produce
suicidality in children or adolescents. The study
performed was a meta-analysis of industry studies. This showed that within the first two weeks
of treatment (and not thereafter), there was an
increase of suicidal thinking (not acting) in more
subjects on the drugs than on placebo. Other studies have borne out this effect in this age group.
It is important to note here that this black
box warning does not lead to the possibility of
analysis of SSRI suicides, because the latter are
exceedingly rare, if they could be identified at all,
according to the very studies of the subject. Although several studies have now shown the same
effect as they FDA studies, none have shown an
increase rate of suicide or suicide attempts with
treatments. (In fact, the opposite is now under
consideration. As the number or prescriptions have
dropped in young people the number of suicides
have increased in the same group in several countries. A clear relationship has not been proven.)
If, in the original study by the FDA, venlafaxine
(Effexor) and paroxetine (Paxil), two very stimulating drugs, are removed from analysis, the effect
disappears.
The warning issued by the FDA should not be
taken lightly, but should be understood for what
it is. The fact that children and young people often respond differently than adults to psychiatric
medication has been known long before SSRIs.

This reflects partly a developmental effect, but

more important for treaters a recognition that
the full form of a disease, if there is a diseases at
all, is not likely to be fully manifest until early
adulthood. Consequently, you may not be medicating only what the child is currently complaining of. The more stimulating the drug, the more
likely anxiety, mania, psychosis, or impulsivity will
manifest. The same is true for adults, but this is
much easier to predict. A recent study in the New
England Journal of Medicine (Walkup et al. 2009)
compared, prospectively, the treatment of anxiety
in children and young adults. Various combinations of sertraline (Zoloft), cognitivebehavioral
therapy (CBT), and placebo were used. In the
medication groups (including 273 subjects), there
was no suicidal ideation or attempts, whereas there
was a 3.6% incidence of suicidal ideation in the
CBT group and no suicide attempts. Medication
with CBT offered the best outcome.
I include these comments to highlight the common but inaccurate assumptions regarding SSRIs
in the philosophical literature. That is, there is
little to no evidence that SSRIs are mood elevators,
mood dampeners, personality improvers, memory
enhancers, or suicide inducers. The reasons for
these effects are much more parsimonious than the
postulation of new actions of drugs that do not
currently exist (excluding drugs of abuse, which
could do all the things listed but not reliably, for
any sustainable period of time, nor safely).
To end, let me return to the corpus and purpose
of this paper. Awareness and self-state have a much
more complex and multilayered quality than current models in psychiatry or philosophy suggest.
Hadreas formulation of a pre-reflective model that
can account for these complexities, as well as for
dimensions such as intentionality, is an opening to
the way out of brain-as-computer theories.
From a psychiatric perspective, it would be
interesting and helpful to begin to weave the
normative functions that go awry into the prereflective space. Such things as mood, anxiety, and
executive capacity are clear candidates. Further
candidates await discovery; although we name
things like reality testing, we really do not have
a psychological or biological normative grounding
for what goes wrong in, this case, delusions. There

60 PPP / Vol. 17, No. 1 / March 2010

are of course many other examples likely waiting

in the pre-reflective, Husserlian mind.

References
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Gorenstein, C., V. Gentil, M. Melo, F. Lotufo-Neto, and
V. Lauriano. 1998. Mood improvement in normal
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