LAW, ETHICS AND MEDICINE
Ethical issues in psychopharmacology
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J Med Ethics 2006;32:405–410. doi: 10.1136/jme.2005.013185
The marketing of selective serotonin reuptake inhibitors in
the psychopharmacological industry presents a serious
moral problem for the corporate model of medicine. In this
paper I examine ethical issues relating to the efficacy and
safety of these drugs. Pharmaceutical companies have a
moral obligation to disclose all information in their
possession bearing on the true risks and benefits of their
drugs. Only then can patients make fully informed
decisions about their treatment.
pharmaceutical industry has created corporate
psychiatry along with industry sponsored clinical
research, direct to consumer marketing of anti-
depressants, ghost writing for medical journals
and a major war for the market share. All the
trappings are in place for marketing the disease
rather than the cure. An illness intervention
industry with no serious ethical commitment to
health care threatens the most basic imperative
of the medical art—‘‘first, do no harm’’—and
demonstrates the weakness in the corporate
model of medicine.
California State University,
Northridge, Department of
Received 15 June 2005
In revised form
29 September 2005
Accepted for publication
30 September 2005
ow more than ever the moral and
scientific integrity of psychopharmacology
deserves closescrutiny.A behemoth
THE SEROTONIN HYPOTHESIS
The controversy over the serotonin hypothesis of
depression lies at the very heart of the matter.
Since, however, the pharmaceutical industry has
an enormous financial interest in protecting the
hypothesis, the problems with the theory are
seldom discussed and less likely to reach publica-
tion. The epistemological virtue of science as the
rigorous pursuit of truth has been corrupted by an
industry that manipulates the process to its own
advantage. Corporate psychiatrists become cocon-
spirators by accepting a paradigm uncritically and
by adopting the language game of chemical
imbalance that entirely satisfies this purpose.
The serotonin hypothesis is a monoamine
theory that advances the view that depression
is caused by neurotransmitter system deficits. It
was originally proposed in the late 1950s by
Edinburgh and gained further support from
Alex Coppen at Surrey and Herman van Praag
at Utrecht in the groundswell of early develop-
ments in biological psychiatry.1 2Low concentra-
tions of serotonin, 5HT (5-hydroxytryptamine)
or its main metabolite, 5-HIAA (5-hydroxyindole
acetic acid), were found in autopsy studies of
brains from suicide victims and in studies of
cerebrospinal fluid from depressed patients.3–6
Although it might appear that the develop-
ment of the new psychotropic drugs, the selective
serotonin reuptake inhibitors (SSRIs), was the
next logical step from the idea of serotonin
deficiency, the actual history shows otherwise.
The norepinephrine hypothesis of depression
(another monoamine theory), not the serotonin
hypothesis, was the leading idea that guided
research in psychopharmacology at the time,
especially in the United States. The SSRIs were
created when it became clear that drugs with an
action on the serotonin system had a recogni-
sably different effect from drugs active on the
norepinephrine system. SSRIs function in the
brain by blocking the breakdown or reuptake of
serotonin from the synapse into the transmitting
cell, thus leaving the serotonin active in the
synapse for a longer period.i‘‘Selective’’ in
‘‘SSRI’’ suggests that the drug’s action is clean
or precise, but this is misleading as the drug has
effects on a range of other neurotransmitter
Although the serotonin theory might offer a
compelling view within our physiochemical
model of the brain, its main problem is over
simplicity in the overall neurochemical scenario.
Even more to the point, however, it is probably
false. The fact of the matter is that there never
was a consistent body of evidence to support the
theory. George Ashcroft, who was one of the
pioneers in serotonin research, abandoned the
idea of lowered serotonin levels by 1970.
Ashcroft makes the crucial point: ‘‘What we
believed was that 5-HIAA levels were probably a
measure of functional activity of the systems and
not a cause. It could just as well have been that
people with depression had low activity in their
system and that 5-HIAA was mirroring that and
then when they got better it didn’t necessarily go
up.’’9With regard to Popperian and Kuhnian
explains the survival of the monoamine theories
despite a wealth of negative evidence. He
describes them as erected on a quicksand of
mistaken assumptions and apparently lacking in
the mortar of supporting evidence.10Although
there seems to be no question about the fact that
SSRIs act on the serotonin system, what has not
been established is an abnormality of serotonin
Abbreviations: FDA, Food and Drug Administration;
SSRI, selective serotonin reuptake inhibitors
iFor a view wholly favourable to the development of
SSRIs and their therapeutic benefits see P D Kramer’s
Listening to Prozac, especially chapter 3.7David Healy
offers an expanded history of this development and a
counterargument to over inflated claims of the benefits of
SSRIs in his Let Them Eat Prozac.8
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