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In
the news ...
Link between serotonin and depression
The widely held
belief that depression is due to low levels of serotonin
in the brain - and that effective treatments raise these
levels - is a myth, argues a leading psychiatrist.
David Healy, Professor of Psychiatry at the Hergest
psychiatric unit in North Wales, points to a misconception
that lowered serotonin levels in depression are an
established fact, which he describes as "the marketing of
a myth."
The serotonin reuptake inhibiting (SSRI)
group of drugs came on stream in the late 1980s, nearly
two decades after first being mooted, writes Healy. The
delay centred on finding an indication.
After concerns emerged about tranquilliser dependence in
the early 1980s, drug companies marketed SSRIs for
depression, "even though they were weaker than older
tricyclic antidepressants, and sold the idea that
depression was the deeper illness behind the superficial
manifestations of anxiety," he explains. The approach was
an astonishing success, "central to which was the notion
that SSRIs restored serotonin levels to normal, a notion
that later transmuted into the idea that they remedied a
chemical imbalance."
In the 1990s, no one knew if SSRIs raised or lowered
serotonin levels, he writes; they still don't know. There
was no evidence that treatment corrected anything, he
argues.
He suggests that the myth "co-opted" many, including the
complementary health market, psychologists, and journals.
But above all the myth co-opted doctors and patients, he
says. "For doctors it provided an easy short hand for
communication with patients. For patients, the idea of
correcting an abnormality has a moral force that can be
expected to overcome the scruples some might have had
about taking a tranquilliser, especially when packaged in
the appealing form that distress is not a weakness."
Meanwhile more effective and less costly treatments were
marginalised, he says.
He stresses that serotonin "is not irrelevant" but says
this history "raises a question about the weight doctors
and others put on biological and epidemiological
plausibility." Does a plausible (but mythical) account of
biology and treatment let everyone put aside clinical
trial data that show no evidence of lives saved or
restored function, he asks? Do clinical trial data
marketed as evidence of effectiveness make it easier to
adopt a mythical account of biology?
These questions are important, he says. "In other areas of
life the products we use, from computers to microwaves,
improve year on year, but this is not the case for
medicines, where this year's treatments may achieve
blockbuster sales despite being less effective and less
safe than yesterday's models."
"The emerging sciences of the brain offer enormous scope
to deploy any amount of neurobabble. We need to understand
the language we use. Until then, so long, and thanks for
all the serotonin," he concludes.
The BMJ
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