Study Explains Why Depression Can Strike Again
Finds 'trait marker' in people recovered
from depression
Physicians and patients have long known that
people who have a major
depressive episode have a greater risk for suffering another. These people,
although ostensibly recovered, also remain unusually
sensitive to emotional
stress.
Now researchers reporting in the November 2002
issue of the American Journal of Psychiatry have identified what may be
a "depression trait marker" in the brain which explains why patients
who have recovered nevertheless remain vulnerable to another depressive
episode.
And in a second study released today, another
research team says it has identified the first gene that leaves
women vulnerable to clinical
depression.
"Depression is not a single event for many
people and each episode, if you're lucky, can be treated and you can be well,
but depressed patients know that they are at risk for more episodes," says
Dr. Helen Mayberg, lead author of the "trait marker" study and a
professor of psychiatry and neurology at the University of Toronto. "The
question is what about your
brain seems to be the area of vulnerability."
Previous research has already demonstrated that
the brains of depressed people work
in different ways than healthy people. This study takes the concept
further.
It "goes to a new level because it talks
about people who have recovered from depression or who have been treated. Their
brains are functioning differently, and it's a question of why they're
functioning differently," says Dr. Kenneth Skodnek, chairman of the
department of psychiatry and psychology at Nassau University Medical Center in
East Meadow, N.Y. "This is special because I believe this is the first
time that there has been evidence even when someone recovers that the brain is
still not functioning normally."
In this study, researchers asked 25 adults to
remember an extremely sad experience in their life, then scanned their brains
with positron emission tomography (PET) while they recalled the event.
The participants belonged to one of three
categories: 10 women who had recovered from a major depression (nine were on medication
and one was not); seven women who were at that time
in the throes of
a major depressive episode (only one was on
antidepressant
medication); and eight healthy women who had no personal or
family history of
depression.
The scans, which measure blood flow, showed
that the brains of the recovered patients and currently depressed women
experienced different changes than the brains of the healthy
participants.
"We saw that recovered patients looked for
all intents and purposes like acutely depressed patients and that there were
some very specific areas of the brain that changed uniquely in depressed
patients that we don't see in healthy subjects and vice versa," Mayberg
says. "Under that emotional stressor, the recovered depressed patients
looked like the worst depressed patients. When we stressed healthy subjects'
brains, we didn't see any decrease in brain activity."
Specifically, the subgenual cingulate and the
medial frontal cortex areas of the brain were involved. The subgenual cingulate
has already been identified as being involved in the experience of intense
sadness even in healthy individuals. It is also a target of antidepressant
medication.
"These people are different even when
they're treated," Skodnek says. "It's almost like someone comes in
with congestive heart failure, you treat them" and the heart appears to be
doing OK. "But if you know what's going on with the heart, it's not
OK."
Whether the differences in brain function are a
cause or effect of a previous depressive episode remains unknown.
Nevertheless, this research and future studies
it spawns will have important implications for identifying people at risk for
depression and in identifying new targets for drug therapy.
Although this appears to be a trait marker for
depression, Mayberg is careful not to overstate the case. "I wouldn't want
anyone to think we've got the glucose tolerance test for depression," she
says.
Meanwhile, researchers at
the University of Pittsburgh say they've found evidence that a gene in
chromosome 2q33-35 leaves women at a
higher risk for depression. However, they found no such correlation in men,
suggesting that vulnerability to the disease is at least in part influenced by
one's gender.
Source: HealthScout News, Oct. 31,
2002
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