阅读理解
Depression(抑郁) can be a destructive illness,
plaguing millions of people worldwide with feelings of sadness, hopelessness,
and fatigue. Despite numerous antidepressant drugs, as many as a third of
patients don't respond to medication. This has forced doctors to be more
creative in finding different treatments for the condition.
In the past two decades, researchers have tied depression to
a seemingly unrelated condition: inflammation(炎症), the body's natural response to
stress. It could rise from injury or inflection, or even emotional issues like
an unhappy marriage or problems at work. Some amount of inflammation is
generally beneficial, as it increases production of cytokines(致癌因子)，proteins that help us heal and protect
us from the effects of overwork.
But excessive cytokine levels, and the inflammation
they bring on, could come at a cost—a number of studies suggests that high
levels of cytokines could contribute to depression.
Cytokines can reach the brain several ways: directly through
the blood-brain barrier or indirectly by binding to nerve fibers elsewhere,
which send signals to the brain to produce the inflammation molecules. In the
brain, cytokines can disturb the production and release of several important
signaling chemicals, including serotonin, dopamine and glutamate, which help
control emotion, appetite, sleep, learning and memory. It's though that a lack
of serotonin activity in the brain causes depression; most antidepressants
increase the activity. But cytokines also have been shown to activate stress
hormone signaling in the brain, which man also serve to develop depression.
With all the evidence implicating inflammation in
depression, doctors have been anxious to test anti-inflammatory drugs as a
potential treatment. Four small studies published between 2006 and 2017 by
research groups in Europe and Iran found that adults diagnosed with depression
who took aspirin or another anti-inflammatory drug called Celecoxib, along with
an antidepressant, got more relief from feelings of sadness, hopelessness,
guilt and fatigue compared with those taking an antidepressant alone. However, Andrew
Miller, a professor of psychiatry at Emory University, thought something was
wrong in these small, limited studies. None of them looked at whether the
participants had to have high levels of cytokines before they'd see a benefit
from anti-inflammatory drugs. "Unfortunately,
much of the field has fallen into the trap of viewing inflammation as the
be-all, end-all," Miller says. He and his colleagues wanted to see whether
the effect of these drugs was limited to the depression patients with high
cytokine levels, or if it helped all people diagnosed with depression.
