I was a young doctor in 1990 when I met a patient with rheumatoid
arthritis. Mrs. P told me quietly but in no uncertain terms that she
ticked all the boxes for a diagnosis of co-occurring depression.
When I reported this to the senior physician in charge of her case, he
said: "Well, you would too, wouldn't you?" and changed the subject. He
meant that her mood was obviously a reasonable reflection on her current
state of disability and a future of inexorably deteriorating health
and mobility. Mrs. P was "understandably" depressed because she was
thinking about, and ruminating on, what it meant to have an inflammatory
disorder. And so there was nothing we physicians could do about it. It
was a matter of the mind, not of the body—the province of psychiatry.
Mrs. P's symptoms, which were intimately interconnected in her lived
experience of arthritis, were split apart by doctors into mental and
physical symptoms. Having diagnostically divided Mrs. P in two, we
proceeded to treat her physical disease—her swollen joints—in completely
different and disconnected way from her mental illness—her depression
and fatigue. We used the medical language of immune cells to treat her
inflammation, and a different team of doctors, in a different hospital, used the language of serotonin and psychotherapy to treat her depression.
Depression is a widely used word of many meanings. The
mainstream clinical sense today is similar to what the ancient Greek
physicians called melancholia—a syndrome of sadness or low mood, low energy, reduced capacity for pleasure (or anhedonia), reduced appetite for sex and food, pessimistic anticipation of the future, guilty rumination on the past, and a strongly self-critical bias in thinking that can lead to self-harming or suicidal behavior.
No question, it's depressing to be sick. But what if depression were
not strictly a disorder of the mind? The notion that Mrs. P might be
depressed because she was inflamed—not because she was thinking about
being inflamed—did not cross my mind in 1990, and such an idea would
have been medical bonkers even if I had been clever enough to conceive
of it back then.
But the notion is very much a matter of investigation today, a
centerpiece of the burgeoning science of neuroimmunology. And it not
only reflects a new way of looking at the disorder but also promises new
ways to treat it, to track it—even new measures to prevent it among
those whose life experience puts them at risk for developing it.
A New Path to Pathology
Epidemiological data put the prevalence of depression at
approximately 10 percent among the general population and significantly
higher among patients with rheumatoid arthritis (25 percent),
inflammatory bowel disease, psoriasis, chronic lung disease, or any
number of other inflammatory or autoimmune disorders. Advocacy groups,
like the National Rheumatoid Arthritis Society in the U.K., highlight
psychological symptoms such as depression, fatigue, and "brain fog," as
key areas of unmet need for many patients who have a physical disease.
Establishing that depression can be caused by inflammation somewhere
—anywhere—in the body demands much evidence. But it also requires more: a
radical shift in mindset, because it overrides one of the
distinguishing features of Western thinking—the deep fault line that
separates ideas about the workings of the body from those about the
workings of the mind.
Even now, in 2019, Mrs. P's experience is not uncommon. Many patients
with inflammatory disorders consult well-meaning specialist physicians,
like rheumatologists, who may recognize the symptoms of depression but
don't feel that they know how to treat them—or understand how they are
linked to the swollen joints that they do feel qualified to treat.
Physicianly disengagement from psychological symptoms is not surprising
in view of the mind-body split of Western medicine, but it is surprising
given that most physicians have some first-hand clinical experience of
the mood-boosting effects of anti-inflammatory drugs.
Steroids are among the most powerful anti-inflammatory drugs
available. They mimic the effects of cortisol, the body's own
anti-inflammatory hormone,
in counteracting the influence of immune activators called cytokines.
Steroid treatment is well known to cause rapid and dramatic improvements
in mood and energy (although such effects are generally not
long-lasting, and chronic steroid use can be associated with depression
and psychosis).
Antibodies against cytokines—one type is marketed as Remicade—have
been a dramatic advance in the treatment of inflammatory disorders in
the last 15 years. They very selectively target and disable inflammatory
hormones and often have an antidepressant effect—called "the Remicade high"—within a few days of treatment.
An antidepressant effect of anti-inflammatory drugs in patients with
comorbid depression—that's exactly what you'd expect if their depression
was directly caused by their inflammation. But it is not usually
explained that way. Instead, the Remicade high is seen as a placebo
response: The patients would have been equally uplifted if they thought
they were getting Remicade but got an innocuous substitute.
Placebo-controlled, randomized trials of anticytokine antibodies in
patients with arthritis, psoriasis, and inflammatory bowel disease have
often demonstrated mood improvements. But it has still been argued that
the mental health effects of anticytokine antibodies are a psychological
reaction to their physical health benefits: Patients are less depressed
because they have less joint pain and swelling and easier mobility. One
way or another, the antidepressant effects of anti-inflammatory drugs
in comorbid depression have been explained away as a function of the
disembodied mind.
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