“Anti-inflammatories for depression? Yeah, okay.”

“So I’m dialed-in on the meds that can help me manage my depression. But isn’t there more on the menu? I mean, let’s get creative here.”

Very dicey stuff, this meds biz. All you have to do is hit the comment section of any of my Viibryd articles. The frustration of “guinea-pig-itis” and crushing side effects is readily apparent.

So within the realm of meds, is there anything else that may help?

Here’s a smidge of new science I find interesting – and you may find hopeful and helpful.

“Anti-inflammatories for depression? Yeah, okay.”

This message was delivered to the June 2011 attendees of the International Congress of the Royal College of Psychiatrists…

The addition of an anti-inflammatory med to an antidepressant regimen may ramp-up efficacy.

Carmine Pariante, MD, PhD of Kings College’s (London) Institute of Psychiatry delivered the news. He went on to say five years worth of studies back him up.

In a statement to Medscape Medical News, Dr. Pariante said…

“Inflammation is a key element in the pathogenesis of depression, and using anti-inflammatory drugs is a novel strategy that uses a completely new antidepressant approach, finally, after 20 years of me-too drugs.”

“High levels of inflammation induce depressive symptoms, especially those that are more somatic, such as tiredness, loss of appetite, and disturbed sleep.”

By the way, did you catch his use of the term “me-too drugs?” I love it!

“This is based upon???”

According to Pariante, it’s well known that long-term illness is a trigger for depression. Okay, I can buy that. He then says individuals enduring chronic medical disorders also have high levels of inflammatory markers or cytokines.

A cytokine is a tiny protein released by a cell that has a specific effect on the interactions between cells or on cell behavior.

At the risk of losing you to biobabble, the cytokines include the interleukins (sounds like an Alps ski lodge), lymphokines, and the interferons. They’re involved with triggering inflammation and responding to infections.

Supporting his argument, Pariante  cites two studies that revealed an increase in depression when patients were given meds for hepatitis C and typhoid vaccinations. They’re both known to raise levels of inflammation.

He also cites an article that showed improved response rate and extended remission time for patients who added aspirin (a non-steroidal anti-inflammatory) to an SSRI (Prozac, Zoloft, Paxil, Celexa, etc.) regimen. These patients hadn’t responded to four weeks of solo SSRI treatment.

“Evolutionary biology. That’s an interesting angle.”

John Potokar, MD, a colleague of Dr. Pariante, shared a theory regarding how anti-inflammatories work in the relief of depression. He points out it’s all about evolutionary biology, which is responsible for depressive traits and inflammation.

According to Potokar…

“All the behavior that we call depression can also be seen in sickness behavior…the behavioral changes that occur during inflammation. It may be that humans evolved these behaviors as a protective mechanism.”

“An antibiotic too?”

It seems Dr. Pariante is also swirling around the idea of using the antibiotic minocycline as an add-on to an antidepressant. The goal, again, being a reduction in inflammation.

He says he chose minocycline because it’s cheap, well tolerated, and has been used for other emotional/mental health situations.

Now, it’s really important to emphasis that minocycline is primarily used as an antibiotic; however, the anti-inflammatory impact (which is counted on to reduce depression) is generated by a different characteristic/action of the med. So it isn’t about minocycline the antibiotic.

That’s actually comforting to know, because in 2009 the FDA (US) added minocycline to its Adverse Event Reporting System (AERS) – a list of medications under investigation by the FDA for potential safety issues.

The AERS cites a potential link between the use of minocycline products and autoimmune disease in pediatric patients.

Other antibiotics are being considered as antidepressant add-ons, as well.

“But didn’t I read somewhere…”

You may have caught this sub-heading in a March ’11 chipur article…

“NSAIDs Squash the Effects of SSRIs”

Seems a research team suggests non-steroidal anti-inflammatory drugs (NSAIDs) reduce the effectiveness of selective serotonin reuptake inhibitor (SSRI) antidepressants. The NSAIDs include aspirin, ibuprofen, and naproxene.

Knowing what I’d learned some four months ago, I was scratching my head when I read the new research. So I went back to the March article and found that the SSRI/NSAID issue especially involves seniors.

One other bit of, “Hmmm.” I wrote an update to the SSRI/NSAID piece two months later. In it I revealed that the interaction of an NSAID and an SSRI increases the risk of an upper GI bleed six-fold.

That Will Do It

Interesting stuff, don’t you think? And I believe these developments are incredibly important.

Sure, we just got Viibryd. But the next antidepressant of note (EB-1010) is likely 18 months away. So in the meantime, we need all of the creative interventions we can come up with.

If you’d like to try using an anti-inflammatory (or antibiotic?) as an add-on to your antidepressant, run it by your psychiatrist.

If you do, update us. I’d really like to know what she/he says – and how it works for you.

Thanks to medscape.com for the heads-up on the topic.

To catch a list of all chipur meds articles, click here.