4 ms·

It's also worth noting that there is no clear causal relationship. There is a strong and well-established association between depression and inflammatory biomar

It's also worth noting that there is no clear causal relationship. There is a strong and well-established association between depression and inflammatory biomarkers, but we have very little idea of whether depression increases the risk of inflammatory illness or vice-versa. http://www.mdedge.com/currentpsychiatry/article/76288/depression/depression-and-inflammation-examining-link http://www.mdedge.com/currentpsychiatry/article/76288/depres...

Reason077 9y ago
You'd think the answer would be easy to figure out. If you successfully treat the inflammatory illness, does the depression go away?
- smallnamespace 9y ago
  > If you successfully treat the inflammatory illness How do you know you completely succeeded?
  - jonlucc 9y ago
    This is not my field, but you can measure inflammation a couple of ways. One is by quantifying cytokines present and another one is to count blood cells.
- jdietrich 9y ago
  The answer to that question just muddies the waters further. Anti-inflammatory drugs have been shown to have some anti-depressant effect, while anti-depressant drugs have been shown to have some anti-inflammatory effect. In both cases, the effect size is fairly small. It would be nice to find a simple cure for a complex and diffuse set of symptoms, but we haven't had any luck so far. In all likelihood there are multiple interacting factors that affect the progression of depressive disorders, with no singular cause. http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2016167a.html?foxtrotcallback=true http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201616... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194072/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194072/
joools 9y ago
The research I'm familiar with (and teach) suggests you see associations prospectively in both directions, but no clear evidence of causality (although I've grown skeptical of causality as a concept). This PNAS paper is nice to see, although as some are pointing out, there's a bit of p-hacking probably going on. My sense is that certain research topics are kind of ground zero in this misled, outdated mind-body war. So you see people trying to demonstrate something along the lines of "see here, there's a biological basis to this, so patients aren't just inventing this," as if the psychosomatic conceptualization of the problem was ever just "inventing it," and as if people with psychogenic psychosomatic problems can't mimic the same things in their subjective reports (what happens when you do have this cytokine screen, and you still have people who look normal on that?) As you're alluding to here, the problem is that even if you do find inflammation markers it's difficult to tell if this is due to stress in a broad sense, and how these markers relate to perceptions of stress across a broad range of individuals. Just to take an example: how do these markers look in psychiatric patients who don't report CFS symptoms? I don't mean to suggest that these individuals have psychiatric problems, but it's unclear to me from this study what is going on with these inflammatory markers. Let's say these cytokines do cause increased pain and fatigue experience. Do CFS patients have a stronger relationship between those inflammatory markers and experienced pain? If so, what does that mean? The paper itself is more appropriate in tone than the NPR article, for what it's worth.
- JPLeRouzic 9y ago
  I am at the half of this long thread, comments are incredibly good and interesting --even for HN-- but yours seems to me outstanding. Thanks for taking the time to write it.
- pablobaz 9y ago
  Many CFS studies use patients with depression as a control for the very reasons you have suggested.

Reason077 9y ago

You'd think the answer would be easy to figure out. If you successfully treat the inflammatory illness, does the depression go away?

smallnamespace 9y ago
> If you successfully treat the inflammatory illness How do you know you completely succeeded?
- jonlucc 9y ago
  This is not my field, but you can measure inflammation a couple of ways. One is by quantifying cytokines present and another one is to count blood cells.
jdietrich 9y ago
The answer to that question just muddies the waters further. Anti-inflammatory drugs have been shown to have some anti-depressant effect, while anti-depressant drugs have been shown to have some anti-inflammatory effect. In both cases, the effect size is fairly small. It would be nice to find a simple cure for a complex and diffuse set of symptoms, but we haven't had any luck so far. In all likelihood there are multiple interacting factors that affect the progression of depressive disorders, with no singular cause. http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2016167a.html?foxtrotcallback=true http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201616... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194072/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3194072/

joools 9y ago

The research I'm familiar with (and teach) suggests you see associations prospectively in both directions, but no clear evidence of causality (although I've grown skeptical of causality as a concept). This PNAS paper is nice to see, although as some are pointing out, there's a bit of p-hacking probably going on. My sense is that certain research topics are kind of ground zero in this misled, outdated mind-body war. So you see people trying to demonstrate something along the lines of "see here, there's a biological basis to this, so patients aren't just inventing this," as if the psychosomatic conceptualization of the problem was ever just "inventing it," and as if people with psychogenic psychosomatic problems can't mimic the same things in their subjective reports (what happens when you do have this cytokine screen, and you still have people who look normal on that?) As you're alluding to here, the problem is that even if you do find inflammation markers it's difficult to tell if this is due to stress in a broad sense, and how these markers relate to perceptions of stress across a broad range of individuals. Just to take an example: how do these markers look in psychiatric patients who don't report CFS symptoms? I don't mean to suggest that these individuals have psychiatric problems, but it's unclear to me from this study what is going on with these inflammatory markers. Let's say these cytokines do cause increased pain and fatigue experience. Do CFS patients have a stronger relationship between those inflammatory markers and experienced pain? If so, what does that mean? The paper itself is more appropriate in tone than the NPR article, for what it's worth.

JPLeRouzic 9y ago
I am at the half of this long thread, comments are incredibly good and interesting --even for HN-- but yours seems to me outstanding. Thanks for taking the time to write it.
pablobaz 9y ago
Many CFS studies use patients with depression as a control for the very reasons you have suggested.