| 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 My sense is that certain research topics are kind of ground zero in this misled, outdated mind-body war.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. |