Effects of anti-inflammatory drugs on the expression of tryptophan-metabolism genes by human macrophages, 2018, Freeman et al

Open access at https://www.researchgate.net/public...ptophan-metabolism_genes_by_human_macrophages

 

Interesting. However, the explanation may be way simpler than this.

If you look carefully at the research suggesting a link between inflammation and depression, you notice that only a subset of people with depression have evidence of inflammation, and only a subset respond to anti-inflammatory interventions. That subset are unusual in other ways too - on self-report measures of depression, they score particularly highly on "physiological" items (I feel tired all the time, I have difficulty concentrating, I have difficulty sleeping). And interventions that involve anti-inflammatory drugs tend to alter responses to these items specifically.

Also, although there's been some studies showing that placing people on interferon can lead to increased scores on self-report measures of depression, the majority of people on interferon score highly mostly on the physiological items. There is only a subset of people that reach clinical levels of depression and that tends to be those who have previously had a depressive episode.

My conclusion: inflammation is probably not linked with depression in the way we normally understand it, its probably associated with some other set of problems that look a bit similar, especially on self-report measures.

Sound familiar?

We need to sort out what depression is before we can start talking about what causes it. To me, it seems like it is a collection of pretty different conditions with different aetiologies.

(Edited to explain myself better)

 

Would it be fair to say that depression is a symptom that means a variety of things, some of which are experienced by healthy people, some of which may be secondary to various other conditions, and one or more which is a disease in its own right?