Surprisingly enough, this partially exposes the link between depression and some of the autoimmunal diseases. One example is how patients with psoriasis have significantly elevated levels of proteins from the IL-17 family (namely, IL-17A, IL-17C, and IL-17F) - up to 4 to 8 times above nominal values.<p>At the same time, bimekizumab, one of the bleeding-edge psoriasis and psoriatic arthritis treatments, suppresses production of IL-17A and IL-17F (methotrexate does that, too, albeit to a much smaller degree). As a result, people receiving IL-17 suppressors become happier over the course of years, and not only due to months-long remission - I had a chance to see this in one of the experimental treatment programs.
I read a study a while ago, the study found common vitamin deficiency in depressed humans.<p>I researched more about it and looks like some of the deficiency in the vitamins in the study are correlated with higher IL-17 levels.<p>Carnitine: Seems to have some effect in decreasing IL-17?<p>Vitamin D: Highly impacts IL-17 (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC4609465/" rel="nofollow">https://pmc.ncbi.nlm.nih.gov/articles/PMC4609465/</a>)<p>COQ10: Decreased plasma levels of IL-17 (<a href="https://www.clinicalnutritionespen.com/article/S2405-4577(22)01049-X/fulltext" rel="nofollow">https://www.clinicalnutritionespen.com/article/S2405-4577(22...</a>)<p>Folic Acid: Reduces IL-17 (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8839991/" rel="nofollow">https://pmc.ncbi.nlm.nih.gov/articles/PMC8839991/</a>)<p>Lutein: I didn't find any study that seems to study the effect on IL-17<p>Citrulline: No relevant studies<p>This is the study I'm referring to: <a href="https://www.nature.com/articles/s41398-023-02696-9" rel="nofollow">https://www.nature.com/articles/s41398-023-02696-9</a><p>I think we're getting closer to find some blood level correlations, so we can fix them!<p>I can say for a fact when I take CoQ10, I feel my energy levels going up so it really has some effect.
Related paper on receptors: <a href="https://www.cell.com/cell/abstract/S0092-8674(25)00279-X" rel="nofollow">https://www.cell.com/cell/abstract/S0092-8674(25)00279-X</a><p>Paper suggesting mood alteration: <a href="https://www.cell.com/cell/abstract/S0092-8674(25)00278-8" rel="nofollow">https://www.cell.com/cell/abstract/S0092-8674(25)00278-8</a>
Related paper on the immune system triggering anxiety: "Stress-Induced Metabolic Disorder in Peripheral CD4+ T Cells Leads to Anxiety-like Behavior" <a href="https://doi.org/10.1016/j.cell.2019.10.001" rel="nofollow">https://doi.org/10.1016/j.cell.2019.10.001</a><p>Related: "N-acetylcysteine as a new prominent approach for treating psychiatric disorders" <a href="https://doi.org/10.1111/bph.15456" rel="nofollow">https://doi.org/10.1111/bph.15456</a> section "2.3 Regulation of inflammatory mediators".<p>N-acetylcysteine (NAC) is considered safe and is sold as a diet supplement in USA and many other countries. If you suffer from anxious feelings, 1200mg/day NAC may reduce them a lot.
This is interesting! I've been having some pretty bad intermittent panic attacks over the past year or so and a thing I've noticed is that I have general inflammation across my body along with the panic attacks. For a long while I thought it was an infected tooth, but with that fixed and the panic attacks still ongoing, I'm not sure! But this is a nice confirmation that there's some correlation.
There are multiple theories that focus on different ethiologies of depression. Besides brain networks, early life adversities, sleep disturbances and the now obsolete monoamine hypothesis I read about the inflamation hypothesis. On a higher level that ties into all the other theories quite well and I don't oppose it. But there has been research into TNF-a, IL-6, IL-4, COX-2, and so on. We know there is inflammation, but we don't know where it starts and why. SSRIs are antiinflammatory in general, but why? Is this a downstream effect? Where is the original target we want to hit?<p>All those possible targets need to be verified by actual treatments. Treating the increased diabetes type 2 risk in depressed people is still advantagous but won't help the depression much. It's like changing tires on a broken car. Pushing is easier, but won't run by itself.
Possibly related to: <a href="https://en.m.wikipedia.org/wiki/Sickness_behavior" rel="nofollow">https://en.m.wikipedia.org/wiki/Sickness_behavior</a>
Interesting. I personally experienced such feelings during periods when my immune system was working to protect me. I find the part of the article where the dual function of our immune system emerges really interesting: on the one hand its job is to fight pathogens, on the other hand to communicate with our brain via cytokines to protect ourselves and the community we live in.
we should always start with the presumption that an effect like this is adaptive, as perhaps as simple as "when you're sick you should not sally forth to fight a dragon you heard about."<p>And while in the modern world we tend to think "well, we can <i>treat</i> this with <i>chemistry</i>", don't be shocked if that course uncovers undesirable side effects down the road, or even direct effects like "hey, you're not fighting infection as effectively".