In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and... 2024 Maes et al

Full title: In major dysmood disorder, physiosomatic, chronic fatigue and fibromyalgia symptoms are driven by immune activation and increased immune-associated neurotoxicity

Abstract

Major depressive disorder (MDD) is accompanied by activated neuro-immune pathways, increased physiosomatic and chronic fatigue-fibromyalgia (FF) symptoms. The most severe MDD phenotype, namely major dysmood disorder (MDMD), is associated with adverse childhood experiences (ACEs) and negative life events (NLEs) which induce cytokines/chemokines/growth factors.

To delineate the impact of ACE + NLEs on physiosomatic and FF symptoms in first episode (FE)-MDMD, and examine whether these effects are mediated by immune profiles. ACEs, NLEs, physiosomatic and FF symptoms, and 48 cytokines/chemokines/growth factors were measured in 64 FE-MDMD patients and 32 normal controls. Physiosomatic, FF and gastro-intestinal symptoms belong to the same factor as depression, anxiety, melancholia, and insomnia. The first factor extracted from these seven domains is labeled the physio-affective phenome of depression. A part (59.0%) of the variance in physiosomatic symptoms is explained by the independent effects of interleukin (IL)-16 and IL-8 (positively), CCL3 and IL-1 receptor antagonist (inversely correlated). A part (46.5%) of the variance in physiosomatic (59.0%) symptoms is explained by the independent effects of interleukin (IL)-16, TNF-related apoptosis-inducing ligand (TRAIL) (positively) and combined activities of negative immunoregulatory cytokines (inversely associated). Partial least squares analysis shows that ACE + NLEs exert a substantial influence on the physio-affective phenome which are partly mediated by an immune network composed of interleukin-16, CCL27, TRAIL, macrophage-colony stimulating factor, and stem cell growth factor.

The physiosomatic and FF symptoms of FE-MDMD are partly caused by immune-associated neurotoxicity due to T helper (Th)-1 polarization and M1 macrophage activation and relative lowered compensatory immunoregulatory protection.

Open access, https://www.nature.com/articles/s41598-024-57350-1

 

Is this interesting research from a respected team, or auto-generated from an immunology book, a psychology article in the People's Friend, and a Victorian novel?

I'm having one of those days where I can't tell.

 

The output from Maes and his varied co-authors tends to give the impression of the latter of those options.

 

I don't think you will find a physio-affective phenome in any of those much!

 

Umm, can we take a moment for the coinage of the word physiosomatic.

It regularly appears to me like peddlers of psychosomatics are so used to psychosomaticing illness that they seem to often use the word "somatic" as shorthand for "psychosomatic" instead of "physical", like it means "spontaneous physical symptoms out of thin air that are caused by the psyche and behaviour really".

And now they invent a new word that denotes that symptoms are actually physical in origin. You can't make this shit up.

 

One of the growing paradigms in AI is Mixture of Experts (MoE), a technique where various independent models are asked the same question and a general language model takes the various inputs and chooses what is most relevant in a single response.

I'm not sure this technique would give anything this incoherent, though. More like Mixture of Eminences.