Altered Tryptophan Metabolism on the Kynurenine Pathway in Depressive Patients with Small Intestinal Bacterial Overgrowth, 2022, Chojnacki et al

Abstract

The causes of depression are diverse and are still not fully understood. Recently, an increasing role is attributed to nutritional and inflammatory factors. The aim of this study was to evaluate selected metabolites of the tryptophan kynurenine pathway in depressive patients with small intestinal bacterial overgrowth (SIBO).

The study involved 40 healthy people (controls) and 40 patients with predominant small intestinal bacterial overgrowth (SIBO-D). The lactulose hydrogen breath test (LHBT) was performed to diagnose SIBO. The severity of symptoms was assessed using the Gastrointestinal Symptom Rating Scale (GSRS–IBS) and the Hamilton Depression Rating Scale (HAM-D). The concentration of tryptophan (TRP), kynurenine (KYN), kynurenic acid (KYNA), and quinolinic acid (QA) in urine was determined using an LC–MS/MS method, before and after cyclic treatment with an antibiotic drug, rifaximin, for three months. The number of intraepithelial lymphocytes (IELs) in the duodenum and small intestinal mucosa, fecal calprotectin (FC) and serum level of C-reactive protein (CRP) were also determined.

In patients with SIBO, a higher level of KYN and QA were found as compared to the control group. These two groups also differed in KYN/TRP (higher in SIBO) and KYNA/KYN ratios (lower in SIBO). A positive correlation was found between HAM-D and the number of IELs and the level of FC. Treatment with rifaximin improves the kynurenic pathway, as well as abdominal and mental complaints. Therefore, small intestinal bacterial overgrowth can be a cause of abdominal symptoms, but also mental disorders.

Open access, https://www.mdpi.com/2072-6643/14/15/3217/htm

 

Interesting results, but their study really needed a control arm to show what they are claiming to show regarding depression.

 

Again following the pattern that the main issue with any research on "depression" is mostly unusable because it's a label slapped onto people for the sake of slapping that label.

Are those "depressed" patients? Or the same old pattern of a group of people with chronic health issues who have been labeled as being depressed for no other reason that depression is just as much a dumping ground of various patients as any discriminated chronic illness:

This is likely the main reason why the evidence is so uncertain, even in very large cohorts of "depressed" patients it's basically guaranteed that they are a heterogeneous group with various problems unified only by superficial labels based on nothing at all.

It reads differently but makes more sense if in any BPS research you simply search-and-replace "depression", MUS or FND with "things medicine doesn't understand yet".

This is simply not serious work. Nothing biopsychosocial is serious.

 

I definitely had the same question reading this (are the patients depressed or do they have other health problems that cause them to answer the questionnaires in that way), but I think the fundamental question here (can improving gut function improve mental state) is pretty reasonable. I'm not at all convinced that this study answers that question, but it's a reasonable one to ask.

This isn't BPS research at all; it's gut-brain axis research.