Another really interesting paper was just published on the subject of the gut biome’s relationship to schizophrenia.[i] I first wrote about this subject back in 2017, and have kept a pretty close on in it since. Firstly, schizophrenia is very closely related to autism, so of course it peaks my interest. Secondly though, if you remember, my after-college roommate had a brother afflicted with the illness, and I’ve never forgotten his (and the whole family’s) suffering.
In this study, 63 patients with schizophrenia had their stool samples analyzed and compared to 69 healthy controls. Significant differences were found.
Firstly, those with the disease had less microbial diversity, with higher levels of several kinds of bacteria (including Veillonellaceae, Prevotellaceae, Bacteroidaceae, and Coribacteriaceae). They also had much lower levels of a variety of other species (including Lachnospiraceae, Ruminococcaceae, Norank, and Enterobacteriaceae).
The scientists then compared the microbiome profile of those with schizophrenia to those with major depressive disorder and found a distinct microbiota fingerprint that was unique to those with schizophrenia.
Now for the best part. The researchers took the fecal samples from the humans with schizophrenia and transplanted them into germ-free mice. They then ran a series of tests on the animals and discovered that, “Collectively, these behavioral tests showed that mice transplanted with SCZ [schizophrenia] microbiota displayed locomotor hyperactivity, decreased anxiety- and depressive-like behaviors, and increased startle responses, suggesting that the disturbed microbial composition of SCZ microbiota recipient mice was associated with several endophenotypes characteristic of mouse models of SCZ…” That is, the mice developed those behaviors associated with the known animal model of schizophrenia. They also found that there were disruptions in glutamate signaling which is generally thought to be relevant to the mental illness. (Glutamate abnormalities are also associated with autism and seizure disorders, among others.)
Of course, an animal model of schizophrenia is not a perfect parallel. But considering that by using fecal transplant, scientists have now been able to transfer (from humans) symptoms of depression, autism, obesity, etc. to mice, the evidence is mounting for microbiota alterations being, at the very least, a major factor in so many human illnesses.
How these microbiota alterations first develop is unknown, but in their discussion the scientists write, “In the context of these findings, several events shown to influence composition of the gut microbiome, especially during the microbiome’s establishment/dynamic period in infancy—e.g., cesarean versus vaginal birth, breast versus formula feeding, or early life antibiotic treatment—have all been associated, to some degree, with risk or onset of SCZ.” So once again, early life events and biome depletion likely play a central role in increasing the risk of developing the disease.
[i]Peng Zheng et al. The gut microbiome from patients with schizophrenia modulates the glutamate-glutamine-GABA cycle and schizophrenia-relevant behaviors in mice, Science Advances (2019). DOI: 10.1126/sciadv.aau8317