It’s no surprise that people experience more depression and anxiety when their inflammatory bowel disease flares up.
The gut and brain are in constant communication through the vagus nerve, immune system, and countless chemical messengers.
When the gut is inflamed, that inflammation can spread systemically and reach the brain.
The immune system in the gut (GALT) talks directly with brain immune cells (microglia),
while the gut microbiome produces most of the body’s neurotransmitters - the same ones that regulate mood and focus.
In Dr Rachel’s practice, many clients notice their mental health symptoms worsen during IBD flares, or even with gut inflammation that doesn’t yet meet diagnostic criteria but is linked to dysbiosis.
When the inflammation is resolved at the root, other issues often fade away too.
Because 70% of the immune system sits in the gut, a leaky intestinal barrier allows bacterial fragments, food particles, and toxins like LPS to leak into the bloodstream - triggering immune activation throughout the body and brain.
Mitochondrial dysfunction, metabolic imbalance, and environmental toxins all contribute to this process.
That’s why Dr Rachel takes a root-cause approach, repairing the gut lining, restoring mitochondrial health, and rebalancing the microbiome - to help the body heal from the inside out.


Berger E, Rath E, Yuan D, Waldschmitt N, Khaloian S, Allgäuer M, Staszewski O, Lobner EM, Schöttl T, Giesbertz P, Coleman OI, Prinz M, Weber A, Gerhard M, Klingenspor M, Janssen KP, Heikenwalder M, Haller D.
Mitochondrial function controls intestinal epithelial stemness and proliferation.
Nature Communications. 2016; 7:13171.
doi: 10.1038/ncomms13171

Citation:Özsoy, M., Stummer, N., Zimmermann, F. A., Feichtinger, R. G., Sperl, W., Weghuber, D., & Schneider, A. M. (2022). Role of Energy Metabolism and Mitochondrial Function in Inflammatory Bowel Disease. Inflammatory Bowel Diseases, 28(9), 1443–1450. https://doi.org/10.1093/ibd/izac024​:contentReference[oaicite:1]{index=1}
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/35247048/PubMed

Sánchez-Quintero, M. J., Rodríguez-Díaz, C., Rodríguez-González, F. J., Fernández-Castañer, A., García-Fuentes, E., & López-Gómez, C. (2023). Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review. International Journal of Molecular Sciences, 24(23), 17124. https://doi.org/10.3390/ijms242317124
You’ve been told gut health is all about probiotics and fiber.
You’ve been told digestion is about what you eat (or perhaps even that diet doesn't matter).
You’ve been told constipation and IBS are “functional disorders” you just have to manage.
What if you’ve been misled?
Because here's the real story:
Your gut runs on a clock. And if you break the clock, you break the gut.
Let’s unpack the truth.
Your gut follows a strict 24-hour rhythm.
This rhythm is controlled by two systems:
These two clocks need to work together.
When they don’t? Digestive chaos follows.
When your circadian rhythm is disrupted — by shift work, jet lag, blue light at night, or irregular eating — your gut suffers.
Here’s what goes wrong:
In short, your gut gets confused about when to move and when to rest.
Result? Bloating, pain, irregular bowel movements, and inflammation.
Studies show genetic variants in circadian clock genes (CLOCK, BMAL1, PER, CRY) can slow down gut motility.
Melatonin — your night hormone — also plays a huge role in gut movement.
You produce 400 times more melatonin in your gut than in your brain.
When your clock is broken, melatonin production drops — and your gut pays the price.
This is biology, not bad luck.
Here’s the good news:
You can reset the clock.
You can get your gut back in sync.
The key is to work with your circadian biology, not against it.
Here’s how:
You must stop thinking of gut problems as random or “functional”. They are rhythm disorders.
Duboc, H., Coffin, B., & Siproudhis, L. (2020). Disruption of Circadian Rhythms and Gut Motility: An Overview of Underlying Mechanisms and Associated Pathologies. Journal of Clinical Gastroenterology, 54(5), 405–414. https://doi.org/10.1097/MCG.0000000000001333
