It is no wonder that studies show higher rates of mental health complaints such as depression or anxiety during times of active relapse in Inflammatory Bowel Disease. 

The gut and the brain are connected in many ways, such as via the vagus nerve and connections via the immune system and other chemical signalling. 

On a basic level, having inflammation in the gut can lead to inflammation in the brain. 

There is cross-talk between the immune system in the gut (GALT) and the immune cells in the brain (microglia), as well as the gut microbiome manufacturing the vast majority of neurotransmitters. 

Dr Rachel has found in her practice that many mental health complaints coincide with flares of IBD or for others it can be significant gut inflammation not amounting to a diagnosis of IBD, accompanied by dysbiosis. 

Dr Rachel has found that fixing the gut inflammation leads to other problems resolving too. 

Autoimmune problems often start in the gut due to 70% of the immune system residing in the gut (GALT) & intestinal permeability leads to bacterial components, food antigens and LPS leaking over into the bloodstream to be picked up by the immune system - cue activation of an immune response in the body (which can include an immune response in the brain). 

Mitochondrial dysfunction, metabolic dysfunction & environmental toxins can all influence the microbiome to raise the risk of dysbiosis and 'leaky gut.'

Therefore taking a root-cause approach to address these issues can overcome even persistent gut inflammation and longstanding dysfunction. 

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.

• Daytime = activity, movement, digestion.
   
• Nighttime = rest, minimal motility.
   

This rhythm is controlled by two systems:

• The central clock in your brain (the suprachiasmatic nucleus or SCN), reset by light.
   
• Peripheral clocks in your gut lining, reset by food and metabolism.
   

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:

• Constipation: Your colon doesn’t wake up properly in the morning.
   
• IBS: Your bowel contractions lose their natural flow, making your gut hypersensitive and unpredictable.
   
• Heartburn at night: Your esophagus loses tone while you sleep.
   
• Slower digestion: Small intestine motility drops after dark.

• Diarrhea & running to the bathroom - increased gut motility.
   

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:

• Avoid excessive blue light from constant screen use
• Get natural light in the morning and throughout the day
• Avoid eating late at night - the gut is supposed to rest & repair overnight.  

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