The Gut-Brain Axis: A woman at a home office desk holding a glass of prepared Ozzi, with the pouch and a stick pack on the desk

The Gut-Brain Axis: What It Is and How to Actually Improve It (2026)

By Brandon, founder of Ozzi · Published July 17, 2026

TL;DR: The gut-brain axis is real, and most of what you've read about it is oversold. Your gut talks to your brain through the vagus nerve, hormones, and immune signaling, and there's decent human evidence that what happens in your colon changes how appetizing a cookie looks. The famous "95% of your serotonin is in your gut" line is technically accurate and almost completely misleading, because serotonin can't cross the blood-brain barrier.

What is the gut-brain axis?

The gut-brain axis is the two-way communication system linking your digestive tract and your central nervous system. It runs on four channels: the vagus nerve (fast electrical signaling), gut hormones like GLP-1 and PYY (slower chemical signaling through the bloodstream), immune and inflammatory messengers, and metabolites produced by your gut bacteria. Your gut microbiome sits on top of all four, shaping the signals your brain receives about hunger, fullness, stress, and reward.

How does your gut actually talk to your brain?

Diagram of the gut-brain axis showing L-cells, short-chain fatty acids, gut hormones and the vagus nerve connecting to the brain

The gut talks to the brain through several routes at once. The vagus nerve is the fastest one.

1. The vagus nerve (milliseconds)

The vagus is the long wandering nerve connecting your gut to your brainstem. Roughly 80% of its fibers run upward, gut to brain, which tells you who's doing most of the talking.

2. Hormones (minutes)

Your gut lining is studded with enteroendocrine cells that release hormones when food shows up. GLP-1 and PYY matter most for appetite. They travel through the blood and act on hunger circuits in the hypothalamus and brainstem.

This is the channel GLP-1 drugs work on, in a much louder way. Full mechanism in what GLP-1 actually is.

3. Immune signaling (hours to weeks)

Your gut houses a majority of your immune tissue. When the gut barrier gets leaky or the microbiome shifts, inflammatory cytokines rise, and those cytokines reach the brain.

4. Bacterial metabolites (hours to days)

Your bacteria ferment fiber and produce short-chain fatty acids: acetate, propionate, butyrate.

They feed your colon cells, they bind receptors on enteroendocrine cells, and some cross into circulation.

Does your gut really control your cravings?

Partly. And the best human evidence for it is a study most gut-health content skips, probably because the result is more complicated than the headline anyone wanted.

Researchers at Imperial College built a molecule that carries propionate to the colon and releases it there, which doses the colon directly instead of hoping fiber gets fermented into something useful. Then they ran it in people.

In the first trial, colonic propionate raised postprandial GLP-1 and PYY and cut energy intake at a test meal. Over 24 weeks, in 60 overweight adults, it reduced weight gain and visceral fat (Chambers et al., Gut, 2015).

The second one is the one I keep thinking about. Same team, 20 adults, fMRI crossover. They gave people colonic propionate and showed them pictures of high-energy food while scanning their brains.

Propionate reduced BOLD signal in the caudate and nucleus accumbens, the reward areas that light up when you want something. People rated the food as less appealing and ate less afterward (Byrne et al., Am J Clin Nutr, 2016).

Then the detail that almost never gets reported. The effect was not mediated by changes in plasma PYY, GLP-1, glucose, or insulin. The researchers measured all four. None explained the brain result.

So something other than GLP-1 is carrying that signal: possibly vagal, possibly direct SCFA action, possibly something not yet characterized. The honest answer is that we don't fully know.

A woman standing at an open refrigerator in a dark kitchen at night

The mouse study everyone cites as if it were human

When you read "SCFAs boost GLP-1," the source is usually Tolhurst et al., Diabetes, 2012. Short-chain fatty acids stimulate GLP-1 secretion via the FFAR2 receptor, and knockout mice lose the response.

Excellent study. It's mice and cell culture.

That distinction gets erased constantly. A mechanism that works in a mouse colon and a mechanism that works in your colon are two different claims, and only one of them has been tested. I go deeper in butyrate and GLP-1, including why I won't tell you butyrate raises GLP-1 in humans. No human study shows that.

What about serotonin? The 95% myth, corrected

Yes, about 95% of your body's serotonin is made in your gut. It still isn't what's making you happy.

Serotonin cannot cross the blood-brain barrier. This has been settled pharmacology for decades. The molecule is polar, it has no dedicated transporter at the barrier, and it stays where it's made.

Your gut serotonin and your brain serotonin are two separate pools. They never mix. The serotonin your enterochromaffin cells produce is doing gut jobs: gut motility, secretion, platelet function, nausea signaling.

What does cross the blood-brain barrier is tryptophan, the amino acid your brain uses to build its own serotonin locally. Tryptophan has a transporter. Serotonin doesn't.

An open canvas tote bag containing keys, a book, a water bottle and two Ozzi stick packs

What actually improves your gut-brain axis?

I graded these on human evidence quality, not on how often they show up in wellness content.

Intervention Grade Best human evidence The honest caveat
Fermented foods A- Stanford randomized trial, 17 weeks. High-fermented-food diet increased microbiota diversity and decreased inflammatory markers. 18 people per arm. Measured immune markers rather than cravings. No trial has shown it stops you eating crackers at 10pm.
Colonic SCFA delivery (propionate) A- Two human RCTs: raised GLP-1/PYY, cut energy intake, reduced 24-week weight gain and visceral fat, reduced brain reward response on fMRI. Used a purpose-built delivery molecule you can't buy. Eating fiber is not the same intervention.
Specific probiotic strains B L. rhamnosus HA-114 RCT, 152 adults: reduced binge eating, disinhibition, and food cravings during weight loss. Strain-specific. Did not increase weight or fat loss. This says nothing about "probiotics" as a category.
Plain added fiber C+ The high-fiber arm of the same Stanford trial missed its primary outcome. Cytokine response score was unchanged. Fiber is still good for you for other reasons. As a gut-brain lever specifically, it underperformed in the trial designed to test it.
Prebiotics for craving D Prebiotic fiber RCT, 50 adults with alcohol use disorder. The prebiotic fiber was no better than placebo on craving, anxiety, or depression. This is a direct negative result. Prebiotics have a defensible role as fermentation substrate. Craving reduction isn't it.

The practical version: eat fermented foods most days, get fiber from actual plants (for general health, not to fix your cravings), sleep, and don't buy anything sold on the serotonin stat. More in gut health and GLP-1 and the best fiber for appetite control.

Where does Ozzi fit into any of this?

Ozzi Crave Crusher is a cold-water drink stick. Per serving: allulose (8g), glucomannan (500mg), L-Lysine Butyrate (500mg), African mango extract (150mg), chromium (300mcg, as Metabolex). No berberine, caffeine, or stimulants. Vegan.

What I'll say: it's formulated around the viscous-fiber side of gut function, and it's designed to support satiety and help manage food noise.

What I won't say: that the butyrate in it raises your GLP-1. No human study shows that. The mechanism is real in mice and in cell studies, and mice aren't you.

If nighttime is your battleground, why you crave sugar at night and how to quiet food noise naturally are more useful to you than anything on this page.

Test it on yourself for 14 days

All I'll promise you is a fair test. 14-Day Ozzi Challenge: Take it for 14 straight days. If your cravings and food noise aren't quieter, we'll refund your first bag.

Try Crave Crusher

Gut-brain axis FAQ

Can improving my gut health stop my night cravings?

Honestly, I don't know, and neither does anyone selling you a confident yes. The best human evidence (colonic propionate reducing brain reward response on fMRI) suggests the gut-to-craving route is real. Whether the things you can actually buy move that dial enough to matter at 10pm isn't established. Nighttime cravings are the single biggest thing Ozzi customers mention, and they're driven by a stack of factors including sleep, stress, and daytime undereating. Food noise is rarely one mechanism.

About the author

Brandon is the founder of Ozzi, maker of Crave Crusher. He reads the primary literature because the summaries kept being wrong, and he answers questions about the formula (including the unflattering ones) in Reddit AMAs and in his inbox. Catch an error in this post and he'll fix it and credit you.

This article is for informational purposes and isn't medical advice. Ozzi Crave Crusher is a dietary supplement. It is not intended to diagnose, treat, cure, or prevent any disease. Talk to your doctor before starting any supplement, especially if you're on medication or managing a health condition.

References

  1. Chambers ES, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut. 2015. Human RCT (n=60, 24 weeks; n=20 acute). doi:10.1136/gutjnl-2014-307913
  2. Byrne CS, et al. Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods. Am J Clin Nutr. 2016. Human fMRI crossover (n=20). doi:10.3945/ajcn.115.126706
  3. Wastyk HC, et al. Gut-microbiota-targeted diets modulate human immune status. Cell. 2021. Human randomized trial, 17 weeks (n=18 per arm). High-fermented-food arm increased diversity and lowered inflammatory markers; high-fiber arm missed its primary outcome. doi:10.1016/j.cell.2021.06.019
  4. Berding K, et al. Feed your microbes to deal with stress: a psychobiotic diet impacts microbial stability and perceived stress. Mol Psychiatry. 2023. Human RCT (n=45). Between-group difference in perceived stress not statistically significant. doi:10.1038/s41380-022-01817-y
  5. Choi BS, et al. Lacticaseibacillus rhamnosus HA-114 improves eating behaviors and mood-related factors in adults with overweight during weight loss. Nutr Neurosci. 2022. Human RCT (n=152). Strain-specific; no effect on weight or fat loss. doi:10.1080/1028415X.2021.1965787
  6. Carbia C, et al. The Microbiome-Gut-Brain axis regulates social cognition & craving in young binge drinkers. EBioMedicine. 2023. Human observational (n=71). Correlational only. doi:10.1016/j.ebiom.2023.104442
  7. Amadieu C, et al. Effect of inulin supplementation on gut microbiota, alcohol craving and psychological symptoms in alcohol use disorder: a pilot randomized controlled trial. Gut Microbes. 2022. Human RCT (n=50). Inulin no better than placebo on craving, anxiety, or depression. doi:10.1080/19490976.2022.2007042
  8. Tolhurst G, et al. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes. 2012. Mouse and in vitro. Not human. doi:10.2337/db11-1019
  9. Kaelberer MM, Buchanan KL, Klein ME, et al. Neuropod Cells: The Emerging Biology of Gut-Brain Sensory Transduction. Annu Rev Neurosci. 2020. Rodent-derived. doi:10.1146/annurev-neuro-091619-022657
  10. O'Mahony SM, Clarke G, Borre YE, Dinan TG, Cryan JF. Serotonin, tryptophan metabolism and the brain-gut-microbiome axis. Behav Brain Res. 2015. Review (largely rodent-derived mechanism). The key tryptophan/kynurenine citation. doi:10.1016/j.bbr.2014.07.027
  11. Interaction of the Vagus Nerve and Serotonin in the Gut-Brain Axis. Int J Mol Sci. 2025. Review (rodent-derived circuit mapping). Gut 5-HT activates vagal afferents to NTS, then dorsal raphe and locus coeruleus. doi:10.3390/ijms26041188
  12. Medawar E, Villringer A, Witte AV. Impact of obesity and diet on brain structure and function: a gut-brain-body crosstalk. Proc Nutr Soc. 2022. Human (LIFE-Adult cohort, ~2,600). Mediation analysis: visceral fat affects brain tissue via systemic low-grade inflammation. doi:10.1017/S0029665122002786
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