CBD Could Treat Inflammatory Bowel Disease, Says New Study

Cannabidiol (CBD) can reduce the permeability of the human gastrointestinal tract and may help to treat conditions such as inflammatory bowel disease (IBD). 

After providing participants with the famously calming endocannabinoid and the endocannabinoid-like molecule palmitoylethanolamide (PEA), the researchers from the University of Nottingham, England found that the two molecules prevented inflammation-induced hyperpermeability in the subjects’ colons. 

The gastrointestinal tract acts a selectively permeable barrier that allows the body to absorb water and nutrients from food and drink, while simultaneously blocking the absorption of harmful bacteria and lipopolysaccharides. Inflammation of the gut can disrupt this delicate process and result in the harmful substances being erroneously absorbed, leading to conditions such as IBD. 

CBD for IBD

The most common symptoms of IBD include stomach pains and cramping, diarrhea, weight loss, and extreme tiredness. Recent figures from the US Centers for Disease Control and Prevention estimate that around 1.3 percent of American adults are currently living with a diagnosed IBD condition, the most common of which are Crohn’s disease and ulcerative colitis. 

The Nottingham researchers hypothesized that CBD and PEA would reduce inflammation-induced hyperpermeability in the human gut as they are both known for their anti-inflammatory effects.

Published in Plos One, the group’s recent research included a randomized, placebo-controlled, double-blind controlled trial to examine the potential of PEA and CBD to modulate intestinal permeability in humans.

In the trial, a temporary state of gut permeability was induced in patients using oral aspirin. The concentrations of lactulose and mannitol – sugars commonly used in constipation treatment – in the participants’ urine were determined using liquid chromatography-mass spectrometry (LC-MS). Urine samples were taken at regular intervals throughout the 6-hour study period.

In participants who received the placebo, there was an observable increase in the urinary concentrations of mannitol and lactulose, which reached a maximum peak two hours after being administered. Participants who were given both CBD and aspirin also showed an increase in urinary lactulose and mannitol content. However, the lactulose to mannitol ratio (LMR) was noticeably lower than the group who received a full placebo. 

D-mannitol is passively absorbed by the small intestine at a steady rate in a healthy body, whereas larger lactulose molecules can only be absorbed during episodes of inflammation. Both sugars are experience similar degradation in the gut before they are excreted, and so comparison of the ratios of both sugars present in urine samples should give a good picture of gut permeability during an episode of induced inflammation. LMR has previously been used to study intestinal permeability in Crohn’s disease. With this in mind, the decrease in LMR in the group receiving CBD and aspirin illustrates a resultant decrease in gut hyperpermeability when inflammation is treated with CBD. 

In the group receiving PEA and aspirin, there was also an observable increase in urinary lactulose concentrations (but not in mannitol concentration) during induced inflammation, but this increase was, again, lower than that seen in the placebo-only group.

Notably, six of the ten participants who received PEA and aspirin had mannitol levels that were undetectable, and so an LMR could not be calculated for these participants. But the other participants saw a significant decrease in LMR as seen in the CBD and aspirin group. 

CBD for Inflammation 

This is the first time that these cannabinoid and cannabinoid-like compounds have been shown to reduce intestinal permeability in vivo and may thus be potentially useful in the treatment of IBD and related conditions.

The researchers do also note several limitations of the study. Firstly, it is not guaranteed that aspirin provides a reliable simulation of gut inflammation like that in IBD, and so the effects of PEA and CBD may not translate in clinical studies. The necessary exclusion of the six participants with undetectable mannitol levels may also have skewed or exaggerated group differences for those receiving oral PEA. It could be that PEA itself was causing this decrease in mannitol levels, which would certainly have implications for the clinical use of PEA, or this may be down to an error in the LC-MS analysis. 

Ultimately, the paper demonstrates that CBD and PEA may have clinical relevance to the treatment increases in gut permeability. It is the recommendation of the researchers that the clinical effectiveness of CBD and PEA should now be investigated in phase one and phase two clinical trials.