Life with IBD
If you have ulcerative colitis and you've ever Googled whether you can still have a glass of wine, or whether smoking might actually help your gut, you're far from alone. These are some of the most common questions UC patients ask, and the answers are more complicated than "just avoid everything." Here's what the research actually says about alcohol, smoking, nicotine, vaping, and cannabis when you're living with UC.
Alcohol and Ulcerative Colitis
Alcohol is probably the substance UC patients ask about most, and the evidence is fairly clear: it increases your risk of flares. A meta-analysis presented at DDW 2025 found that alcohol consumption was associated with a UC flare risk ratio of 2.62, meaning drinkers were roughly two and a half times more likely to experience a flare than non-drinkers.
The reasons are well understood at a biological level. Ethanol disrupts the intestinal epithelial barrier, the physical lining that keeps bacteria and toxins on the inside of your gut and away from your immune system. When that barrier becomes more permeable, luminal bacteria and endotoxins leak through and trigger an inflammatory cascade involving tumor necrosis factor-alpha, interleukin-1, and interleukin-6. The result can be mucosal ulcerations, crypt microabscesses, and the familiar symptoms of a flare. Alcohol also generates reactive oxygen species that cause additional oxidative damage to the colonic lining.
Beyond flare risk, alcohol interacts with many common UC medications. Methotrexate combined with heavy drinking raises the risk of liver damage. Immunosuppressants like thiopurines are metabolized through pathways that alcohol can disrupt. And because alcohol itself suppresses immune function while simultaneously driving inflammation, it can work against the medications designed to manage your disease. There isn't yet enough data to define a universally "safe" amount, but the research supports reducing intake, and many gastroenterologists advise avoiding alcohol entirely during active flares.
The Paradox of Smoking and UC
Here is where the evidence gets genuinely surprising. Unlike almost every other disease, where smoking makes things worse, current smoking is associated with a lower risk of developing ulcerative colitis. This isn't a fringe finding. Multiple meta-analyses over decades have confirmed the association, and a 2025 meta-analysis in Scientific Reports reaffirmed that current smokers have significantly lower odds of UC compared to non-smokers and former smokers.
The mechanisms behind this protective effect are becoming clearer. A 2025 study found that Streptococcus mitis, a bacterium influenced by smoking, triggers Th1 helper cells that counteract the Th2-driven immune response characteristic of UC, reducing colonic inflammation. Smoking also appears to enhance mucin production and strengthen the epithelial barrier, and it alters the gut microbiota in ways that may promote anti-inflammatory bacterial species like Lachnospira.
But before anyone considers picking up a cigarette, the caveats are critical. The protective effect is temporary and disappears after quitting, at which point the risk of UC actually rises above that of people who never smoked. Former smokers have a higher risk of developing UC than never-smokers, and they tend to have more extensive disease, more hospitalizations, and higher rates of surgery. The cardiovascular, pulmonary, and cancer risks of smoking vastly outweigh any gut-specific benefit. No gastroenterologist recommends smoking as a UC treatment.
Nicotine Without the Smoke
Because nicotine appears to be the active ingredient behind smoking's UC effects, researchers have tested nicotine patches as a treatment. The results are mixed but instructive. In a landmark trial published in the New England Journal of Medicine, non-smoking UC patients with active disease who wore nicotine patches for six weeks achieved complete symptom resolution in 48.6% of cases compared to 24.3% with placebo. A US trial found 39% clinical improvement with nicotine versus 9% with placebo at four weeks.
However, nicotine patches failed as maintenance therapy. A six-month trial in patients already in remission found no difference in relapse rates between nicotine and placebo groups. And when nicotine was compared head-to-head with standard medications, it didn't outperform them. Side effects were also significant: nausea, lightheadedness, tremors, headache, sleep disturbances, and skin irritation were all common. Nicotine patches remain a research curiosity rather than a recommended therapy, and they should not be used without medical supervision.
Vaping and UC: Almost No Evidence
If you're wondering whether vaping might deliver nicotine's potential benefits without smoking's risks, the honest answer is that the research barely exists. There have been no clinical trials studying e-cigarette use in UC patients. What little evidence does exist comes from animal models, and it's not encouraging. A study in rats found that e-cigarette exposure caused heavy colonic infiltration with inflammatory cells, suggesting that the non-nicotine components of vape liquid, including propylene glycol, vegetable glycerin, and flavorings, may independently damage the colon.
Because e-cigarettes are not standardized, nicotine concentrations vary between products and even between puffs. The additional chemicals used in vape liquids have not been tested for colonic safety. Until direct evidence exists, treating vaping as an untested exposure rather than a therapeutic option is the more cautious approach.
Cannabis, CBD, and UC
Cannabis use among UC patients is common. Surveys show that many patients use it to manage pain, nausea, and appetite loss, and several report symptom improvement. The research partially supports these observations, but with an important distinction.
A randomized controlled trial found that short-term treatment with THC-rich cannabis induced clinical remission and improved quality of life in patients with mild to moderately active UC. Patients reported less pain, better appetite, and fewer urgent bowel movements. However, this clinical improvement did not translate to reduced inflammation. Endoscopic scores and laboratory inflammatory markers showed no significant change. A Cochrane review concluded that no firm conclusions about the effectiveness or safety of cannabis for UC can be drawn from existing evidence.
This gap between how patients feel and what's happening at the tissue level matters. Feeling better without actually reducing inflammation means the disease can progress silently. Cannabis may have a role in symptom management alongside conventional treatment, but it is not a substitute for anti-inflammatory therapy. CBD-only products have even less evidence behind them for UC specifically, with most studies focusing on THC or whole-plant cannabis. Anyone considering cannabis for UC symptom management should discuss it with their gastroenterologist, particularly because cannabis can interact with immunosuppressants and other IBD medications.
Making Informed Decisions
The research on substances and UC doesn't fit neatly into simple rules. Alcohol has the clearest evidence for harm. Smoking has a real but paradoxical protective association that no one should act on given the broader health consequences. Nicotine patches showed promise for active flares but not for maintenance. Vaping is essentially unstudied. Cannabis may help with symptoms but does not appear to reduce the underlying inflammation.
What ties all of these together is that individual responses vary. Some UC patients can tolerate moderate alcohol without issues; others find that a single drink triggers symptoms within hours. The same variability applies to cannabis and nicotine. Tracking your own intake alongside your symptoms gives you data that's far more useful than general advice. Wondering how alcohol or other substances affect your UC? Track your intake alongside your symptoms in Aidy to see your personal patterns with real data.