Abdominal pain is one of the most common, most misunderstood and most stubborn symptoms in Crohn’s and ulcerative colitis. Around 70% of patients report it at diagnosis or during a flare, and a huge number continue to experience pain even when every test says “You’re in remission.”
This is why pain becomes such a big driver of fear, healthcare use, unnecessary medication and poor quality of life. If someone is hurting, they don’t care what their calprotectin says — they assume something is wrong. And unless you understand the physiology behind IBD pain, it’s easy to misread symptoms or miss the wider contributors entirely.
Abdominal pain in IBD is not a single mechanism. It’s an interplay between inflammation, structural complications, nervous system sensitisation, psychological load, diet, medications and previous surgical trauma. If you only treat one layer, the pain stays.
Let’s break it down properly.
Pain is one of the biggest reasons IBD patients seek medical help, miss work, restrict food or assume they’re relapsing. It also drives the use of medications that can worsen gut symptoms (NSAIDs, opioids, etc.).
Even more important
Pain can exist even when the bowel looks fine. Studies show that up to:
…still have ongoing abdominal pain without visible inflammatory activity.
So pain ≠ inflammation. And missing that nuance causes a lot of unnecessary fear.
Chronic abdominal pain in IBD has been linked to:
It also changes behaviours
People begin to avoid food, social events, exercise, intimacy and anything that “might trigger symptoms.” This fuels hypervigilance and keeps the pain pathways switched on.
This is why the psychological layer matters. Nervous system dysregulation amplifies visceral pain signals. Fear-based avoidance makes the system even more sensitive.
This pattern is common in Crohn’s, UC, IBS and any brain–gut disorder.
Here’s where most people go wrong. They try to pin pain on one factor. The research is clear — pain in IBD is multifactorial.
Active inflammation sensitises the nerves in the gut. Even mild inflammation can create significant pain for some people.
Remission doesn’t always remove the sensitisation straight away. Some people retain low-grade inflammation, even when their scopes look “good.”
All of these can produce mechanical or neuropathic pain.
Can happen when strictures or post-surgical anatomy slow gut transit. Often presents exactly like IBD pain, even without inflammation.
IBS rates double in IBD compared to the general population.
IBD + IBS overlap often explains pain in “remission”.
This is where the gut–brain axis becomes central. Hypervigilance, stress and previous traumatic flares can condition the nervous system to over-react to normal gut sensations.
Pain perception is not a purely physical process. The research shows increased anxiety, depression, somatisation, stress and catastrophising in IBD patients with pain even when the disease is quiet.
Fear changes pain pathways.
Stress amplifies visceral signalling.
Avoidance behaviours worsen sensitivity.
This is exactly why my psychological layer in MGHM exists.
FODMAP sensitivity, lactose intolerance, high-fat foods and specific irritants can trigger pain without inflammation.
IBD patients with chronic pain show differences in:
None of this is “in your head”. It’s neuroplasticity. Pain pathways can hard-wire.
When a patient with IBD reports abdominal pain, the job isn’t to jump to panic or assume a flare. The job is to get clear. Pain is a symptom with multiple potential drivers and the more precise you are about which driver is active, the better your intervention.
Most people skip this step which is why they stay scared, confused or overly medicated.
Here’s what a grounded, evidence-led assessment actually looks like.
Understand the pain properly
A good history does more than half the work. You want clarity on:
IBD pain comes in patterns. Once you learn the patterns, you stop guessing.
Use validated tools... but know their limitations
No survey has been built specifically to measure abdominal pain in IBD, but several IBD activity indices include pain scoring:
These are useful for trend monitoring but not for differentiating inflammation driven pain from brain–gut-driven pain.
They tell you how much, not why.
For more nuance, you can use tools like:
But again... helpful descriptors, not diagnostic answers.
Essentially, surveys are supportive data points. You still need clinical reasoning.
Test properly (not excessively) and combine data
History alone misses inflammation in a significant number of cases.
So you pair history with objective measures:
Useful but not diagnostic on their own.
If calprotectin is normal and stable over time, the likelihood of active inflammation is low, but not zero.
Used to detect:
The most sensitive tools include:
Still considered central for:
But even scopes can miss:
No single test can “rule out” inflammation.
The best approach is a multimodal assessment: symptoms + labs + imaging.
This is where most patients panic, most clinicians rush and most unnecessary medication changes happen.
If calprotectin is normal, imaging is clean and scopes are stable the priority shifts to exploring the non-inflammatory drivers:
Look for:
Extremely common and often missed.
Look for bloating, gas trapping, motility changes, fear-based food avoidance and symptom–stress correlation.
High FODMAP foods, under-eating, skipping meals, high-fat meals, fibre overload or under-consumption.
Anxiety, hypervigilance, catastrophising and unresolved trauma can amplify visceral pain circuits.
The research is clear:
IBD patients with anxiety, depression, or catastrophising experience far more pain — even in full remission.
Adhesions
Nerve entrapment
Hernias
Altered motility post-surgery
All of these create mechanical or neuropathic pain that won’t show up on lab tests.
Especially if:
Gallbladder, kidneys, pancreas all need consideration. IBD patients have increased risk.
This is the point where clients often spiral. The way you anchor them is simple:
“This is miserable, but it’s not dangerous. If I was worried, I’d tell you straight.”
Identify red flags early
These require urgent medical assessment:
Everything else tends to fall into the manageable category once you understand the mechanism.
What the evidence actually supports
Your clinical strategy should follow this order:
If there is active disease, pain will not settle until inflammatory load reduces.
Biologics, steroids, immunomodulators and nutritional therapy (exclusive enteral nutrition) can all reduce pain by reducing inflammation.
Strictures, abscesses, fistulas, adhesions, hernias — these often need surgical input.
NSAIDs and opioids are the biggest offenders.
Opioid-induced hyperalgesia and narcotic bowel syndrome are very real in IBD patients.
Low FODMAP
Lactose reduction
Gentle fibre modulation
Trigger mapping
Nutrient optimisation
This is where personalised guidance matters and not blanket restriction.
Tricyclics, antispasmodics, gabapentinoids, SSRIs/SNRIs and psychological therapies all have targeted roles but should be used intentionally, not scatter gunned.
This is the missing layer in most care pathways.
Pain circuits amplify when:
This is exactly where REWIRE Series™ sits:
Down-training the threat response → reducing pain sensitivity → restoring gut–brain balance.
Gentle reintroduction of foods, movement and normal routines prevents long-term sensitisation.
Clear explanation reduces fear. Fear reduction calms the pain pathways.
This is psychology + physiology... not mindset fluff.
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