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A Gutsy Girl | Cornerstone Reference | Conditions that coincide with gut disorders

This is not a checklist telling you that you have 9 diseases. Most people who read this will find one or two rows that fit. That’s the point. It’s a tool for a better appointment, not a diagnosis.

Conditions That Commonly Coincide With Gut Disorders: The Complete Research Guide

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Before you read this

You were told you have IBS. Or SIBO. Or reflux.

And then nobody mentioned the migraines. Or the joint pain. Or the anemia that keeps coming back no matter how much iron you take.

That gap is what this guide fixes.

Gut conditions do not stay in the gut. The research on this is not new and it is not thin. It is just rarely handed to the patient. So I pulled it together in one place: what overlaps with what, how often, why, and what to actually ask your doctor to check.

For me personally, this is the guide I wish someone had put in my hands 20 years ago. I spent years treating IBS as a standalone problem when there was also SIBO, a low-functioning thyroid, “adrenal fatigue,” and motility issues underneath it. In order to fix a problem, you need to understand the cause of that problem. That applies to the conditions sitting next to your diagnosis too.

How to read the numbers

Three terms show up constantly below. Here is what each one actually means.

Prevalence. The percentage of people with condition A who also have condition B. “SIBO prevalence in systemic sclerosis is 39.9%” means about 4 in 10 people with scleroderma test positive for SIBO.

Odds ratio (OR). How much more likely the overlap is compared to people without the first condition. An OR of 3.0 means roughly 3 times the odds. An OR of 1.0 means no association at all.

Confidence interval (CI). The range the true number probably sits in. A tight range (2.4 to 4.1) is a more reliable finding than a wide one (9.7 to 37.2). When you see a wide interval below, I say so.

Note: a high odds ratio with a small absolute risk still means a small absolute risk. Both numbers matter.

Section 1: IBS

39.1% of people with IBS have anxiety symptoms. Almost none were told that.

IBS is the most studied overlap cluster in this entire guide, and the pattern is consistent. The conditions that travel with IBS are largely conditions of the nervous system and pain processing.

IBS and anxiety

Prevalence: 39.1% of people with IBS have anxiety symptoms (95% CI: 32.4 to 45.8). 23% meet criteria for a diagnosable anxiety disorder (95% CI: 17.2 to 28.8).

Odds ratio: 3.11 for anxiety symptoms versus healthy controls (95% CI: 2.43 to 3.98).

Source: Zamani M, et al. Systematic review with meta-analysis: the prevalence of anxiety and depression in patients with irritable bowel syndrome. Aliment Pharmacol Ther. 2019. 73 studies.¹

IBS and depression

Prevalence: 28.8% have depressive symptoms (95% CI: 23.6 to 34). 23.3% meet criteria for a depressive disorder (95% CI: 17.2 to 29.4).

Odds ratio: 3.04 for depressive symptoms (95% CI: 2.37 to 3.91).

By subtype: IBS-C carries the highest rates. 38% depression, 40% anxiety.

Sources:

• Zamani M, et al. 2019.²
• Hu Z, et al. The level and prevalence of depression and anxiety among patients with different subtypes of IBS: a network meta-analysis. BMC Gastroenterol. 2021.³

The one-line version: people with IBS have roughly 3 times the odds of anxiety or depression compared to healthy controls.

IBS and migraine

Prevalence: 25% to 50% of people with IBS report migraine or headache. In control groups the range is 4% to 19%.

Odds ratio: roughly 2.66.

The reverse direction: people with migraine develop IBS at a hazard ratio of 1.62 (95% CI: 1.29 to 2.03). The relationship runs both ways.

Source: Kim JH, et al. Systematic review and meta-analysis of calculating degree of comorbidity of irritable bowel syndrome with migraine. J Headache Pain. 2023.⁴

IBS and fibromyalgia

Prevalence: chronic pain comorbidities in fibromyalgia patients run 39% to 76%, a cluster that includes IBS, migraine, tension headache, and temporomandibular disorder.

Source: Kleykamp BA, et al. The prevalence of psychiatric and chronic pain comorbidities in fibromyalgia: an ACTTION systematic review. Semin Arthritis Rheum. 2021.⁵

IBS and endometriosis

The average endometriosis diagnosis takes years. ‘You have IBS’ is often the label during the wait.

This one is the most underdiagnosed overlap in the entire guide, and it is worth sitting with.

Prevalence: 23.4% of women with endometriosis meet IBS criteria (95% CI: 9.7 to 37.2). Individual studies range from 10.6% to 52%, which is why that interval is so wide. Treat 23.4% as a floor, not a precise figure.

Odds ratio: 2.97 versus healthy controls (95% CI: 2.17 to 4.06). Roughly 3-fold.

In adolescents: 24% of girls with endometriosis had comorbid IBS versus 7.1% without. OR 5.26 (95% CI: 2.13 to 13.0).

Sources:

• Nabi MY, et al. Endometriosis and irritable bowel syndrome: a systematic review and meta-analyses. Front Med. 2022. 96,119 subjects.⁶
• Saidi K, et al. Overlap between irritable bowel syndrome diagnosis and endometriosis in adolescents. Clin Gastroenterol Hepatol. 2020.⁷

Why this matters practically: the average delay to an endometriosis diagnosis is measured in years, and “you have IBS” is one of the most common labels applied during that delay. If your gut symptoms track your menstrual cycle, that is information.

If You Have IBS, Consider Screening For	What The Research Shows	Priority
Anxiety and depression	39.1% anxiety, 28.8% depression symptoms; ~3x odds	High
Endometriosis	23.4% pooled prevalence; OR 2.97	High
SIBO	31% test positive; OR 3.7 to 5.7	High
Bile acid diarrhea	41% pooled in IBS-D populations	High
Celiac disease	Standard exclusion in any IBS workup	High
Migraine	25% to 50% report it; OR 2.66	Moderate
Microscopic colitis	3% pooled prevalence	Moderate

Why IBS overlaps with all of these

Four mechanisms, and they compound.

1. The gut-brain axis is a two-way road. The enteric nervous system and the central nervous system talk constantly, through the vagus nerve, the HPA axis, immune signaling, and microbial metabolites. Gut inflammation changes brain signaling. Stress changes gut motility and permeability. Neither one is downstream of the other in a clean way.

2. Central sensitization. The nervous system turns up the volume on pain signals. Once it does, the amplification is not organ-specific. This is why IBS, fibromyalgia, migraine, interstitial cystitis, and TMJ pain cluster in the same people. Researchers group these as central sensitivity syndromes for exactly this reason.

3. Visceral hypersensitivity. Normal gut distension gets read as pain. Endometriosis and IBS both feature this, which is part of why they are so easily confused.

4. Shared genetics. GWAS work has found meaningful genetic overlap between endometriosis, IBS, migraine, and fibromyalgia.

IBS: testing considerations

Bring this list. Do not order it yourself.

Consider screening for	Why	How it is usually assessed
Anxiety and depression	~3x odds; drives long-term quality of life more than GI symptoms do	GAD-7, PHQ-9
Endometriosis	~3x odds; commonly mislabeled as IBS for years	Pelvic exam, imaging, gynecology referral; laparoscopy is definitive
Celiac disease	Standard IBS workup exclusion	tTG-IgA with total IgA, on a gluten-containing diet
SIBO	Pooled prevalence 31% in IBS	Glucose or lactulose breath test
Bile acid diarrhea	Pooled prevalence 41% in IBS-D populations	SeHCAT or 7C4 where available
Microscopic colitis	3% pooled prevalence	Colonoscopy with biopsy
Migraine	~2.7x odds	Clinical history

Source for the misdiagnosis rates: Black CJ, et al. A systematic review and meta-analysis on the prevalence of non-malignant, organic gastrointestinal disorders misdiagnosed as irritable bowel syndrome. Sci Rep. 2022.⁸

Make note: that last source is one of the most useful papers in this entire guide. It found that a meaningful share of people carrying an IBS label in secondary care have a treatable organic condition instead. Bile acid diarrhea at 41% is the headline. Most people have never heard of it.

Section 2: Ulcerative Colitis

Roughly 1 in 4 people with IBD develop at least one manifestation outside the gut. In UC specifically, the pooled figure for at least one joint, eye, or skin manifestation is 27%.

Source: Massano A, et al. Prevalence of extraintestinal manifestations in inflammatory bowel disease: a systematic review and meta-analysis. Inflamm Bowel Dis. 2024.⁹

UC and arthritis / spondyloarthritis

Prevalence: arthritis in UC runs about 7.1% (95% CI: 2.6 to 18.2). Arthralgia, meaning joint pain without confirmed arthritis, runs 18.4% (95% CI: 14.3 to 23.3). Musculoskeletal involvement is the single most common extraintestinal category across all IBD.

The important distinction: peripheral arthritis usually flares with bowel disease activity. Axial disease, meaning ankylosing spondylitis and sacroiliitis, runs on its own timeline independent of gut flares. That difference changes treatment.¹⁰

UC and primary sclerosing cholangitis

PSC is rare in the general population and much less rare in UC. It is a progressive bile duct disease and it carries real cancer surveillance implications, which is why it belongs on this list even though the percentage is small.

Prevalence: approximately 5% in pediatric UC cohorts (95% CI: 4 to 7). Adult figures vary by population.

Key point: PSC in UC does not follow gut disease activity. Your colitis can be in complete remission while PSC progresses.¹¹

UC and skin manifestations

Erythema nodosum: tender red nodules, usually on the shins. Roughly 2% in pediatric UC (95% CI: 1 to 4). Typically flares with bowel activity.

Pyoderma gangrenosum: painful ulcerating lesions. 1% or less. More common in UC than Crohn’s. Runs independent of gut activity.

Overall skin involvement in IBD: approximately 9.9% in one regional meta-analysis; the literature range across studies is 2% to 34%.¹²

UC and eye inflammation

Prevalence: uveitis and episcleritis at 1% or less in pediatric UC. In mixed adult cohorts, episcleritis and uveitis combined reach approximately 6.5%.

Crohn’s versus UC: the odds of uveitis are higher in Crohn’s than UC (pooled OR 1.603, 95% CI: 1.254 to 2.049).

This is the one that is genuinely time-sensitive. Episcleritis is irritating. Acute anterior uveitis can threaten vision and needs same-week ophthalmology, not a wait-and-see. Eye pain, light sensitivity, and blurred vision in someone with IBD is an urgent call.

Source: Lin CJ, et al. The prevalence of ocular extra-intestinal manifestations in adults inflammatory bowel disease: a systematic review and meta-analysis. 2022.¹³

UC and venous thromboembolism

Risk: IBD is associated with roughly a 2-fold increased risk of venous thromboembolic events.

Source: Papa A, et al. The risk of venous thromboembolic events in patients with inflammatory bowel disease: a systematic review and meta-analysis. 2021.¹⁴

Why it belongs in a patient guide: the risk is highest during active flares and hospitalization. Most patients are never told. Unilateral leg swelling, calf pain, or sudden shortness of breath during a flare is an emergency, not a wait-until-Monday.

Why UC overlaps with all of these

1. Shared immune pathways. The same immune activation driving colonic inflammation, particularly the IL-23/Th17 pathway, also drives joint, skin, and eye inflammation. These are not side effects of colitis. They are the same disease process showing up in different tissue.

2. Molecular mimicry and shared HLA associations. HLA-B27 links gut inflammation and spondyloarthritis. Bacterial antigens crossing a permeable gut barrier can trigger immune responses that cross-react with joint and eye tissue.

3. Bacterial translocation. A damaged barrier lets microbial products reach systemic circulation, which drives inflammation far from the colon.

4. Chronic inflammation shifts coagulation. Active IBD raises fibrinogen and platelets and lowers antithrombin. That is the VTE mechanism, and it is why risk tracks flare activity.

UC: testing considerations

If you have UC, consider screening for	Trigger to raise it	Typical assessment
Primary sclerosing cholangitis	Any abnormal liver enzymes, especially ALP	LFTs, then MRCP
Spondyloarthritis	Morning stiffness over 30 min, back pain improving with movement	Rheumatology referral, HLA-B27, imaging
Uveitis	Eye pain, redness, light sensitivity, vision change	Same-week ophthalmology
Anemia	Fatigue disproportionate to disease activity	CBC, ferritin, CRP, B12, folate
VTE	Leg swelling, calf pain, breathlessness during a flare	Urgent care, not routine
Bone density loss	Steroid exposure, long disease duration	DEXA
Colorectal cancer surveillance	8+ years of extensive colitis; earlier with PSC	Surveillance colonoscopy per guideline

Section 3: Crohn’s Disease

Crohn’s carries the highest extraintestinal burden of the IBD group. Pooled prevalence of at least one joint, eye, or skin manifestation: 35%.

One prospective cohort of 480 Crohn’s patients found the cumulative probability of extraintestinal manifestations rose from 22% at diagnosis to 40% at 10 years. It accumulates.¹⁵

Crohn’s and arthritis

Prevalence: 13.5% (95% CI: 2.6 to 47.3). That interval is very wide, reflecting real differences in how studies defined arthritis. The direction is reliable; the precision is not.¹⁶

Crohn’s and eye inflammation

Higher than UC. Pooled OR for uveitis in Crohn’s versus UC: 1.603 (95% CI: 1.254 to 2.049). In European populations the gap is larger still for both uveitis and episcleritis.¹⁷

Crohn’s and osteopenia / osteoporosis

Risk: pooled OR 1.32 for osteoporosis in IBD versus controls (95% CI: 1.2 to 1.4).

Source: Hidalgo DF, et al. Inflammatory bowel disease and risk of osteoporotic fractures: a meta-analysis. Cureus. 2019.¹⁸

Why Crohn’s specifically: small bowel involvement means malabsorption of calcium and vitamin D. Add repeated corticosteroid courses and chronic inflammatory cytokines that directly stimulate bone resorption, and you have three mechanisms stacking.

Crohn’s and SIBO

This overlap is large and routinely missed, because SIBO symptoms and Crohn’s symptoms are close to identical.

Prevalence: 32.2% of Crohn’s patients test SIBO-positive (95% CI: 25.9 to 38.8). Across all IBD it is 31.0% (95% CI: 25.2 to 37.1).

Odds ratio: 5.25 versus healthy controls (95% CI: 2.96 to 9.32).

Predictors within IBD: bloating (OR 3.02), flatulence (OR 4.70), prior abdominal surgery (OR 2.05), stricturing or penetrating disease behavior (OR 3.51), lower BMI.

Source: Zhang M, et al. Prevalence and predictors of small intestinal bacterial overgrowth in inflammatory bowel disease: a meta-analysis. 2025. 29 studies, 3,250 IBD patients.¹⁹

The clinical trap: ongoing bloating and diarrhea in a Crohn’s patient whose inflammatory markers look fine is often read as “your Crohn’s is worse than the labs suggest,” which leads to escalating immunosuppression. Sometimes it is SIBO, and SIBO is treated completely differently. That predictor list, especially prior surgery and stricturing disease, is the tell.

Crohn’s: testing considerations

Consider screening for	Trigger	Assessment
SIBO	Bloating or flatulence out of proportion to inflammatory markers; prior surgery; strictures	Glucose or lactulose breath test
Osteoporosis	Steroid exposure, small bowel disease, low BMI	DEXA, vitamin D, calcium
B12 deficiency	Ileal disease or ileal resection	B12, methylmalonic acid
Iron deficiency	Fatigue, heavy periods, active disease	Ferritin with CRP, transferrin saturation
Uveitis	Any eye symptom	Same-week ophthalmology
Spondyloarthritis	Inflammatory back pain	Rheumatology referral
Fat-soluble vitamin deficiency	Extensive small bowel disease or resection	Vitamin A, D, E, K

Section 4: SIBO

SIBO is less a standalone diagnosis than a consequence. Something upstream broke, usually motility, structure, or acid. That is why it recurs when only the bacteria get treated.

For me personally, my main issue with the recurring SIBO was slow motility. Treating the overgrowth without treating the motility meant it came back. Every time.

SIBO and IBS

Prevalence: 31% of IBS patients test positive (95% CI: 29.4 to 32.6) in a 2020 meta-analysis of 25 case-control studies covering 3,192 IBS patients and 3,320 controls.

Odds ratio: 3.7 versus controls (95% CI: 2.3 to 6.0). A more recent meta-analysis puts the pooled odds at 5.71 (95% CI: 3.45 to 9.45).

The test method problem, and it is a big one: prevalence estimates in IBS come out at 49% with the lactulose breath test (95% CI: 40 to 57) versus 19% with glucose (95% CI: 13 to 27). Aspirate culture gives 13% to 14%. Same patients. Same condition. Wildly different answers depending on the test.

Sources:

• Black CJ, et al. Sci Rep. 2022.²⁰
• Frontiers in Microbiology, 2026, 25 studies.²¹

Be honest about this one. Anyone quoting a single confident SIBO-in-IBS percentage is picking a test method and not telling you. The range is real. Lactulose overcalls; glucose undercalls distal overgrowth. This is why breath test results need a clinician who knows the limitations.

SIBO and systemic sclerosis

The single strongest association in this entire guide.

Prevalence: 39.9% (95% CI: 33.1 to 47.1) across 28 studies and 1,112 patients. A separate meta-analysis found 34% (95% CI: 27 to 42).

Odds ratio: 9.6 versus controls (95% CI: 5.6 to 16.5). Roughly 10-fold. A second meta-analysis found 12.51 (95% CI: 6.51 to 24.03).

Sources:^{22 23}

The mechanism is clean: scleroderma causes fibrosis of intestinal smooth muscle. The migrating motor complex, the wave that sweeps the small intestine clean between meals, stops working. Bacteria accumulate because nothing is clearing them.

SIBO and Crohn’s disease

32.2% (95% CI: 25.9 to 38.8). See Section 3.

SIBO and gastroparesis / motility disorders

Parkinson’s disease, as the clearest motility example: roughly half of Parkinson’s patients test SIBO-positive. Pooled OR 5.22 (95% CI: 3.33 to 8.19).

Diabetes: pooled SIBO prevalence 29% (95% CI: 20 to 39).

Sources: ^{24 25}

SIBO and celiac disease

This one is real, and it has a specific answer: SIBO is a recognized cause of celiac symptoms that persist despite a strict gluten-free diet.

Prevalence: the pooled mean across studies is 20% (95% CI: 10 to 30). But the number that matters clinically is higher. In celiac patients who still have symptoms on a gluten-free diet, pooled SIBO prevalence is 28% (95% CI: 10 to 47). In asymptomatic celiac patients it drops to 10%.

Odds ratio: 10.52 versus healthy controls (95% CI: 2.69 to 41.21). That interval is very wide, so read the direction, not the precision. The association is strong; the exact multiple is not nailed down.

The test-method split shows up here too: jejunal aspirate culture found 11% (95% CI: 3 to 19), while breath tests found 23% (95% CI: 10 to 37). Same pattern as everywhere else in this guide. The test you use changes the answer.

Source: Losurdo G, et al. Small intestinal bacterial overgrowth and celiac disease: a systematic review with pooled-data analysis. Neurogastroenterol Motil. 2017. 11 studies.²⁶

The practical version: if you have celiac disease, you are strict with gluten, your antibodies have normalized, and you are still bloated and symptomatic, SIBO is one of the first things to check. That is the scenario the 28% figure describes. It is common enough to belong at the top of the differential, not the bottom.

Why SIBO overlaps with all of these

Three defenses normally keep the small intestine relatively clean. SIBO shows up when one fails.

1. Motility. The migrating motor complex sweeps every 90 to 120 minutes between meals. Scleroderma, diabetic neuropathy, Parkinson’s, opioids, and post-infectious nerve damage all disable it. This is the dominant mechanism.

2. Stomach acid. Acid sterilizes what you swallow. Low acid, whether from atrophic gastritis, H. pylori, or long-term acid suppression, means more bacteria reaching the small intestine alive.

3. Structure. Strictures, surgical blind loops, adhesions, and an incompetent ileocecal valve all create places where bacteria pool.

Slow motility does not occur on its own. There is always a reason for it. Find the reason, fix the issue, and the recurrence problem gets much smaller.

SIBO: testing considerations

If SIBO keeps coming back, consider evaluating	Why
Gastric emptying	Gastroparesis and SIBO share a motility root
Thyroid function	Hypothyroidism slows transit
Autoimmune screen, especially scleroderma	~10x odds; ANA, anti-centromere, Scl-70
Celiac serology	Standard exclusion
Structural imaging	Strictures, adhesions, prior surgery, blind loops
Medication review	Opioids, anticholinergics, long-term PPIs
Diabetes screening	HbA1c; autonomic neuropathy is a motility cause

Section 5: Increased Intestinal Permeability

Handle this section with more care than the others. Barrier dysfunction is measurable and real in specific diseases. The popular version of “leaky gut” as a universal explanation for everything runs well ahead of what the research supports. I am going to tell you where the evidence is solid and where it is not.

Where the evidence is strong

Celiac disease. Gliadin triggers zonulin release, which opens tight junctions. This is well characterized and it is the clearest human model of the mechanism.

Crohn’s disease. Barrier dysfunction is documented in patients and, importantly, in their healthy first-degree relatives. That last detail suggests permeability can precede disease rather than only result from it.

Ulcerative colitis. Barrier dysfunction is present during active disease.

Where the evidence is developing

IBS. A subset of IBS patients show increased permeability, particularly post-infectious IBS and IBS-D. Not all IBS patients. Subset is the operative word.

Metabolic disease. Associations exist between barrier dysfunction and obesity, fatty liver, and type 2 diabetes. The direction of causation is not settled.

The mechanism, plainly

The intestinal lining is a single cell layer. Cells are joined by tight junction proteins, mainly occludin and the claudins, held in place by scaffolding proteins including ZO-1. On top sits the mucus layer, secretory IgA, and antimicrobial peptides.

Zonulin loosens tight junctions when released. Gliadin triggers it. So do certain bacteria. Inflammatory cytokines, particularly TNF-alpha and IFN-gamma, disassemble the junctions directly. Short-chain fatty acids from fiber fermentation, especially butyrate, fuel colonocytes and support the barrier, which is why microbiome composition matters here.

When the barrier loosens, bacterial products, particularly lipopolysaccharide, reach circulation. That drives systemic inflammation. Inflammation further damages the barrier. That is the loop.

The honest caveat

Permeability testing outside of research settings is not standardized and not clinically validated. Lactulose-mannitol ratios are a research tool. Serum zonulin assays have known specificity problems. Direct-to-consumer “leaky gut panels” are not diagnostic and I would not spend money on one.

Make note: treat increased permeability as a mechanism that shows up in specific diseases, not as a diagnosis you can go get and then treat. The productive move is finding and treating the underlying condition driving it.

Section 6: Gastroparesis

Gastroparesis and diabetes

Prevalence: pooled global estimate of gastroparesis in diabetes is 9.3%. By type: 12.5% in type 2 (95% CI: 7.7 to 17.3) and 8.3% in type 1 (95% CI: 6.4 to 10.2) in that meta-analysis.

The Olmsted County population data tells a different story, and the difference is worth understanding: 10-year cumulative incidence was about 5% in type 1 and 1% in type 2, versus 1% in controls. Hazard ratio 33 for type 1 (95% CI: 4.0 to 274, and yes that interval is enormous).

Why the two disagree: the meta-analysis pooled mostly symptom-based and clinic-based studies. The Olmsted data captured only people who presented for care and had formal gastric emptying testing. The meta-analysis catches more; the population data is more conservative. Reality sits between them.

Sources: ^{27 28}

In symptom terms: one study of type 2 diabetes patients found 44% had clinical features of gastroparesis. Early satiety 45.1%, stomach fullness 44.5%, bloating 38.3%, nausea 33.1%. Strongly linked to disease duration over 10 years, high HbA1c, and polyneuropathy.²⁹

Gastroparesis and autonomic neuropathy

The vagus nerve controls gastric emptying. Damage it and emptying slows. In diabetes this is a length-dependent autonomic neuropathy, which is why gastroparesis clusters with other autonomic signs: orthostatic hypotension, resting tachycardia, gustatory sweating, bladder dysfunction, erectile dysfunction.

Practical version: if you have gastroparesis symptoms plus dizziness on standing, get the autonomic picture evaluated as a whole, not organ by organ.

Gastroparesis and systemic sclerosis

Same fibrotic process described in Section 4, affecting the stomach as well as the small bowel.

Gastroparesis and SIBO

Direct causal chain. Delayed emptying means retained contents, which means bacterial proliferation. Roughly half of Parkinson’s patients, a population defined by impaired GI motility, test SIBO-positive.

Gastroparesis and neurologic disorders

Parkinson’s is the best-studied. Alpha-synuclein pathology appears in the enteric nervous system, often years before motor symptoms. Constipation and delayed gastric emptying are recognized prodromal features.³⁰

Gastroparesis: testing considerations

Consider evaluating	Why
Gastric emptying scintigraphy	The diagnostic standard; 4-hour protocol, not 90-minute
HbA1c and diabetes screening	The most common identified cause
Thyroid function	Hypothyroidism slows emptying
Autonomic function	Orthostatic vitals at minimum
SIBO breath test	Direct downstream consequence
Medication review	Opioids, GLP-1 agonists, anticholinergics all delay emptying
Scleroderma screen	If Raynaud’s, skin tightening, or reflux present

Note on GLP-1 medications: they delay gastric emptying by design. That is part of the mechanism. Symptoms that look exactly like gastroparesis in someone on a GLP-1 need that conversation with the prescriber first.

Section 7: GERD

GERD and hiatal hernia

Odds ratio for Barrett’s esophagus given hiatal hernia: 3.94 (95% CI: 3.02 to 5.13) for Barrett’s of any length. For long-segment Barrett’s specifically the OR is 12.67 (95% CI: 8.33 to 19.25). An updated meta-analysis using adjusted data found aOR 3.26 (95% CI: 2.44 to 4.35).

Source: Andrici J, et al. Hiatal hernia and the risk of Barrett’s esophagus. J Gastroenterol Hepatol. 2013. 33 studies.³¹

GERD and Barrett’s esophagus

Prevalence by population:

Population	Barrett’s Prevalence	95% CI
Low-risk general population	0.8%	0.6 to 1.1
Obesity (BMI over 35)	1.9%	1.2 to 3
GERD alone	3%	2.3 to 4
Age over 50	6.1%	4.6 to 8.1
Male sex	6.8%	5.3 to 8.6
GERD plus any other risk factor	12.2%	10.2 to 14.6
Family history of BE or EAC	23.4%	13.7 to 37.2

Source: Qumseya BJ, et al. Systematic review and meta-analysis of prevalence and risk factors for Barrett’s esophagus. Gastrointest Endosc. 2019. 49 studies, 307,273 individuals.³²

Read that table as a screening argument. GERD alone at 3% is not a strong indication for endoscopy. GERD plus one more risk factor at 12.2% is a different conversation. That is what “risk factor stacking” means in practice.

Progression risk: approximately 0.33% of Barrett’s patients progress to esophageal adenocarcinoma per year. The relative risk is high, the annual absolute risk is low. Both facts are true and patients deserve both.

GERD and obesity

Central adiposity raises intra-abdominal pressure, which mechanically promotes reflux and hiatal hernia formation. Visceral fat is also metabolically active and pro-inflammatory. Two mechanisms, not one.

GERD and asthma / respiratory symptoms

Two directions, both real. Microaspiration of refluxate irritates the airway directly. Separately, esophageal acid triggers a vagally mediated bronchoconstriction reflex without anything reaching the lungs. Asthma medications, particularly beta-agonists and theophylline, also relax the lower esophageal sphincter, which makes reflux worse. That is a loop worth naming out loud to your doctor.

GERD and esophagitis / stricture

Repeated acid exposure causes erosive esophagitis. Chronic inflammation causes fibrosis. Fibrosis narrows the lumen. Progressive difficulty swallowing solids is the symptom that should never be watched and waited on.

GERD: testing considerations

Consider evaluating	Trigger
Upper endoscopy	Alarm features: dysphagia, weight loss, anemia, vomiting, GI bleeding
Barrett’s screening	GERD plus 1+ risk factors (male, over 50, white, obesity, smoking, family history)
H. pylori testing	Region-dependent; discuss with your clinician
Hiatal hernia assessment	Part of endoscopy
Sleep study	Loud snoring plus nocturnal reflux; OSA and GERD travel together
Eosinophilic esophagitis	Dysphagia or food impaction, particularly with atopy
Manometry and pH study	Before any anti-reflux surgery; also for PPI non-response

Section 8: H. pylori

Iron that won’t come up, with no bleeding, is a reason to test for a stomach bacteria almost nobody checks.

Roughly half the world carries it. Most people never develop disease. The reason it matters is that the small percentage who do develop serious disease, and eradication changes that trajectory.

Global prevalence: approximately 48.5%. Range by country from 18.9% in Switzerland to 87.7% in Nigeria.

What actually develops in carriers

Outcome	Approximate risk among infected people
Duodenal or gastric ulcer	1% to 10%
Gastric cancer	0.1% to 3%
Gastric MALT lymphoma	under 0.01%

Source:³³

H. pylori and chronic gastritis

Essentially universal in carriers. H. pylori is the principal cause of chronic gastritis worldwide. Where it settles determines what follows: antral-predominant gastritis raises acid and tends toward duodenal ulcer, while corpus-predominant gastritis lowers acid and tends toward atrophy and cancer risk.

H. pylori and peptic ulcer disease

H. pylori colonizes approximately 80% of duodenal ulcers and approximately 50% of gastric ulcers. ³⁴

H. pylori and gastric adenocarcinoma

Classified by the IARC as a Group 1 human carcinogen. Infected people have 6 to 8 times the risk of non-cardia gastric cancer versus uninfected people, per the National Cancer Institute.

Note the direction reversal: H. pylori appears to decrease risk of esophageal adenocarcinoma and gastric cardia cancer, likely through reduced acid output. This is a genuinely complicated organism.

H. pylori and gastric MALT lymphoma

Infected patients are approximately 6 times more likely to develop MALT lymphoma. Absolute risk under 0.01%.

Worth knowing: early-stage gastric MALT lymphoma often regresses with H. pylori eradication alone. A cancer treated with antibiotics.

H. pylori and iron-deficiency anemia

Two mechanisms. Bleeding lesions cause obvious iron loss. Separately, H. pylori-associated gastritis causes refractory iron deficiency without any bleeding at all, through impaired iron absorption and bacterial iron sequestration.

One study found H. pylori-associated chronic gastritis, with no erosions or ulcers, in a meaningful share of patients with otherwise unexplained refractory iron deficiency.^{35 36}

This is the practical takeaway of the whole section. Iron deficiency that will not correct with supplementation, in someone with no obvious bleeding source, is a reason to test for H. pylori. That connection is missed constantly.

H. pylori: testing considerations

Consider	Note
Urea breath test or stool antigen	Preferred non-invasive tests. Must stop PPIs 2 weeks and antibiotics 4 weeks prior or you get false negatives
Endoscopy with biopsy	If alarm features present
Confirm eradication	4+ weeks after treatment. Do not assume it worked
Ferritin and CBC	Especially with unexplained iron deficiency
B12	Atrophic gastritis impairs absorption
Family screening	Discuss if a first-degree relative had gastric cancer

Important testing caveat: breath and stool antigen tests give false negatives at meaningful rates in atrophic gastritis, MALT lymphoma, bleeding ulcers, and during PPI or antibiotic use. If clinical suspicion is high and the test is negative, that is a conversation to have, not a closed case.

Section 9: The Master Cross-Reference Table

If you have	Consider screening for	Approximate strength	Priority
IBS	Anxiety / depression	~3x odds; 23% to 39% prevalence	High
IBS	Endometriosis (if female)	~3x odds; 23.4% pooled prevalence	High
IBS	SIBO	31% prevalence; OR 3.7 to 5.7	High
IBS	Bile acid diarrhea	41% in IBS-D populations	High
IBS	Celiac disease	Standard exclusion	High
IBS	Migraine	~2.7x odds	Moderate
IBS	Fibromyalgia	39% to 76% pain-condition clustering	Moderate
IBS	Microscopic colitis	3% pooled	Moderate
Ulcerative colitis	Spondyloarthritis	7.1% arthritis, 18.4% arthralgia	High
Ulcerative colitis	PSC	~5%; changes cancer surveillance	High
Ulcerative colitis	Uveitis	Time-sensitive; vision risk	High
Ulcerative colitis	VTE (during flares)	~2x risk	High
Ulcerative colitis	Erythema nodosum / PG	2% and under 1%	Moderate
Crohn’s disease	SIBO	32.2%; OR 5.25	High
Crohn’s disease	Osteoporosis	OR 1.32	High
Crohn’s disease	B12 deficiency	If ileal disease or resection	High
Crohn’s disease	Uveitis	Higher than UC (OR 1.6 vs UC)	High
Crohn’s disease	Spondyloarthritis	13.5%	Moderate
SIBO	Systemic sclerosis	39.9% prevalence; OR ~9.6	High
SIBO	Gastroparesis / motility	Direct causal mechanism	High
SIBO	Celiac disease	28% if symptomatic on GFD; OR ~10.5	High
SIBO	Thyroid dysfunction	Motility mechanism	Moderate
SIBO	Diabetes	29% SIBO prevalence in diabetes	Moderate
Gastroparesis	Diabetes	9.3% pooled prevalence in diabetes	High
Gastroparesis	SIBO	Direct downstream consequence	High
Gastroparesis	Autonomic neuropathy	Shared vagal mechanism	High
Gastroparesis	Systemic sclerosis	Fibrotic mechanism	Moderate
GERD	Barrett’s esophagus	3% GERD alone; 12.2% GERD + 1 risk factor	High
GERD	Hiatal hernia	OR 3.94 for Barrett’s	High
GERD	Sleep apnea	Bidirectional	Moderate
GERD	Asthma	Bidirectional; meds worsen reflux	Moderate
H. pylori	Iron-deficiency anemia	Refractory IDA without bleeding	High
H. pylori	Peptic ulcer	80% of duodenal ulcers	High
H. pylori	Gastric cancer	6 to 8x risk; 0.1% to 3% absolute	High
H. pylori	B12 deficiency	Via atrophic gastritis	Moderate

Section 10: Symptom Overlap

The reason these conditions get confused is that they share a symptom vocabulary. Here is where the confusion happens and what actually distinguishes them.

Bloating

Appears in: IBS, SIBO, gastroparesis, celiac, ovarian pathology, endometriosis, constipation.

The Bloating Pattern	Points Toward
Within 30 to 90 minutes of eating, worse with fermentable carbs	SIBO
With early satiety and nausea, worse with fat and fiber	Gastroparesis
Tracks the menstrual cycle	Endometriosis
Relieved by a bowel movement, with stool changes	IBS
Persistent early satiety plus weight loss	Needs ovarian evaluation

Abdominal pain

Appears in: nearly everything in this guide.

What distinguishes them:

• Relieved by defecation, associated with stool changes: IBS pattern
• Cyclical, worse around menstruation, with dyspareunia: endometriosis pattern
• Right lower quadrant, with weight loss and raised inflammatory markers: Crohn’s pattern
• Epigastric, related to meals, night waking: peptic ulcer pattern

Fatigue

Appears in: all of them, which makes it useless as a differentiator and important as a flag.

What to check: ferritin (with CRP, since inflammation falsely raises ferritin), B12, vitamin D, thyroid, and disease activity markers. Fatigue disproportionate to everything else deserves a workup, not reassurance.

Nausea

• With early satiety and vomiting undigested food hours later: gastroparesis
• With epigastric burning: gastritis or ulcer
• With migraine and light sensitivity: migraine, and the GI symptoms are part of the migraine

Joint pain

• Morning stiffness over 30 minutes, improves with movement: inflammatory, needs rheumatology
• Worse with activity, better with rest: mechanical
• Widespread, with tender points, sleep disruption, cognitive fog: fibromyalgia pattern

Skin changes

• Tender red nodules on shins: erythema nodosum, tracks IBD activity
• Painful ulcerating lesions: pyoderma gangrenosum, urgent dermatology
• Itchy blistering rash on elbows, knees, buttocks: dermatitis herpetiformis, essentially diagnostic of celiac

Section 11: Questions to Take to Your Appointment

Copy these. Save them. Adapt as necessary. Bring the specific one that fits.

What to do with all of this

Do not read this and conclude you have 9 conditions. That is not what the numbers say.

Read it, find the one or two rows that describe your actual pattern, and take those to a doctor who will look. The odds ratios in this guide are population statistics. Your job is not to diagnose yourself. Your job is to ask the question nobody thought to ask.

I have been the person sitting in an appointment with a list. It changes the appointment.

If you liked this article, you might also enjoy:

1. How to Heal SIBO: 5 Steps to Start (From Someone Who Did)
2. Shop by symptom
3. Where to start healing your gut: your step-by-step path

Xox,

SKH

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