Coeliac disease
Based on Wikipedia: Coeliac disease
Here's something unsettling to consider: you might have a disease that's slowly damaging your body, and you've simply gotten used to feeling unwell. Many people with coeliac disease spend years—sometimes decades—assuming their fatigue, brain fog, and digestive troubles are just normal life. It's only after they eliminate gluten and start feeling genuinely healthy that they realize what they'd been missing all along.
Coeliac disease is one of medicine's great masqueraders.
It can present as chronic diarrhea in a toddler, unexplained anemia in a teenager, osteoporosis in a thirty-year-old, or persistent headaches in someone who's otherwise healthy. It can cause infertility, liver problems, neurological symptoms, or nothing at all—at least nothing obvious. This chameleon-like nature makes it both fascinating and frustrating, often leading to diagnostic delays that span years.
What Exactly Is Coeliac Disease?
At its core, coeliac disease is a case of mistaken identity by your immune system. When someone with a genetic predisposition eats gluten—a protein found in wheat, barley, and rye—their immune system doesn't just ignore it the way most people's do. Instead, it treats gluten as a dangerous invader and launches an inflammatory attack.
The battlefield is the small intestine, specifically its lining.
Your small intestine isn't smooth inside. It's covered with millions of tiny finger-like projections called villi, which dramatically increase the surface area available for absorbing nutrients. Think of them like the pile on a carpet, maximizing contact with whatever passes through. In coeliac disease, the immune system's inflammatory response damages these villi, flattening them over time. Less surface area means less absorption. Less absorption means nutritional deficiencies, even when you're eating well.
This isn't an allergy. Allergies involve a different part of the immune system—they're typically immediate reactions involving antibodies called immunoglobulin E. Coeliac disease is an autoimmune condition, meaning the body is attacking its own tissues. It's more akin to type 1 diabetes or rheumatoid arthritis than to a peanut allergy, though the trigger happens to be something you eat.
The Genetic Lottery
You can't develop coeliac disease without the right genes. Almost everyone with the condition carries one of two genetic variants: Human Leukocyte Antigen DQ2 (found in about ninety percent of cases) or Human Leukocyte Antigen DQ8 (found in most of the remaining cases).
But here's where it gets interesting.
About forty percent of the general population carries one of these variants, yet only a small fraction develop coeliac disease. Having the gene is necessary but not sufficient—something else has to flip the switch. Researchers believe environmental factors play a role: infections, the composition of gut bacteria, even the timing and amount of gluten introduced during infancy. The disease seems to require both genetic susceptibility and environmental triggers, though we don't fully understand what that second piece looks like.
This genetic requirement creates an evolutionary puzzle. Coeliac disease causes serious health problems and can affect fertility. Natural selection should have eliminated these gene variants over thousands of years. Instead, they're most common in populations that have been eating gluten-rich grains the longest. One theory suggests that the Human Leukocyte Antigen DQ2 gene might have provided an advantage that outweighed its drawbacks—possibly protection against tooth decay, of all things. Evolution often involves such trade-offs.
Classic Versus Non-Classic: Two Faces of the Same Disease
Doctors used to think coeliac disease looked one way: a young child with chronic diarrhea, a swollen belly, and failure to thrive. This "classic" presentation still exists and remains the most recognizable form. The child has pale, voluminous, foul-smelling stools—the kind that make parents wince. They're losing weight or not gaining it properly. They might be irritable and lethargic.
Then researchers realized that classic coeliac was just the tip of the iceberg.
Non-classic coeliac disease—more commonly seen in adults—plays a different game entirely. The primary symptoms happen outside the gut. Someone might present with unexplained iron-deficiency anemia that doesn't respond to supplements. Or osteoporosis at an age when their bones should be strong. Or infertility, recurrent miscarriages, chronic fatigue, joint pain, headaches, or what's colloquially called "brain fog"—a persistent mental haziness that makes concentration difficult.
The digestive symptoms, if present at all, might be vague: occasional bloating, mild abdominal discomfort, nothing dramatic enough to warrant serious investigation. Many people with non-classic coeliac disease have been diagnosed with irritable bowel syndrome and told their symptoms are just stress, or their imagination, or something they need to learn to live with.
The Diagnostic Journey
Getting diagnosed with coeliac disease can feel like solving a mystery novel where half the clues are missing. The average time from symptom onset to diagnosis has historically been measured in years—sometimes more than a decade.
The process typically starts with blood tests that look for specific antibodies. The most useful is tissue transglutaminase antibody, often abbreviated as tTG-IgA. If this test is positive, the next step is usually a biopsy of the small intestine, performed during an upper endoscopy. A gastroenterologist threads a thin tube through your mouth, down your esophagus, through your stomach, and into the first part of your small intestine, where they snip tiny tissue samples.
Under a microscope, a pathologist looks for the telltale signs: damaged villi, increased inflammatory cells, and the architectural changes characteristic of untreated coeliac disease.
Here's the catch: you must be eating gluten for these tests to work.
If you've already eliminated gluten from your diet—perhaps because you suspected it was causing problems—the immune response quiets down. Your antibody levels drop. Your intestinal lining begins to heal. The tests come back negative, and you're left wondering if you really had coeliac disease at all. For an accurate diagnosis in someone already avoiding gluten, doctors often recommend a "gluten challenge": deliberately eating gluten for several weeks before testing. It's unpleasant for someone who reacts badly to gluten, but it's often the only way to get a definitive answer.
The Spectrum of Severity
Coeliac disease doesn't affect everyone equally. Some people are exquisitely sensitive—a crumb of bread can trigger days of symptoms. Others seem to tolerate small amounts of gluten with minimal apparent effect, though the intestinal damage may still be occurring silently.
There's also a subset of people with what's called "potential coeliac disease." They have the antibodies in their blood, but when doctors biopsy their small intestine, it looks normal. They're at risk—possibly in an early stage of the disease—but they haven't yet developed the classic intestinal damage. What to do with these patients is debated. Some doctors recommend they adopt a gluten-free diet as a preventive measure; others suggest watchful waiting.
At the other end of the spectrum is refractory coeliac disease, a rare and serious form where the intestine continues to be damaged even after twelve months of strict gluten avoidance. Type one refractory disease looks similar to untreated coeliac disease under the microscope; type two shows abnormal cell changes and carries a higher risk of complications, including a rare type of intestinal lymphoma.
Between these extremes are the "slow responders"—people whose symptoms persist despite their best efforts to avoid gluten. Most of them don't have truly refractory disease. Instead, they're accidentally consuming hidden gluten (it lurks in surprising places), or they have a second condition contributing to their symptoms, or their intestines simply need more time to heal.
Gluten: The Trigger Explained
Gluten isn't a single protein. It's actually a family of proteins found in certain grains, primarily the storage proteins that help seeds nourish new plants. In wheat, the main culprits are called gliadins and glutenins. Barley has hordeins. Rye has secalins. These proteins share enough structural similarity that the immune system of someone with coeliac disease reacts to all of them.
The problematic grains belong to a botanical group called the tribe Triticeae. This includes not just common wheat, but also its ancient relatives and hybrids: spelt, durum wheat (used in pasta), khorasan wheat (marketed as Kamut), and triticale (a wheat-rye hybrid). All of these trigger the disease.
Oats occupy a gray zone.
Pure oats contain a protein called avenin, which is chemically different enough from wheat gluten that most people with coeliac disease can tolerate it. The problem is that commercial oats are frequently contaminated with wheat during growing, harvesting, or processing. If you buy regular oats at the grocery store, there's a good chance they contain traces of wheat. Certified gluten-free oats exist, processed in dedicated facilities with careful testing, and these are generally safe for most coeliac patients. However, a small percentage of people react to pure oats anyway, for reasons that aren't fully understood.
What's safe to eat? Rice, corn, millet, sorghum, teff, quinoa, buckwheat (despite its name, it's not related to wheat), and amaranth are all naturally gluten-free. So are potatoes, legumes, fruits, vegetables, meat, fish, eggs, and dairy—though processed versions of these foods might contain added gluten as a thickener or filler.
Beyond the Gut: A Whole-Body Disease
The damage in coeliac disease extends far beyond the intestine. This is a systemic condition, meaning it can affect virtually any organ system. Understanding this is crucial because many people—including some doctors—still think of coeliac disease as purely a digestive problem.
Nutritional deficiencies are the most direct consequence of intestinal damage. When your gut can't absorb nutrients properly, deficiencies develop even with a healthy diet. Iron is commonly affected, leading to anemia that doesn't respond to oral supplements (the iron passes through without being absorbed). Folate, vitamin B12, zinc, and vitamin D are frequently low. Vitamin D deficiency can trigger secondary hyperparathyroidism, where the parathyroid glands work overtime trying to maintain calcium levels, sometimes at the expense of bone density.
Speaking of bones: coeliac disease is a major but underrecognized cause of osteoporosis in young adults. When a thirty-five-year-old presents with bones that look like those of a seventy-year-old, coeliac disease should be on the differential diagnosis. The mechanism involves not just poor calcium and vitamin D absorption, but also direct effects of inflammation on bone metabolism.
Reproductive health suffers too. Untreated coeliac disease is associated with delayed puberty, irregular periods, infertility, and pregnancy complications including miscarriage and fetal growth restriction. The reasons are probably multifactorial: nutritional deficiencies (especially zinc, iron, folate, and selenium), inflammation, and possibly direct immune effects on reproductive tissues.
Neurological symptoms are more mysterious. Some people with coeliac disease develop peripheral neuropathy—tingling, numbness, or pain in their hands and feet. Others experience what's been called "gluten ataxia," a condition affecting coordination and balance. Brain fog is common enough that many patients mention it spontaneously, though it's hard to measure objectively. Whether these neurological effects stem from nutritional deficiencies, direct immune attack on nerve tissue, or something else entirely remains an active area of research.
The liver is affected in about forty percent of untreated cases, typically showing up as mildly elevated liver enzymes on routine blood tests. This "coeliac hepatitis" is usually silent—no symptoms, no jaundice—and resolves with a gluten-free diet. Occasionally, coeliac disease coexists with or triggers other liver conditions.
The Treatment: Simple in Theory, Challenging in Practice
There is currently only one treatment for coeliac disease: a strict, lifelong gluten-free diet.
No medications can prevent the immune reaction. No supplements can protect the intestine. No amount of building up tolerance helps. The only option is to completely remove the trigger.
The good news is that this works remarkably well. Symptoms often improve within days of eliminating gluten. The intestinal lining begins to heal, though complete recovery can take months to years in adults (children tend to heal faster). Nutritional deficiencies correct themselves as absorption improves. Bone density can increase. The excess risk of complications diminishes.
The challenging part is that gluten is everywhere.
It's in bread, pasta, cereal, and baked goods—obvious sources. But it's also in soy sauce (fermented with wheat), many salad dressings, some medications, communion wafers, beer, malt flavoring, certain candies, and countless processed foods where it serves as a thickener or binder. Cross-contamination is a constant concern: a knife used to cut regular bread, a shared toaster, a deep fryer used for breaded foods, even a wooden cutting board that has absorbed gluten over years of use.
Maintaining a strict gluten-free diet requires eternal vigilance, careful label reading, difficult conversations at restaurants, and sometimes opting out of social eating situations entirely. Studies suggest that even people who try their best often ingest small amounts of gluten inadvertently. Whether these trace exposures matter clinically is debated—some people seem to tolerate occasional contamination without apparent harm, while others react to minuscule amounts.
How Common Is Coeliac Disease?
Estimates suggest that somewhere between one in two hundred and one in fifty people have coeliac disease—roughly half to one percent of the population in countries where it's been studied. That makes it one of the most common genetic disorders in people of European descent.
Here's the sobering part: most of these people don't know they have it.
Studies that have screened general populations with blood tests and biopsies consistently find that the majority of coeliac disease cases are undiagnosed. For every person who knows they have the condition, there may be several others walking around with damaged intestines and no idea why they feel vaguely unwell.
Diagnosis rates have increased dramatically over the past few decades, driven by greater awareness among doctors and the availability of accurate blood tests. But this increased diagnosis has mostly captured the low-hanging fruit—the more obvious cases. The silent cases, the non-classic presentations, the people whose symptoms were attributed to stress or aging or irritable bowel syndrome, remain largely undetected.
Whether we should screen everyone is controversial. Mass screening would certainly find many undiagnosed cases. But screening healthy people who feel fine is complicated: Would they follow a restrictive diet for a disease they can't feel? Would the label of "disease" cause them harm? Would the benefits of treatment outweigh the burdens and costs? Current evidence doesn't clearly support universal screening, so most guidelines recommend testing only those with symptoms or risk factors.
The Name Itself
A brief note on spelling: if you've seen it both ways, you're not imagining things. "Coeliac" is the preferred spelling in British and Commonwealth English, while "celiac" dominates in American usage. Both derive from the Greek koiliakos, meaning "of the abdomen." The condition has accumulated a remarkable number of synonyms over the years—coeliac sprue, non-tropical sprue, gluten-sensitive enteropathy, idiopathic steatorrhea—though most of these have fallen out of common use.
There's also some confusion about related terms. "Gluten intolerance" and "gluten sensitivity" are sometimes used as synonyms for coeliac disease, but they're also applied to people who react badly to gluten without having the autoimmune intestinal damage that defines true coeliac disease. This "non-coeliac gluten sensitivity" is a real phenomenon—these people genuinely feel better without gluten—but it's distinct from coeliac disease and doesn't carry the same long-term health risks.
Dermatitis herpetiformis is coeliac disease's skin manifestation: an intensely itchy, blistering rash that shares the same underlying cause and responds to the same gluten-free diet. Gluten ataxia is a neurological form affecting coordination. These conditions, along with wheat allergy (which involves a completely different immune mechanism), are collectively grouped under "gluten-related disorders."
What We're Still Learning
Despite decades of research, significant mysteries remain. Why do some people with the genetic variants develop coeliac disease while most don't? What environmental factors flip the switch? Why does the disease sometimes appear in childhood, sometimes in middle age, and sometimes not until the senior years? Can anything prevent it in genetically susceptible individuals?
Researchers are working on alternative treatments that might allow coeliac patients to tolerate some gluten—enzymes that break down gluten before it can trigger the immune response, medications that block the intestinal damage, even vaccines that might retrain the immune system. None of these have reached clinical practice yet, but the science is advancing.
For now, the gluten-free diet remains the only option. It's imperfect—socially difficult, expensive (gluten-free products cost more than their conventional counterparts), and not always completely effective at preventing every trace of exposure. But for those who follow it strictly, it offers something remarkable: the chance to reverse the damage, correct the deficiencies, and finally understand what it feels like to be truly healthy.
If you've been told your symptoms are "just stress" or "probably irritable bowel syndrome," if you're tired all the time for no clear reason, if you have unexplained anemia or early osteoporosis or any of the constellation of seemingly unrelated problems that coeliac disease can cause—it might be worth asking your doctor about testing. Just make sure you're still eating gluten when they draw the blood.