I remember the exact moment my doctor said the words "celiac disease" back in 2014. I had spent months exhausted, with symptoms I could not explain. The diagnosis brought relief, then a flood of questions. The biggest one was simple: why? What actually causes this? The two-word answer everyone gives is gluten. I assumed that was the whole story. Then my daughter was diagnosed in 2020, and I went back through the research. What I found reads like a detective story that took nearly two thousand years to solve.

Around 1.4 percent of people worldwide have celiac disease, according to a 2018 meta-analysis published in Clinical Gastroenterology and Hepatology. The cause is a chain of three conditions:

• Gluten in wheat, barley, and rye
• Genetic susceptibility, mostly from two specific immune gene variants
• An immune trigger, often an infection or other stress at a particular moment

Separating those conditions took centuries. The story starts with a Greek physician who described the illness without knowing what triggered it.

A Greek physician saw the illness but not the trigger

Aretaeus of Cappadocia, working in the second century, wrote about a wasting bowel disease he called koiliakos. The word literally means "of the abdomen," which is where he placed the blame. His patients had diarrhea, pale stools, and bodies that could not absorb nourishment. He described the damage in detail, noting how food seemed to pass through without doing any good. The name stuck. The cause stayed unknown for another sixteen hundred years.

Reading his descriptions today, I recognize the symptoms from my own experience and from what parents describe in support groups. The illness was visible, but the mechanism was invisible. That gap between what doctors could see and what they could explain defined celiac disease for most of human history.

1888: Samuel Gee's food observation

In 1888, a British physician named Samuel Gee gave a lecture on what he called the coeliac affection. He told fellow doctors something that sounds obvious now but was radical then: if the patient can be cured at all, it must be by means of diet. Gee suspected starchy foods, but he never identified gluten as the specific offender. He advised regulating food with care, which was a step toward the truth. That sentence from 1888 came closer to the cause than almost anything said in the previous eighteen centuries.

What strikes me about Gee's observation is that he was working from pure clinical observation. No blood tests, no genetic screens, no endoscopes. He watched patients improve when food changed. That is the same thing I noticed in my own kitchen years later, but Gee lacked the tool to see which ingredient mattered. The answer was hiding inside a staple food people ate every day.

A Dutch famine forced the answer into view

The breakthrough came from a famine. Willem-Karel Dicke was a Dutch pediatrician in the Netherlands during World War II. In the winter of 1944 and 1945, a blockade cut off wheat and rye flour. Bakeries had almost nothing to sell. Bread disappeared from daily life. Dicke noticed something extraordinary: children with celiac symptoms did better when wheat was scarce. When wheat flour returned after the famine, their symptoms came back.

Dicke and his colleagues later showed that wheat gluten was the dietary trigger. Their work turned gluten from a guess into a documented cause. It also explained why the condition had looked so confusing for so long. The trigger sat inside a food people ate at nearly every meal. No one thought to remove the most ordinary food on the table.

I think about that famine often when I hear parents say they felt lost after a diagnosis. The cause of celiac disease was hiding in plain sight. It took a war and a famine to reveal it. Sometimes the hardest problems are the ones woven into our daily routines.

Genetics: why most people with the genes never get sick

The next layer arrived decades later. Researchers found that nearly everyone with celiac carries one of two gene variants, HLA-DQ2 or HLA-DQ8. The University of Chicago Celiac Disease Center states that about 95 percent of people with celiac carry HLA-DQ2, and most of the rest carry HLA-DQ8. Those genes help the immune system recognize gluten as a threat. Here is the part that confused me at first: the same genes show up in a large minority of people who never develop the disease. Carrying the genes is necessary but not enough.

When I learned this, it reframed the question. Genetic testing can tell you who is at risk, but not who will get sick. My daughter and I both carry the genes, and both of us developed celiac. Plenty of people with the same genes do not. Researchers call that gap the third layer, and it is the part still being worked out.

The third layer: infections and timing

A 2017 study in Science gave one concrete example of what that third layer might look like. Researchers found that a common intestinal virus, a reovirus, made mice lose tolerance to gluten. People with celiac also had higher levels of antibodies against that virus. The researchers interpreted the result as evidence that the immune system's history matters. A child's past infections shape how the body first sees gluten. Other research has looked at early gut infections and the amount of gluten introduced during infancy. Those findings are mixed, which is honest but frustrating.

As a mom reading this research, I describe it this way: celiac develops when gluten meets a genetically susceptible immune system that has been pushed by something else, often an infection or other stress, at a particular moment. The timing matters, and timing is hard to study in humans. That is why the third layer remains under investigation. I do not pretend to have the answer, and I leave medical decisions to our doctors and dietitians.

What this means in our kitchen and our family

For years I thought of celiac as a wheat allergy. The history shows it is different. Gluten drives an autoimmune response, which is not the same as an allergy. That is why the standard of care is strict gluten avoidance rather than medication. Our medical team guides that part. What I bring to the kitchen is simpler: I make meals without gluten, dairy, and soy because our family needs them.

Learning the cause story helped me stop blaming myself for not catching it sooner. The cause was a chain I could not see, and no parent could have spotted it without the right tests. That is also why I started Clean Monday Meals. When my daughter wanted ramen after her diagnosis, I could not find a gluten-free, dairy-free, soy-free option that tasted like the food she missed. We made our own instead. You can find our ramen and seasonings on our website if you need them. The free Clean Monday Meals Recipe App has hundreds of gluten-free, dairy-free recipes that got us through the first six months after diagnosis. It is the resource I wish I had in 2014.

Ask your doctor about antibody screening if celiac runs in your family. That conversation belongs in a clinic. What I can offer from my own research is the story of how we finally figured out the cause, and the hope that comes from understanding the chain. The more we learn, the less alone this diagnosis feels.