Celiac disease is obviously extremely common. But gluten sensitivity (which is not celiac disease) is thought to be even more so. No good prevalence studies have been done for nonceliac gluten sensitivity, but some experts estimate that the majority of people have some form of gluten sensitivity.

      People often wonder, if celiac disease is so common, why don’t more people have it? They do! They just don’t know it yet (and may never know it).

      Pinpointing Who Develops Celiac Disease and Why

      Doctors have no way to identify who will develop celiac disease. What they do know is that you need at least three parts of the puzzle to develop the condition:

      Even if you have all three, you may never develop celiac disease. You can say, though, that if you’re missing one of these three pieces, you won’t develop celiac disease (but you may still have gluten sensitivity).

      Celiac disease is a nondiscriminatory condition, found in all races and nationalities. It’s commonly thought to be more prevalent in people with Northern European ancestry, but that distinction is diminishing as people are becoming more diverse and intermingled.

      

Prevalence studies do show differences in the incidence of celiac disease in different ethnicities. But those figures are skewed by the fact that some nations test more than others. Northern Europe, for instance, has been way ahead of the United States in its awareness of celiac disease for decades. Testing has been far more comprehensive, which may explain why that region reports more people with the disease. Northern Europe doesn’t necessarily have more affected people – just more people have been diagnosed.

      

Some people think that civilizations that developed between the Tigris and Euphrates rivers in the Middle East, where grain was first cultivated, have had longer to evolve to cope successfully with gluten-containing grains; that’s why the prevalence of gluten sensitivity among these people is lower. Other groups, like the Germans, the Scandinavians, and the Celts of England, Scotland, and Ireland, began cultivating wheat only in limited amounts in the post-Roman era. They were mostly hunter-gatherers until the Middle Ages, so those populations have had less time to adjust to gluten-containing grains.

      No one knows all the genes that are involved in developing celiac disease, but researchers do know of two key players: HLA DQ2 and HLA DQ8. You don’t need to have both – just one will do – and DQ2 is the one seen most often in people with celiac disease.

      The DQ gene comes in different types, called alleles. Researchers have identified the combination of these alleles that results in the highest risk of developing celiac disease.

      But about one-third of the general population has these genes and doesn’t develop celiac disease, so knowing whether you have them is valuable if you want to rule out celiac disease. In other words, if you have the genes, you may or may not develop celiac disease. But if you don’t have either gene, there’s a 99 percent chance that you won’t develop celiac disease (which may leave you wondering about that 1 percent!). Keep in mind also that if you don’t have these genes, you can still have nonceliac gluten sensitivity.

      

Celiac disease isn’t dominant or recessive – it’s multifactorial or multigenic, meaning that several different types of genes play a part in the development of the condition.

      People use the word trigger in two ways when they talk about celiac disease. The first refers to gluten being the “trigger” for initiating a response of the body’s immune system (you can delve into that topic more deeply in the next section). The other meaning is an environmental trigger that “flips a switch,” so to speak, launching celiac disease into an active mode.

      Most people have a pretty clear idea of when their celiac disease was triggered, because in many cases they’re relatively healthy, and then boom! Their symptoms appear “out of the blue,” and they have no idea why.

      Common triggers include the following:

      Understanding Celiac Disease and What It Does to the Body

      Celiac disease is an autoimmune disease (a disease in which the immune system attacks the body) that gets activated when someone eats gluten. To help you understand exactly what damage is being done, this section gives you just a taste of basic human anatomy, specifically focusing on the gastrointestinal tract.

      

Some people think that because celiac disease is an autoimmune disease, someone with celiac disease has a compromised immune system. Not at all! In fact, the opposite is true – the immune system in people with celiac disease is working overtime to fight what it perceives to be bad guys – like gluten.

      You’ve got guts, but do you know how they work? Help is here. When food gets to the upper part of your small intestine, it has already been chewed, swallowed, passed through the stomach, and broken down by enzymes into nutrients that the body can use to nourish itself.

The small intestine is lined with hairlike projections called villi. The purpose of the villi, shown in Figure 3-1, is to increase the surface area of the intestine so they have more room to absorb important nutrients.

       Figure 3-1: The villi of the small intestine absorb nutrients.

      The lining of the small intestine is basically a solid wall. All the cells on the lining are joined by tight junctions. When the body is ready to absorb the nutrients, these tight junctions open the space between cells and let the good stuff in – but keep the bigger bad stuff, like toxins, out.

      How do the tight junctions know how far to

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