[ed. note: Michael Jorrin, who I like to call “Doc Gumshoe,” is a medical writer (not a doctor) who shares his thoughts with our readers a couple times a month. He does not generally cover investing topics, but I find his discussions of broader health issues interesting and useful. Enjoy!]
Doc Gumshoe would not be posting a piece about celiac disease if it weren’t for the fact that he (along with just about everybody else alive and breathing, in these parts at least) is daily assailed by offerings of gluten-free this and that. In our own town a cute little shop has sprung up to supply residents with gluten-free treats, and of course the grocery store has lots and lots of gluten-free items.
So what’s going on? Are there really that many people with celiac disease who require a gluten-free diet? Or is it something else?
As a jumping-off place into this potentially tricky quagmire, permit me to stake out my own basic position on this. I am not doing this because I wish to engage the proponents of the gluten-free diet – who are also likely to be partisans of managing health through diet, life-style adjustments, and supplements – in a protracted war of words. I have already, in a previous post, made it as clear as I could that the feud between advocates of mainline medicine and those of alternative health is mostly unnecessary and unproductive. At the same time, it’s also clear that there are fashions and trends in health, and some of them don’t make a whole lot of sense.
Here’s the Doc Gumshoe position in a nutshell:
• Celiac disease is a serious, potentially fatal medical condition, for which there is no known treatment other than the gluten-free diet.
• However, celiac disease is relatively uncommon, and lots of people without celiac disease have adopted the gluten-free diet based on the belief that it is somehow “healthy.” But this diet confers no benefit whatsoever on persons who do not have this condition – in fact, it is likely to bring significant and specific harms.
What, exactly, is celiac disease?
In normal digestion, the contents of the stomach pass into the small intestine, which is where almost all of the nutrient extraction takes place. In the stomach, whatever we ate has been churned up and subjected to an acid bath, and sugars have already been converted into glucose and absorbed into the circulation, and the resulting slurry descends into the small intestine. There, nutrients from this slurry are removed. The agents for this removal are called villi, plural of the Latin villus, meaning “tuft of hair. In effect, the mucosal lining of our small intestine is totally covered with these villi, which extract all manner of nutrients from the matter passing through.
In celiac disease, for reasons that are not totally understood, the villi atrophy. Instead of being covered with villi, the lining of the small intestine in persons with celiac disease are relatively smooth. This has a number of consequences, ranging from deficiencies in a number of nutrients to effects on the quality of the stool, which is now carrying matter that would, in the normal process of digestion, have been removed from the intestinal tract.
The symptoms of celiac disease arising from this can be mild or severe. Some individuals with mild or early stage disease may experience only fatigue or anemia. Diarrhea is common, and the character of the diarrhea is somewhat unusual: it is light-colored, greasy (because lipids have not been absorbed), voluminous, and evil-smelling. Severe pain, stomach cramps, and bloating may occur because of the volume of gas generated in the gut. As the disease progresses, individuals can become severely malnourished. Persons with untreated celiac disease appear to be at a higher risk for non-Hodgkin’s lymphoma and also risk of developing ulcers of the small intestine.
The nutrients in which persons with celiac disease may be deficient include carbohydrates and fats, several minerals (iron, calcium, and others), and several vitamins (A, B12, D, E, K, and folic acid).
And celiac disease symptoms are not limited to the digestive system. Celiac patients have a higher incidence of other autoimmune diseases including Type 1 diabetes mellitus and some skin diseases, as well as liver abnormalities and increased risk of infections.
The term “celiac disease” is singularly imprecise. “Celiac” means nothing more specific than “abdominal.” It is derived from the Greek κοιλιακός (koiliakós), “pertaining to the stomach cavity.” It used to be called “nontropical sprue” or “celiac sprue,” sprue being usually a tropical disease causing some symptoms similar to those in celiac disease.
In other words – to repeat myself – celiac disease is a serious and potentially fatal condition. The question immediately arises, what gives rise to this dadly disease?
How does celiac disease occur?
You notice that I am avoiding the word “cause.” The trigger has been confidently identified as gliadin, which is a gluten protein found in wheat. Some other grains such as barley, rye, and some wheat varieties such as durum and spelt, have similar gluten proteins. These gluten proteins react with an enzyme called tissue transglutaminase (tTG) which modifies the gluten protein such that it sets off an autoimmune reaction. The specific mechanism of this reaction at the cellular or molecular level is exceedingly complex, and there is debate as to which of the actors – the gliadin/gluten protein or the tTG enzyme – is responsible for the several manifestations of celiac disease. The T cells are involved, and it’s thought that these busy reservists in the immune army may be subverted to attack villi. Immunoglobulin A (IgA) is also involved, and along with tTG is considered a celiac disease marker.
However, to call gluten proteins the “cause” of celiac disease, as many commonly available sources do, is a considerable overstatement. I say this confidently, seeing that the great majority of the planet’s population consumes gluten without developing celiac disease. What makes gluten trigger celiac disease in a small minority while having no adverse effect at all on the majority is the question which much research is trying to answer. Favored candidates are a couple of variants of the HLA-DQ protein; most celiac patients have one or the other of those two. However, HLA-DQ cannot be said to be determinative, since up to a third of the general population has those genetic components and most of these people do not have celiac disease. Therefore, some additional factors must be involved.
Identifying the cause of celiac disease is a major part of the puzzle. Another part, perhaps with less impact on treatment, is figuring out why a genetic disposition to celiac disease has persisted in our species, since it is clearly the opposite of a survival characteristic. Consider for a moment the condition of lactose intolerance. This condition emerges gradually as infants are weaned; obviously, newborns cannot be lactose-intolerant or they would not survive. But as a child’s diet moves away from dependence on milk, the capacity to absorb lactose can diminish and disappear, and this happens very commonl