Mucus, Carbs, and Fiber

I have a love/hate relationship with mucus. I appreciate what it does for me, but when it leaks out of my face as part of an immune response, it always feels a bit overdone. Do I really need that much mucus?

One of the effects I noticed after reducing my carb intake was an apparent reduction in face-oozing mucus. My sinuses were clearer, my eyes rarely had any discharge in the morning, and I spit less when I ran.

So this made me both happy and curious: which was the normal state? Could dietary carb restriction be responsible for these changes, and if so, was I making enough mucus to protect my lungs and intestines?

I’ll share what I learned, including some spelling. Mucus is a noun — it refers to the actual stuff coating the epithelial cells. Mucous is an adjective, as in mucous membrane.

Mucus is primary comprised of mucin, a glycoprotein.

The dense “sugar coating” of mucins gives them considerable water-holding capacity and also makes them resistant to proteolysis, which may be important in maintaining mucosal barriers.

Given the glucose content of mucin, is it possible to be deficient if we restrict dietary carbs?

Paul Jaminet says yes, and he suggests that a deficiency might expose us to cancer risk:

There’s good reason to suspect that at least some of the Optimal Dieters developed mucin deficiencies as a result of the body’s effort to conserve glucose and protein. This would have substantially elevated risk of gastrointestinal cancers. Thus, it’s not a great surprise that many Optimal Dieters have been coming down with GI cancers after 15-20 years on the diet.

Lucas Tafur says no, but that protein deficiencies can be causal:

Mucin biosynthesis is highly sensitive to protein malnutrition, specially threonine deficiency (1,2,3). Other aminoacids like serine, proline and cysteine can also promote mucin synthesis (4). When intestinal epithelial goblet cells are deprived of glucose, butyrate modulates MUC gene expression and becomes the main regulator of mucin synthesis (5). There is no evidence that the abscence of dietary glucose affects mucin synthesis.

That last reference to butyrate regulating MUC expression is interesting.   Butyrate is produced by the fermentation of fiber in our gut.    Low-carbers often eat diets low in fiber.    Could that be another cancer risk factor?

Here’s a study with possible mechanisms for the well-documented anti-cancer properties of fiber: Mechanisms linking dietary fiber, gut microbiota and colon cancer prevention, which again suggests that butyrate (a SCFA), as well as the fiber itself, protects against cancer via multiple mechanisms:

First, dietary fiber resists digestion in the small intestine, and enters the colon where it is fermented to produce SCFAs that may enhance the healthy composition of gut microbiota. Second, SCFAs have anticancer properties which include the promotion of cancer cell cycle arrest, apoptosis, and the inhibition of chronic inflammatory process and cancer cell migration/invasion in the colon. Importantly, these molecular activities are effective only within a certain physiological concentration range of the SCFAs. Third, dietary fiber increases fecal bulking and viscosity, reduces the time for proteolytic fermentation that results in harmful substances, and shortens the contact between potential carcinogens and mucosal cells. In addition, dietary fiber can bind/excrete potential luminal carcinogens (e.g., secondary bile acids), lower fecal pH in the colon, and thus provide a healthy intestinal environment.

I plan to keep eating moderate protein and moderate carbs, including fibrous veggies.