Hey MotherofCFBoy11yrs. Thank you for posting that study, it was unexpectedly interesting! It sent me down a wild rabbit hole of research and I discovered some really interesting things to contemplate (see below)! Regarding your last sentence - I hope you are not referring to the artificial bovine growth hormone that they give the cows which gives them mastitis and other diseases, and is also unsafe for human consumption. And I agree, grains are certainly concerning and difficult to digest for everyone, not just those with CF, Celiac, or both.
But first off, after reading through the study carefully I had to conclude that this study was too poorly designed and way too small to make any CF population-wide conclusions about lactose intolerance. I could go into great detail (and will if you're interested), but the main issues with the study are thus: 1) its sample size is very small (only tested 52 CFers for lactose intolerance using the hydrogen breath test). 2) only those CFers who had the genes for lactose intolerance (52 out of 289) were tested for lactose intolerance with the breath test. The other CFers with genes for lactase persistence (a.k.a. lactose tolerance) were not tested. This does not make sense since there are many other ways to become lactose intolerant other than genetics (and the study admitted this - they call it "secondary hypolactasia" and encouraged in the discussion section doctors to test all CFers for lactose intolerance, not just those with the genes for it. 3) the CFers tested were Polish nationals only (it was a Polish study). Since lactose intolerance is a ethnically-determined genetic trait, it does not make sense that we make projections from this study on 52 Polish nationals onto the worldwide CF population. Rates of lactose intolerance vary greatly depending on ethnicity (check out this
sweet map), even within Western Europe. 4) conclusions about similar rates of lactose intolerance in CF vs. non-CF populations were made for "mild-type" CF mutations only. Although "mild-type" is not defined, it is certain that deltaF508 is not in the mild category. In fact, in the discussion section it is stated that studies have shown deltaF508's are more likely to be lactose intolerant than the general population, and furthermore studies have shown that very young CFers in general (considering all mutations, not limited to mild-type) are more predisposed to non-genetic lactose intolerance (i.e. "secondary hypolactasia").
It is important to note, as this study does, that genes are not the only thing that can cause lactose intolerance. It can be caused by gut infections or dysbiosis which destroy the microvilli that house the lactase enzyme. Lactase is required to break down lactose. Pancreatic insufficiency and CF epithelial cell disregulation may be enough to destroy gut lactase. Even stress or viral infections can destroy lactase in the guts (one reason why it is suggested to avoid dairy when you have a cold or flu). Furthermore, lactose intolerance is not the only reason why dairy can cause health problems. Even if someone is lactose tolerant, they can be casein-sensitive, or even allergic to casein. Casein is the protein in milk, and casein sensitivities and allergies are very common, and go hand in hand with gluten sensitivities. This is mediated by leaky gut syndrome, another result of gut dysbiosis.
So this study is not large, thorough, or well-designed enough to make any conclusions about the relationship between CF and lactose intolerance in the general CF population, unfortunately.
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All that said, the discussion section of this study was FASCINATING!!!!! Did you get a chance to look at it? I am SO glad you posted this article because it led me to other sources that discuss the issue of possibly reasons WHY CF developed in the first place (evolutionarily). I have been aware for a few years now that researchers hypothesized that CF developed as an adaptation to cholera, since carriers and those with double-alleles (CFers) do not develop the lethal diarrhea that causes death from cholera. In fact, CFers and carriers do not suffer from any kind of lethal pathogen-mediated diarrhea (I guess this is why I never had any kind of digestive problems when traveling abroad when ALL of my friends did). This led other researchers to conclude (and this is where it gets really interesting) that CF (particularly the deltaF508 mutation) may have developed as a response to the diarrhea induced by lactose intolerance! What?! Crazy right? So what's the significance? Well, when Europeans starting eating dairy 9,000 years ago, the theory goes that they developed two genetic strategies to avoid the diarrhea from lactose intolerance that can cause death: 1) lactase persistence, which leads to lactose Tolerance, and 2) the gene that codes for CF, particularly the deltaF508 mutation. It even says that people with the deltaF508 mutation are less likely to have the gene for lactase persistence than mild-type CF mutations, which makes sense since the mild-type mutations may be younger (conjecture) and maybe not related to lactose intolerance, so a CFer with a mild-type mutation may need lactase persistence to avoid lactose-mediated diarrhea whereas someone with deltaF508 wouldn't! That is why the gene for lactase persistence may be more common in mild mutations than in deltaF508. This is my conclusion given what was said in the article, if anyone has another interpretation, please correct me. The other cool thing that was mentioned in a different aricle on the deltaF508 mutation is that there were two migrations of the gene into Europe at different times, once 52,000 years ago (maybe an epigenetic response to pathogen-borne diarrhea) and a second time 9,000 years ago (most likely as a response to dairying). So maybe both cholera AND lactose intolerance caused CF?!?!
Does any one else find this as ridiculously interesting as me?
