An Infestation of Bacteria

One of those things you probably don’t need to know (but I am going to tell you anyway) is that there are more bacterial cells in your gut than there are cells in your body. This may seem weird, but remember much of your body, like water, is not cellular. And, of course, there is more than just one type of bacteria, indeed according to a Naturearticle from last year, there more than one hundred times the number of genes in the gut than there are in the human host. That, of course, gives a lot of scope for studying, er, colonic material. And yes, some people apparently do that, and there are some “interesting outputs”.

With such a range of “starting material” to study, the first step was to break the bacteria into four enterotypes. One of those sets, labeled Bacteroides 2, is associated with inflammation. Thus 75% of those with inflammatory bowel disease have this enterotype, while fewer than 15% of those who do not have the disease harbor it. This enterotype has another problem: if you have this enterotype it suppresses the manufacture of butyric acid, which is argued to preserve the barrier function of the epithelial cells lining the gut. In short, too little butyric acid and you get more inflammation. This suggests a corrective measure: eat butter, various fats, milk, parmesan cheese, and some rather unpleasant sources. The problem is that such foods still do not give enough. As an aside, butyric acid is quite foul smelling, and is a significant component of vomit. This suggests that supplements are unlikely to be chosen.

Gut bacteria can make trimethylamine oxide, which is claimed to accelerate atherosclerosis and lead to adverse cardiovascular outcomes, and the article adds, “including death”. Yes, that could be described as an adverse effect. Apparently a research group made a study on 2000 individuals and sorted out something like 1400 variables. For me that is far too small a number of subjects for that number of variables, but nevertheless they came out with the claim that a higher prevalence of this Bact-2  enterotype led to a higher probability of cardiovascular disease, but also it correlated with a  higher body-mass index and with obesity.  Note that correlation does not imply causation, and excess weight has been correlated with cardiovascular difficulties before. 

But there was more. If we consider only the obese, it was found that those taking statins have a pronounced reduction in this Bact-2 enterophyte, in which case they presumably help build up butyric acid. Statins also inhibit an enzyme on the route for making cholesterol, leading to cells to boost low-density lipoprotein (LDL), which in turn captures more cholesterol, which is supposed to lower the risk of cardiovascular disease. Statins also have anti-inflammatory action.This leads to a problem that in my opinion confounds medical research. We have an observation from a study in which there were almost as many variables as subjects that in one very small subset statins reduced the level of a gut bacteria group that can be correlated with cardiovascular problems. It seemed particularly effective at doing this in obese patients. Do you notice some rather tenuous links? In this study there were a huge number of variables that were not separated. Could we argue that we have been on the wrong track and something else is the cause of this effect, assuming the effect is real and not an accidental outcome of a small subset? How can we be sure that those taking statins were not better treated or more health conscious? On the other hand, if the effect is real, should not statin consumption, under proper medical prescription, be encouraged? What I hope this shows is how easy it is to find correlations, with the risk you are misleading everybody, which is why there are so many articles on medical issues that seem to contradict other ones. It is not an easy subject to analyse data, but we all have an interest in delaying death and misery.