“Let food be thy medicine, and let thy medicine be food.” Hippocrates
Wouldn’t that be great? The news channels were buzzing with reports of a recent study on the topic of caffeine and Alzheimer’s.
Last month, a team led by Jonathan Geiger at the University of North Dakota published a paper titled “Caffeine blocks disruption of blood brain barrier in a rabbit model of Alzheimer’s disease” in the Journal of Neuroinflammation. This is a peer-reviewed publication, so some credibility should certainly be attached; accordingly, I read the paper several times. I also read a few of the papers the authors cited, as well as a few more I turned up in a PubMed search. Since I’m an engineer and not officially a scientist, I also had some of my scientist friends (you know who you are, thanks!) explain the some of the technical details about the role of IgG and certain proteins such as tight junction proteins in the body.
So what does this study say, in a nutshell? The theory starts with cholesterol and the blood brain barrier (BBB). The role of the BBB is to isolate the brain from the rest of the body, allowing it to have its own “environment” essential to the correct function of the central nervous system (CNS). The BBB is the reason many CNS disorders are difficult to treat with systemic therapy – it keeps all kinds of things, like many therapeutic drugs, from crossing out of systemic circulation into the brain. Apparently, high levels of serum cholesterol have been implicated in allowing more leakage of things across the BBB, which in most cases would be bad.
So what does this have to do with Alzheimer’s? That’s a little less than completely clear, but the pathology of Alzheimer’s includes elevated Aβ plaque formation which is apparently linked to high levels of cholesterol in the brain. So a hypothesis would be that increased cholesterol crossing the BBB leads to elevated elevated Aβ plaque formation which is known to be present in Alzheimer’s patients. So presumably of you could prevent elevated Aβ plaque formation by preventing excess cholesterol from crossing the BBB.
Which leads us to the authors’ tests, which I will grossly oversimplify. In essence they had four groups of rabbits. One got normal feed, one got normal feed + caffeine, one got high cholesterol feed, and one got high cholesterol feed + caffeine. Histology showed that the caffeine apparently reduced the amount of a blue dye administered to the abdomen that ultimately was able to cross the BBB. They measured various other physiological parameters (amounts of important regulatory proteins) which they suggest were responsible for enhanced performance of the BBB in caffeine “protected” animals.
So what does this all mean to people? To me, the most important take-away is that I would certainly NOT alter my caffeine intake based on the results of this study in the hope of preventing Alzheimer’s. I thought it was an interesting study, well run and well written, but it is only a beginning. First of all, the etiology of the disease is largely unknown. Correlation and causation are different things. Second, related to the study, the most obvious questions are the validity of the animal model, and how a dose-response relationship translates to humans. These are not criticisms of the study, mind you, but they are criticisms of most of the news reports I read that tried to make huge leaps from a very nice initial study to the cure for a terrible human disease.
Keep trying guys! It would be great if coffee were part of the solution.