And more evidence that gut inflammation promotes Alzheimer's disease

We've written quite a bit about how events in the gut affect what happens in the brain.  I remain amazed at how bacteria and archaea in the gut (your gut microbiome) are mysteriously controlling what happens in your brain.

Sometimes they call it "gut flora," indicating plants growing in your gut.  Really?  This hearkens back to the 1950s and 1960s when they thought all life could be force-fit into a template of either animal or vegetable.  So bacteria were considered a strange kind of plant, and I'm not sure they even knew how different archaea was from bacteria. Today, we see things differently.  Archaea and a bacteria are each in their own "domains," while all of the other "kingdoms," perhaps five of them, are lumped into a third domain, the eukaryotes.  (Actually, how this is all organized depends on who you ask.  But this is how I taught it as a biology teacher.)

One of the things that goes wrong in the gut is inflammation.  What's important to us is that this inflammation involving the gut microbiome has long been suspected of influencing development and progression of Alzheimer's disease.  After all, Alzheimer's disease is known to be an inflammatory disease.  So inflammatory agents leaking from an aging gut are suspected of promoting inflammation in the brain.  So if these agents are released into the blood, how do they get past the blood-brain barrier to promote inflammation in the brain?  I can't find anyone with a good explanation for that. 

So why am I writing about this?  I came across a new study just published in the journal Scientific Reports, entitled "Gut inflammation associated with age and Alzheimer’s disease pathology: a human cohort study."  It describes research in which fecal matter of 125 participants was analyzed for the protein complex calprotectin which is known to be present when the intestines experience inflammation.  The presence of the proteins was then correlated in the test participants with markers for Alzheimer's disease.  This included cerebrospinal fluid analysis, PET scans, and cognitive and memory tests.  (Of course, I've been subjected to all of these diagnostic tests.)

What did they find?  The researchers wrote, "Calprotectin levels were elevated in advanced age and were higher in participants diagnosed with amyloid-confirmed AD dementia.  Additionally, among individuals with AD dementia, higher calprotectin was associated with greater amyloid burden as measured with PET. Exploratory analyses indicated that calprotectin levels were also associated with cerebrospinal fluid markers of AD, and with lower verbal memory function even among cognitively unimpaired participants. Taken together, these findings suggest that intestinal inflammation is linked with brain pathology even in the earliest disease stages. Moreover, intestinal inflammation may exacerbate the progression toward AD."  (The emphasis is mine.)

So what do we do with this?  From everything I've learned, it is most important to eat in ways that don't promote inflammation.  I stay away from foods that promote inflammation, primarily refined sugar and flour.  I also place importance on prebiotic and probiotic foods.  So I get a lot of fiber in my diet, and I eat fermented foods, like kimchee.  Also, yogurt.  And beans don't hurt.  Non-inflammatory eating is central to all of the brain-healthy diets we discussed in Beating the Dementia Monster; the MIND diet, the DASH diet, and the Mediterranean diet.

This just in: I had posted this entry and gone back to reading a book on intermittent fasting.  More on that book in a future post.  But what I read in a few minutes made me stop and return to this blog post.  I was able to stop the post just before it went out so I could add the following.  

I read in the book about a study with mice in which they took fecal matter from mice that had been undergoing intermittent fasting and implanted it in mice that had been sedentary.  The fasting mice had low inflammation, while the sedentary mice had high inflammation.  (Just like in people.)  This caused a remarkable reduction of inflammation in the sedentary mice.  The inference was that the gut microbiome in fasting mice has a different bacterial makeup than that of sedentary mice.  The bacteria in the fasting mice was anti-inflammatory, while the bacteria in the sedentary mice seemed to promote inflammation ... and disease.