I’ve been covering the growing body of research confirming a link between Alzheimer’s disease and the biome since the inception of this blog years ago. My grandmother – one of my best friends on earth – died of dementia years ago and the horror of that will never leave me. Thus, over the weekend, when I spotted a new article out of the University Hospitals of Geneva supposedly confirming this link, it really caught my attention.[i]
The researchers noted a link between inflammation (detected via blood test), certain intestinal bacteria and Alzheimer’s, leading them to wonder if inflammation seen in the blood could be the link between the gut and the brain. They used PET imaging to measure amyloid plaque buildup and blood inflammation markers in 89 people between the ages of 65 and 85, some with Alzheimer’s/dementia, some without. In particular they were looking for the presence of lipopolysaccharides (LPS), which you may remember from previous posts, are proteins found on the surface of pro-inflammatory bacteria. Such bacteria have been found in amyloid plaques and blood vessels in the brains of those with AD. You’ll also remember, I’m sure (since I talk about it endlessly!) that gut bacteria also make short chain fatty acids (SCFA), and that abnormal levels of these are also associated with disease. (Read more about that here and here, for example.)
Their findings are pretty remarkable. Says the lead author of the study, “Our results are indisputable: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain…Indeed, high blood levels of lipopolysaccharides and certain short-chain fatty acids (acetate and valerate) were associated with both large amyloid deposits in the brain. Conversely, high levels of another short-chain fatty acid, butyrate, were associated with less amyloid pathology.”[ii]
Specifically, the plaques were associated with: LPS in the blood, the SCFAs acetate and valerate, pro-inflammatory cytokines, and endothelial dysfunction (i.e. leaky gut). They were negatively associated with butyrate and the regulatory cytokine, IL-10.
The question is, of course – what do you do about it? The authors suggest that in the future, a probiotic cocktail could be used early in the disease to halt its progression. However, as this would likely only be effective very early on, and diagnosis of such illnesses only occur after symptoms become detectable (which may already be too late), better identification of high-risk individuals is needed. Seeing as this testing or protocol doesn’t exist yet – and who knows when it will – it seems to me, as always, that everyone’s only course of action is to do all the things we know improve the gut biome, reduce inflammation, boost IL-10, etc. as of today. An article was published earlier this year on the links between the biome, aging, our modern lifestyle and Alzheimer’s which states that the gut microbiome is “…highly sensitive to negative external lifestyle aspects, such as diet, sleep deprivation, circadian rhythm disturbance, chronic noise, and sedentary behavior, which are also considered as important risk factors…” in terms of developing Alzheimer’s, as they are linked to neurodegeneration.[iii]
So the moral of the story is – take care of yourself now. Just do it.
[i] Marizzoni, M, et. al. Short-chain fatty acids and lipopolysaccharide as mediators between gut dysbiosis and amyloid pathology in Alzheimer’s disease. Journal of Alzheimer’s Disease. 2020;78(2):683-697. DOI: 10.3233/JAD-200306
[iii] Askarova, S, et. al. The links between the gut microbiome, aging, modern lifestyle and Alzheimer’s disease. Frontiers in Cellular and Infection Microbiology. 202;10(104). doi: 10.3389/fcimb.2020.00104