This is what kicked everything off for Dr. Crandall and what has basically brought about this Blog post and our two sister websites: Curing-Alzheimers & CuringAlzheimersDisease.com
Way back, when we first noticed that his cognition was steroid-responsive, we thought inflammation WAS the issue in his brain. But then, when he was exposed for the first-time to antibiotics – and not just any antibiotic, the right one (MORE ON THAT LATER) and within 12 hours of adding the new medication he noticed even greater cognitive improvements than seen with steroids alone.
Enter, the famous Urinary Tract Infection (UTI) that literally plagues every older person at some point or other. What’s so fascinating about UTI and what we will discuss in greater detail later, is that when the young get them, they don’t experience neurological changes. But when older people get UTI’s – they go literally crazy. Not just a little crazy, but A LOT CRAZY. There’s a key to Alzheimer’s in this observable difference between how UTIs affect us as we age. MORE ON THAT LATER.
Anyhow, the irony was that the medical profession thought it was simply treating an infection that they’d just found through culture, but much by accident, they were actually treating a second infection which our current commercial lab resources are not able to culture – which is an anaerobic bacterial infection in the brain (Dave’s in this instance). And in so doing, my dad’s cognition rebounded exponentially. The nurses and Docs were so surprised at how well – and how fast – dad was improving neurologically. He was discharged faster than expected. And had regained lots of capabilities he’d lost before (continence, walking independently, talking in full sentences).
But when the treatment for the UTI ended, Dave was quickly back to his old base-line. Behaviors and all.
One might think that this amazing improvement was because we fixed the UTI that was making my dad crazy. At least the medical doctors did. As soon as my dad’s condition reversed, they restarted the antibiotic and repeated a UA/UC -and to their surprise, both cultures were negative. They even allowed the cultures to grow for over 1 week – and still no growth! Still on antibiotics he was great, off- he got worse again. Over a 3 month period, docs tested and retested my dad for a UTI and all 8 times the cultures were negative. And each time, the docs put him on antibiotics while the UA/UC were being run – and each time he got amazingly better on the antibiotics despite testing negative for UTI.
It’s at this point (and you can see this in other posts) we started researching why antibiotics would improve cognition. Back out to the researchers we went. As they were the ones investigating what’s unknown to the medical community.
I mean, hearing from medical doctors that dad’s astounding reversal (8 separate times) was coincidence was almost too much to take. In a nutshell – we disagreed. As did the researchers from such distant places as Germany, the UK, Singapore and Canada. Oh – and quite a few here in the US.
Docs then said it was because antibiotics have anti-inflammatory properties. But we researched that, and found inconsistencies here too:
Effectiveness of anti-inflammatory treatment versus antibiotic therapy and placebo for patients
https://bmcpulmmed.biomedcentral.com/articles/10.1186/1471-2466-11-38 in this study, researchers looked at the improvement in symptoms (the inflammatory process was bronchitis) between steroids and antibiotics. The conclusion was that steroids far outpaced anti-biotics in their ability to reduce inflammation and improve the patients’ condition.
The Other Side of Antibiotics
https://www.reviewofophthalmology.com/article/the-other-side-of-antibiotics in this study, which came from the world of ophthalmology, the researchers come straight out and say that 1) the reason antibiotics work is in their ability to somehow modulate the immune response (and that they don’t know how they accomplish this yet) and 2) the anti-inflammatory properties of steroids far exceed the meager effort put forth by antibiotics.
Antibiotics as anti-inflammatory agents
https://www.ncbi.nlm.nih.gov/pubmed/12054075.
And in this article, the authors point to Cyclines and Macrolides and possibly Qyinolones as exhibiting anti-inflammatory potential – which also doesn’t explain DEC’s case as the antibiotics that work on him do not fall into any of these classifications.
So we looked for other reasons and formed a new hypothesis:
If antibiotics work on Dr. Crandall’s cognition, then it’s highly likely due to the microbial properties of the drugs.
And the Docs went crazy. But by this point we were realizing that they often say things to unpaint themselves out of a corner. And position their half-truths as fact until someone questions them (which rarely happens).
And so, instead of letting them stall us, just the direction of our research changed. And suddenly, the world of current research flooded in. And the first hit, was likely the most compelling. It was a study done at Bristol University wherein researchers biopsied Alzheimer’s Diseased brains (dead ones) and to their surprise and astonishment, bacteria was found:
Bacteria found in Alzheimer’s brains
https://www.sciencedaily.com/releases/2017/07/170717100425.htm
In this 2017 study, research using new techniques for identifying cell signatures found larger bacterial colonies in diseased brains (compared to healthy brains). Furthermore, the researchers found a different bacterial composition in the diseased brains than in the healthy brains. These discoveries opened the floodgate to new ways of looking at AD by challenging old conceptions about our blood-brain-barrier. If the BBB is so protective, how did the bacterium get there? And why didn’t the bacteria kill the host in a manner that would indicate infection? And what about the Alzheimer’s patients prevented their brains from keeping the bacteria at manageable levels like that which was found in healthy patient brains? And what about the diseased brains attracted the different types of bacteria not found in healthy brains?
And so our search to answer these questions began…
Within just a little time, we were able to identify what bacteria was most consistently coming up in recent studies of Alzheimer’s Brains: Polymorphous Gingivalis (P. Gingivalis).
Since Dr. Crandall was a dentist, this bacterium is of particular interest to us for two reasons:
1) we know that P. Gingivalis is the main culprit in Periodontal Disease (which we see every day in the clinic). In order to get to its food source (blood) it destroys the “tight junction” system that prevents all those 500+ bacteria from getting below the gum’s line. And no small coincidence – the blood brain barrier employs this same “tight junction” technology to prevent foreign invaders from getting into it. So if P. Gingivalis can break through the oral TJ system – it most surely can break through the Brain’s TJ system…
2) Dr. Crandall practiced dentistry back when there were no mask requirements for dental health professionals (masks were not mandated until 1991 here in the USA) – this means that he would have been nearly 60 when he was first required to wear a mask – and as the trajectory for exposure-to-symptoms for Alzheimer’s is approximated 20 years…the genesis of Dr. Crandall’s AD infection would be when he wasn’t masked during clinic. And as a dentist – every day he practiced he was aerosolizing oral bacteria into his breathing field. That provided more than enough opportunity to have contracted P. Gingivalis from all those periodontal patients – which by that point was a strong percentage of his aging patient population.
Here are some more articles that helped us to focus our study on P. Gingivalis as a likely suspect for Dr. Crandall’s cognitive decline.
Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357742
In this 2019 article, researchers were able to successfully identify P. Gingivalis in the CSF of 7 out of 10 AD suspected patients – and cross testing of the saliva of all 10 yielded a positive P. Gingivalis result in the mouths of 10 out of 10. In their conclusion, the authors write: “The CSF data provide additional evidence for P. gingivalis infection in the brain of AD patients.”
As Dr. Crandall had Periodontal Disease (which is ironic as he has exemplary oral hygiene) we followed this connection first: and immediately found this article that highlights how having a P. Gingivalis based Periodontal Disease statistically doubles the risk of developing Alzheimer’s.
Assessing the role of Porphyromonas gingivalis in periodontitis to determine a causative relationship with Alzheimer’s disease
https://www.tandfonline.com/doi/full/10.1080/20002297.2018.1563405
This next article, titled: Porphyromonas Gingivalis Periodontal Infection and Its Putative Links with Alzheimer’s Disease https://www.hindawi.com/journals/mi/2015/137357/abs/ references how P. Gingivalis is able to break down the tight Epithelial Junction that connects our teeth to our gums in order to infect/destroy subgingival tissue and bone. This is significant to our hypothesis because the Blood Brain Barrier also uses tight junctions to form a restrictive paracellular diffusion barrier which morphologically is more similar to epithelial tight junctions than to endothelial tight junctions in peripheral blood vessels. https://www.ncbi.nlm.nih.gov/pubmed/10690502 This raises the question: if P. Gingivalis can break down the tight junctions of the gum tissue, is it possible that it can also break down the tight junctions of the BBB?
And here’s another interesting study:
Active Invasion of Oral and Aortic Tissues by Porphyromonas gingivalis in Mice Causally Links Periodontitis and Atherosclerosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4024021
In this study that links P. Gingivalis to Arteriosclerosis, researchers injected P. Gingivalis into the mouths of wild mice to encourage periodontal disease. In so doing, they found that the mice also developed aortic inflammation, viable bacteria in oral epithelium and aorta, and plaque development. This study raises the question: If P. Gingivalis can affect one distant part of the body (heart) from its origin in the mouth, is it possible that the P. Gingivalis bacteria from our mouths can travel to other distant parts of the body (brain)?
This is by no means an exhaustive list of research on the topic. It’s just a sampling of what we have been looking at.
We invite you to do your own Google Search using the following search terms:
P. Gingivalis, Alzheimer’s Disease to see for yourself how THE current scientific race being run to cure AD involves something as simple as bacteria.
