We spoke on Friday about microbes that hide themselves in our body.  Waiting for the right opportunity to infect our body with diseases- coronary disease, type 2 diabetes, Alzheimer’s, renal failure, macular degeneration, even some cancers.

Now would be a good time to look up Porphyromonas gingivalis.  This microbes disrupts the normal microbial communities in our body, creating long-term inflammation conditions.  P. gingivalis just blocks some- but not all- inflammatory responses, which is why the inflammation prevails for such long periods of time.  So, it’s our cells that get destroyed by our immune system, providing more fodder upon which P. gingivalis can subsume- including the iron needed for its electron transport system.  The problem is that while the infected tooth may fall out- it won’t be before P. gingivalis  has managed to invade our blood stream.

Those of us who have antibodies to P. gingivalis are more likely to succumb to rheumatoid arthritis, heart attack, or stroke- within the next decade of invasion.  Why? Because P. gingivalis is able to manipulate its surface proteins- allowing it to “hide” inside white blood cells (the vital component of our immune system) or within the cells that form our artery walls.  Why did I say hide?  Because it remains dormant, so our immune defenses and even antibiotics pass the hidden bugs by.  But, it’s always ready to become active given the right immune signals within the body.

The theory is that we need to develop immunity from this pathogen early.  So, a vaccine that attacks gingipains (the enzyme from P. gingivalis  that digests proteins) may be the best answer.  Immunizing us with  such a vaccine when we are really young would mean the opportunistic bug never gets a chance to develop a foothold in our bodies.  (Right now, the American Heart Association considers gum disease an “independent” factor in heart disease- but not causal.)

Which brings up an interesting study that has just been reported in the literature.  Cortexyme (based in San Francisco) has developed an antibiotic that can kill the microbe in mice.  For a short period.  After which, microbial resistance to the antibiotic prevails.  (Yes, that means this can’t be a long-term solution.)

They also have concocted a small molecule (they’ve called it COR388, which should inform you they’ve tried a whole bunch of compounds already) that inhibits gingipains.  When administered to mice, COR388 was able to reverse the brain damage (as in Alzheimer’s) without allowing the microbe develop resistance.  In a VERY small human trial, cognition improved and inflammation responses were augmented.

But, there’s science behind this- causation and not just correlation. A bunch of scientists – from Poland, Norway, New Zealand, UCSF Periodontology, Louisville Dental School,  Harvard Dental, Melbourne Dental School, and Cortexyme – found two enzymes (gingipains) from P. gingivalis in more than 96% (and up to 99%) of samples from the hippocampus (the brain’s memory region) that had succumbed to Alzheimer’s disease (54 such patients).  Moreover, when the brain tissue had tau fragments (and more cognitive decline), the enzyme levels were even higher.

For patients without Alzheimer’s, much lower levels of both gingipain and amyloids were present.  Since we know it can take 20 years for Alzheimer’s symptoms to manifest, it may be due to accumulated gingipain damage.

Further substantiation from other researchers in Sweden gave more credence to this theory.   Patients with the highest genetic risk to develop Alzheimer’s produce ApoE (an immune protein).   And- you guesses it- gingipains are very effective in destroying this protective immune protein.  It’s when the enzymes break down these large lipoproteins into fragments that Alzheimer’s can prevail.

And, what about cardiac disease?  P. gingivalis prevails in the fatty deposits that line arterial walls- the kind that break off and cause blood clots (which is the primary cause of strokes and/or heart attacks).  Moreover, the bug produces the lipoproteins fragment that trigger atherosclerosis (as mentioned above for Alzheimer’s), as if one were enjoying (pigging out?) on a high fat diet.  (Dr. L Kesavalu [Florida] terms this evidence ‘causal’.)

Or, type 2 diabetes?  That’s the ailment when our bodies have lost their sensitivity to insulin, so we can’t really control our blood sugar levels. Well, we know that diabetes worsens gum disease (high sugar levels impair the ability of our immune system)- but gum disease also worsens diabetes- so much so that the Academy of Periodontology recommends the use of a drug to combat drug disease, along with the normal therapy for type 2 diabetes.  (The data indicates that P. gingivitis isn’t just inflating the immune response, but it acting directly on and in the liver and the pancreas to reduce our sensitivity to insulin.)

There’s some more bad news.  Tobacco smoke is an adjuvant (it promotes the effects) of microbes to invade our gum cells.  So, smoking simply makes the situation worse.

But, exercise, which dampens inflammation and improves our response to gum disease is a critical issue.  It seems that exercise makes it tough for P. gingivitis to prevail in our bodies.

Let’s hope that COR388 proves as potent as Cortexyme hopes.  

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