Alzheimer's disease - a neurospirochetosis.

I am going to spread this around!

(BTW I have used tooth powder for more than 12 years, hated toothpaste due to its sicky sweet taste. Now I make my own powder with clay, baking soda, salt and some herb powders. I’ll just cut out the salt now and increase the b. soda.)

Thank you very much for this wonderful and useful info!

So if I’m understanding you right, swordmaker, you’re saying the plaques, or at least the core of the plaques, are made of tangled masses of spirochete bodies but no one has noticed this fact. Presumably because all the researchers so far have used the wrong kind of microscope. Is this correct?

Perhaps... Something forms the framework that catches the crud... It may be hidden by all the rest of the stuff that accreted over years of build up. We SEE the spirochetes forming these masses. . . why, we simply don't know. Maybe they are spirochete orgies. Sometimes they die in those masses. We see them in the oral environment, not in the body. Not enough is known about the spirochete life cycle because there has been no way to follow the entire life cycle!

Most blood born studies have been done with stained slides—I.e., dead bugs, immotile—so they could see them. Only more recently have studies started using the phase contrast microscopes, but even that is difficult. We have to look at these very tiny bacteria at 1200X, and they are STILL very small in the field of view, so finding and following a living spirochete in a 3D media, to spy on its lifestyle is tedious. The one we found that invaded and killed the leukocyte and then left the dead body, did it over a period of six hours! We couldn't watch the whole procedure, we just left the microscope aimed at it and kept checking back on the situation, and recorded it.

Once, we found what we thought was a giant spirochete that extended from one side of the field of view to the other! We watched it for a while then it suddenly broke apart into at least a dozen spirochetes! They had formed an end to end daisy chain out of themselves for a reason known only to spirochetes! Do they repeat these behaviors in the bodies of hosts, or only in oral environments, or only while being watched under a phase contrast microscope? Who knows? I certainly don't!

We've seen other Spirochetes suddenly start moving in the same direction across the entire field of view moving in an entirely synchronized fashion! It's very strange and eerie!

Thanks for the post, Swordmaker, and the pings, grey_whiskers and decimon. Yowser, if this pans out!

Interesting thread. Worth reading the whole thing.

Well, I’ll never be 90. People in my family die in their 50s. I’m already on borrowed time.

I have most of my teeth still, and I’m back on baking soda again. My next purchases will be Chlorox blue-capped bleach and a water pik.

My toothpaste, peroxide, and Listerine budgets just sank to zero as well.

Thank you very much.

If you have a ping list for updates, will you please add me to it.

Swordmaker, I recently went to the dentist (I go infrequently due to not much $) and he did a little test to see bacteria level; he was sure I had a lot since I hadn’t had my teeth professionally cleaned in years. He was quite surprised at the test results and said the level was very low, and also not much plaque. But I have had crappy teeth my whole life.

How can someone have low bacteria but not good teeth?

(Picking your brain here - feel free to ignore since it’s a bit beyond the topic although I haven’t used toothpaste in years, maybe that’s why!)

>> “I’m 50 with Alzheimers in my family.” <<

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But what swordmaker is presenting here doesn’t run “in the family” except possibly if a weak immune response runs in your family.

>> “ I was told NOT to use baking soda or salt because it scratches them” <<

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Baking soda doesn’t scratch anything. Its even used to clean furniture that has natural lacquer finish.

This has to be one of the most significant posts that has ever been posted here in all the time I have been here.

I pray that posting this doesn’t cause you any difficulties professionally.

LJ, I haven’t used toothpaste since the early ‘70s.

I haven’t warmed a dentist’s chair since the early ‘90s when I had to have a partial denture remade.

I had a root abcess about four or five years ago, that I cured with a Hulda Clark type “zapper” with special electrodes that I made out of 1/8” copper tubing, to reach into my gums.

I usually brush with clear water, unless my mouth feels irritated, in which case I use 5% food grade peroxide.

I still see my old dentist, but now its when I do work for him when he needs a house laid out on a steep lot.

He is constantly amazed at how long its been since any actual dental work (over 20 years)

When I was young, my teeth were prone to cavities, but I think it was just lifestyle.

This test is capable of recognizing only the fourteen species of spirochetes that cause Lyme disease, out of more than two hundred so far identified and named species of spirochetes!

Adding exclamations points does not change the fact that the reason that this refutation is significant is that Miklossy's best data, both in the original 1993 paper and in the 2011 preprint, claim the strongest correlation (both positive and negative) for exactly this family of pathogens. The test is determinative, and has no subjectivity, and it finds NO no incidence of Lyme spirochetes in any AD victim.

The authors of the paper do not equivocate: It is a complete ass-kicking.

None of those happen to be oral spirochetes. The borellea family is not really implicated in this set of hypotheses,

Not in your set of hypotheses, but certainly it is in Miklossy's paper.

In fact, in addressing the fact that at least three other researchers failed to verify her claims in a 2004 paper, Miklossy makes the following extraordinarily bizarre claim:

In order to study the particular involvement of Borrelia burgdorferi in AD, it is important to analyze AD patients with a positive serology for Borrelia burgdorferi. Different types of spirochetes may be similarly involved in other AD cases [29,44].

This says nothing more or less than that Borrelia burgdorferi isn't likely to be present in AD cases except in areas where Borrelia burgdorferi is common. That's really NOT even convincing evidence of correlation, forget about causation.

The second 1999 paper refers to a study that attempted to find spirochetes by looking with a microscope at the blood of living patients, and a few autopsied brain samples (n=7). I could not read the entire report, but I am aware of the extreme difficulty most microscopy studies have of even SEEING spirochetes because spirochetes are transparent!

This claim is laughable.

You are suggesting that a peer-reviewed paper challenging a published result got past referees with specialization in this field because of poor experimental technique. Whatever experimental technique and apparatus were available to Miklossy when she started making these claims in 1993 were certainly available to any number of researchers who have been unable to reproduce her findings, especially in 2000 when this paper was written.

As for your notes on transmissibility in another post, you appear determined to miss the point about this. It is immaterial how long the progression of plaques produced by spirochetes to AD takes, or even if the patients keep reinfecting themselves. People are initially infected with these spirochetes somehow, and spirochetes are transmitted orally. That means epidemiologists should be seeing a significant correlation between AD patients and family members. We do not see this correlation when we correct for heritability according to the critical letter in the first citation.

Finally, your claims that you see elevated cholesterol, Type II diabetes and heart disease in patients with oral spirochetosis, is, quite frankly, not a scientific claim.

It might be interesting and it might be worth investigating, but, like the claim that walking under a ladder leads to BAD THINGS, it is essentially superstition on your part, and nothing more. Some superstitions have a basis in fact; some don't.

Metaboloic Syndrome is common, and is an accepted underlying explanation for these conditions in a large number of adults. The simultaneous presence of pathogens (of any kind) isn't dispositive of anything if those pathogens are as common in the oral microecology as you claim, because Metabolic Syndrome is also so common.

These people also all drink water. Or to take a more pertinent correlation, they all apparently go to the same dentist.

Can I therefore conclude that dentistry is the cause of Metabolic Syndrome? AD? Oral spirochetosis? [Hint: NO]

I wish I’d stopped tooth paste in the 70s! ANything wrong with my teeth for the last bunch of years is old fillings pretty much.

I lived on candy when I was a kid and everyone in my family has poor teeth. Some people just seem to have stronger teeth. Interesting about the Hulda Clark zapper things, so they are good for some things!

Thanks for your posts.

You are a fine writer and do a great job in presenting some complex, difficult material.

Hope to see more.

They are good for anything that involves a microbe that has invaded your body!

Recently I got a Freepmail that stated that Etanercept/Enbrel is the only thing that works against Alzheimer.

From the Wikipedia site:
Experimental and off-label uses

Given the central role of TNF-alpha in many diseases, etanercept is being studied as treatment for a number of these disease, including over 150 clinical trials. This includes certain forms of vasculitis (such as Wegener’s granulomatosis, in which it was not effective).

Alzheimer's disease: A 2006 pilot study showed small but significant improvements in various cognitive rating scales in patients with Alzheimer's disease (AD) after treatment with etanercept. A further study, administering to a single AD patient via perispinal infusion, showed rapid and significant improvement in Alzheimer's symptoms. A small number of US physicians offer etanercept treatment for AD at a cost of $10,000 to $40,000 per annum.

http://en.wikipedia.org/wiki/Etanercept

If we assume that Alzheimer is an autoimmune disease the effect of the Etanercept is due to its anti-TNF-alpha function as the Tumor necrosis factor promotes the inflammatory response. This might as well explain why curcumin and cathecins are working.

It might be the case the some spirichete is responsible for this autoimmune disease.

- - -

This video http://www.youtube.com/watch?v=bApY90Bh9Do shows a very nice example of quorum sensing among the spirochetes.

We think that in addition to Alzheimer's Disease, several other plaque related diseases, Chronic Artery Disease and Heart Disease, and Adult Onset Type 2 Diabetes, are also caused by Oral Spriochetes invading the body over long term exposure.

I didn't see anyone mention the Borrellia is the bacteria that causes Lyme disease. It would be interesting to see if Alzheimer's is more prevalent in endemic Lyme's regions of the country.

The other interesting fact that my research on longevity showed that tribes in Peru I believe that were reported to live beyond 100 YO all lost their teeth around age 25. The implication being that oral bacteria from gingivitis had a detrimental effect on life span.

On a final note while neurosyphilis is certainly a cause of dementia. Patients that I have seen in the hospital with dementia and who get a neurological work up that includes tests for syphilis have yet to be positive. Granted this is not a scientific study and only anecdotal.

Finally, your claims that you see elevated cholesterol, Type II diabetes and heart disease in patients with oral spirochetosis, is, quite frankly, not a scientific claim.

WHERE did I ever claim that we see ELEVATED cholesterol???? That is NOT chronic heart disease! Elevated cholesterol is merely high-cholesterol. Many people have high cholesterol with out having chronic heart disease. Don't put words in my post that are NOT THERE!

Your pre-article publications from 1994 and 1999 ARE NOT refutations of a 2011 peer-reviewed article.

You keep hitting on the Borrelia Burgdorferi, and it's family of spirochetes and make the claim the 2011 paper has the strongest correlation for that family... but the research focuses on the Treponema family of oral spirochetes...

"Periodontal pathogen spirochetes Oral anaerobic Treponema (T) spirochetes are predominant periodontal pathogens, which are highly prevalent in the population. Several of them revealed to be invasive in vivo and in vitro [94, 95]. Six different periodontal pathogen spirochetes, specifically, T. denticola, T. pectinovorum, T. vincenti, T. amylovorum, T. maltophilum, T. medium and T. socranskii were detected in the brains of AD patients using species specific PCR. At 7 least one oral Treponema species was detected in 14 of 16 AD cases, and in 4 of 18 controls [96]. Species-specific antigens of T. pectinovorum and T. socranskii were observed in 15 AD and in 7 controls (P<0.001). Six different Treponema species were detected in the brain in one AD patient, five species in four, four or three species each in one, and one species in seven AD cases. Of the four controls with Treponema spirochetes, one had two Treponema species and three one species each. The number of diverse Treponema species was significantly higher in the brains of AD patients compared to controls [96]. Treponema antigens were detected both in the hippocampus and frontal cortex. These important results, as proposed earlier [70, 80-82], indicate that periodontal pathogen spirochetes in an identical way to T. pallidum have the ability to invade the brain, persist in the brain and cause dementia. They also indicate that co- infection by several spirochetes occurs in AD. These findings are in agreement with recent observations showing an association between periodontal diseases and AD [97]"
. . .
". burgdorferi (Table 1, Fig. 1) was observed 13 times more frequently in the brain in AD (19/75, 25.3%) compared to controls (1/52, 1.9%) (P = 2.9 x 10-4, OR = 17; 95% CI: 2 – 732; N = 127). The low prevalence of Lyme disease compared to AD is well reflected by the lower frequency (25.3%) of B. burgdorferi compared to the higher, more than 90% frequency of all types of spirochetes detected with neutral techniques or the highly prevalent periodontal pathogen spirochetes."

Yet you focus on the least significant spirochete and harp on it? Why? Lyme disease is not vectored in a similar way as oral spirochetes vector. Perhaps these patients have never been exposed to a lyme disease laden tick? Do you suppose that may be why some of these AD patients don't present with B. Burgdorferi?

The lack of finding B. Burdorferi in a few AD patients is hardly an "ass-kicking, Fred.

"The association between periodontal pathogen spirochetes and AD was statistically significant as well (Table 1, Fig. 2). They were detected in the brain in 93.7% of AD and in 33.3% of control cases (P = 3.6 x 10-4; OR = 30; 95% CI = 2.8-1364; N = 34)."

A 93.7% association of periodontal pathogen spirochetes in the brains of Alzheimer's Disease cases IS statistically significant... regardless of your attempted obfuscations of the issues with outdated papers from 13 years and longer ago.

You are suggesting that a peer-reviewed paper challenging a published result got past referees with specialization in this field because of poor experimental technique. Whatever experimental technique and apparatus were available to Miklossy when she started making these claims in 1993 were certainly available to any number of researchers who have been unable to reproduce her findings, especially in 2000 when this paper was written.

Miklossy addresses the 1999 McLaughlin et al paper you linked to:

"McLaughlin et al., [90] did not find spirochetes by dark field and electron microscopy in the brains of 7 AD cases tested. They observed spirochetes in the blood in one of 22 clinically diagnosed AD patients (Table 1). The spirochete illustrated by the authors corresponds to a regularly spiral vegetative form. It is not clear, whether the atypical, pleomorphic spirochete forms, which are common in blood and in infected tissues [89, 91-93] were considered or not in this study. The authors have suggested that the spirochete observed could correspond to oral Treponema." (Stress added by Swordmaker)

And it turns out it is just as I thought! They used an old technique called "dark field" microscopy, using old style, standard microscopes. So, yes, Fred, they DID indeed use less than the best in their research, i.e. poor experimental technique! They did not use phase contrast microscopes. Perhaps they are a poor school laboratory and couldn't afford them? That "dark field" method, while it 'sort of works", makes it very hard to find the spirochetes... but it is the only method that works with regular microscopes.

The electron microscopy is better... but you have to be lucky to find the right area... especially with dead samples. And the scope time and prep makes the use costly...

Further, as Miklossy points out, they were essentially looking for only one specific type of spirochete and did not make clear whether they did not find, or ignored, other fairly common blood born spirochetes. Their commentary concentrated on the one case of B. Burgdorferi they found in the brain of the one AD patient... but they did mention in their paper they had observed other spirochetes that "could correspond to oral Treponema," but weren't interested in them.

As for your notes on transmissibility in another post, you appear determined to miss the point about this. It is immaterial how long the progression of plaques produced by spirochetes to AD takes, or even if the patients keep reinfecting themselves. People are initially infected with these spirochetes somehow, and spirochetes are transmitted orally. That means epidemiologists should be seeing a significant correlation between AD patients and family members.

WHY???? What makes you think that there should be? Fred, have you MISSED the fact that 85-90% of the population has Trepanoma species spirochetes ENDEMIC in their oral cavities? This is a fact. The Alzheimer's patients may indeed be infecting their family members... but they are infecting the ALREADY infected! Any re-infection data from an Alzheimer's patient to his family would be just noise amongst the over all data. The secondary factor to the problem is poor dental health at some point for an extended period. Do these people infect their family members with poor dental health as well?

What we DON'T know is how long an exposure through bleeding gums, or what degree of exposure for how long, it takes, or what the "tipping point" is that results in the infection taking root in the body... or why some take root in the brain, some in the blood vessel walls, and some in the Islets of Langerhans.

There is a lot we don't know. Is there a third, perhaps environmental component to the infection that allows the spirochetes to settle in where before they were easily fought off? Is the breeding ground the mouth, and suddenly the body becomes hospitable for reproduction as well? We simply do not know. These things need to be studied.