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Alzheimer's disease - a neurospirochetosis?
Internal Administrator
Posted: Saturday, January 7, 2012 7:55 AM
Joined: 1/14/2015
Posts: 40463


Originally posted by: onward

Don't know what to make of this. As always, input and analysis would be appreciated.
__________________________________________


Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Judith Miklossy

Correspondence: Judith Miklossy judithmiklossy@bluewin.ch
Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional)

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis.

Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD).

Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill.

The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247).

When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases.

Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls.

Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies.

Importantly, co-infection with several spirochetes occurs in AD.

The pathological and biological hallmarks of AD were reproduced in vitro.

The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD.

Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity.

As suggested by Hill, once the probability of a causal relationship is established prompt action is needed.

Support and attention should be given to this field of AD research.

Spirochetal infection occurs years or decades before the manifestation of dementia.

As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

...

Conclusion

Various types of spirochetes, including B. burgdorferi, and six periodontal pathogen spirochetes ((T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of AD patients.

The pathological and biological hallmarks of AD, including increased AβPP level, Aβ
deposition and tau phosphorylation were induced by spirochetes in vitro.

The statistical analysis showed a significant association between spirochetes and AD. The strongly significant association, the high risk factor and the analysis of data following Koch’s and Hill’s criteria, are indicative of a causal relationship between neurospirochetoses and AD.

Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation.

In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced AD-type host reactions and Aβ-plaque, “tangle” and “granulovacuolar” formation.

The characterization of all types of
spirochetes and co-infecting bacteria and viruses is needed, in order to develop
serological tests for the early detection of infection.

The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia.

Persisting spirochetal infection and their persisting toxic components can initiate
and sustain chronic inflammatory processes through the activation of the innate and
adaptive immune system involving various signaling pathways.

In the affected brain the pathogens and their toxic components can be observed, along with host immunological responses.

The response itself is characteristic of chronic inflammatory processes associated with the site of tissue damage.

The outcome of infection is determined by the genetic predisposition of the patient, by the virulence and biology of the infecting agent
and by various environmental factors, such as exercise, stress and nutrition.

The accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of AD form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection.

As suggested by Hill, once the probability of a
causal relationship is established prompt action is needed. Similarly to syphilis, one may
prevent and eradicate dementia in AD.

The impact on healthcare costs and on the
suffering of the patients would be substantial.

Abstract: http://www.jneuroinflammation....tent/8/1/90/abstract

MUCH more info in the provisional pdf: http://www.jneuroinflammation....f/1742-2094-8-90.pdf
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

quote:
3 rounded teaspoons per day

I got the link wrong in above post. It should be:

http://alzheimers.infopop.cc/e...=411309124#411309124

sorry
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

quote:
"...spirochetes were observed in the brain in more than 90% of AD cases"


IN THE BRAINS... an infection starting in the mouth and traveling to the brain via the olfactory nerve like the three people who died this summer from that amoeba Naegleria fowleri http://www.washingtontimes.com..._Feed&utm_medium=RSS

If the infection is in the brain, then that would explain why even after fixing all the problems with bad teeth and gums that people still decline. I would explain why people seem to do better when the take antibiotics. It would explain why Embrel helps for a time, but since it also suppresses the immune system, long-term use is disappointing. It does not explain all cases, but there are probably many paths that lead to the same destination.

I didn't realize that an infection with the bacteria that causes Lyme disease was so common, nor that the bacteria that cause periodontal disease was related, nor that syphilis bacteria was related!

But I'm always looking at the practical side: If this theory is correct, what does it allow us to do?

I wonder if methylene blue (Rember) actually kills off the bacteria?

I wonder if, when treating H.pylori, these other bugs are killed off in the process.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: DLMifm

quote:
Originally posted by JAB:

The idea that an antibiotic or antiviral can help treat Alzheimer's has been around for an equally long time ... and the results from clinical trials on using antibiotics or antivirals to treat Alzheimer's have been conflicting and confusing.


antibiotics or antivirals do they do harm?

DLM
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: amelia99

http://en.wikipedia.org/wiki/Alzheimer's_disease_clinical_research

the link to the page that I saw the info about doxycycline and AD. In the footnotes at the bottom is the link to the clinical trial that was provided. One trial out of Canada that found improvement with Doxycycline and another antibiotic administered together.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by needs help:

my LO has flossed three time a day for 50 years,never an infection in her mouth butdoes flossing below the gum line hide the infecton?


Sorry, I don't know the answer to your question. And by the way, if indeed it's true that spirochetes are a/the root cause of AD, my guess is that the offending spirochetes are entering the brain through multiple routes, not just confined to periodontal, though that may be a primary route. But I don't really know.

Anyway, for anyone interested, below are a couple of interesting quotes from the paper about periodontal spirochetes and AD:

quote:
… periodontal pathogen spirochetes... have the ability to invade the brain, persist in the brain and cause dementia... coinfection by several spirochetes occurs in AD. These findings are in agreement with recent observations showing an association between periodontal diseases and AD...


quote:
... The strong neurotropism of spirochetes is well known. Spirochetes can invade the brain and generate latent, persistent infection... In addition to hematogenous dissemination, they can spread via the lymphatics and along nerve fiber tracts.

Accordingly, periodontal invasive spirochetes were detected along the trigeminal nerve
and in trigeminal ganglia... They might also propagate along the fila olfactoria and
tractus olfactorius, which would be in harmony with the olfactory hypothesis... and with previous observations showing that the olfactory tract and bulb are affected in
the earliest stages of the degenerative process in AD...

Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

quote:
Originally posted by onward:
In an article quoted above -
of 13 essential oils tested, "Cinnamomum verum bark" was found to have "the highest antimicrobial activity, particularly against resistant strains."

Swarfmaker, in the version of cinnamon tea that you make do you feel that you are capturing the oily parts?

According to Wikipedia:

quote:
"Cinnamomum verum ("True cinnamon", Sri Lanka cinnamon or Ceylon cinnamon)"


So isn't it interesting that Ceylon cinnamon, which some on this discussion board have already chosen as the best cinnamon supplement for their AD LOs, turns out to have notable antimicrobial activity. Hmmm...

And cinnamon has been reported in a number of cases (on this discussion board) to produce at least a temporary improvement in AD symptoms.

And maybe this result is due to a variety of functions of cinnamon, antibacterial (anti-spirochete) being an important one of them?


Yes, but the work of Anderson and Graves' study of Cinnamon Verum in vitro was done with the WATER SOLUBLE part of the bark. Sounds like in vivo we should be taking all of it according to your comment on essential oils.

"Abstract. An aqueous extract of Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation,
hallmarks of Alzheimer’s disease (AD). The extract can also promote complete disassembly of recombinant tau filaments and
cause substantial alteration of the morphology of paired-helical filaments isolated from AD brain."

http://www.diabetesaction.org/...ers_09.pdf?docID=781
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by needs help:

My LO has been having blood tests every year can these tests show the spirochetes? and who can recommend the list of blood markers that should be in a healthy brain and what should not be ie. etc heavy metals


Needs-help, I'm sorry I can't answer your questions, but I just wanted to repost them here (because they accidentally got mixed in with a quote from one of my posts, making it look like they were something I'd already posted). Maybe someone else here can help you.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: needs help

quote:
Originally posted by onward:
Don't know what to make of this. As always, input and analysis would be appreciated.
__________________________________________


Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Judith Miklossy

Correspondence: Judith Miklossy judithmiklossy@bluewin.ch
Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional)

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis.

Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD).

Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill.

The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247).

When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases.

Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls.

Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies.

Importantly, co-infection with several spirochetes occurs in AD.

The pathological and biological hallmarks of AD were reproduced in vitro.

The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD.

Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity.

As suggested by Hill, once the probability of a causal relationship is established prompt action is needed.

Support and attention should be given to this field of AD research.

Spirochetal infection occurs years or decades before the manifestation of dementia.

As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

...

Conclusion

Various types of spirochetes, including B. burgdorferi, and six periodontal pathogen spirochetes ((T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of AD patients.

The pathological and biological hallmarks of AD, including increased AβPP level, Aβ
deposition and tau phosphorylation were induced by spirochetes in vitro.

The statistical analysis showed a significant association between spirochetes and AD. The strongly significant association, the high risk factor and the analysis of data following Koch’s and Hill’s criteria, are indicative of a causal relationship between neurospirochetoses and AD.

Spirochetes are able to escape destruction by the host immune reactions and establish chronic infection and sustained inflammation.

In vivo studies with long exposure times will be necessary to efficiently study the sequence of events and the cellular mechanisms involved in spirochete induced AD-type host reactions and Aβ-plaque, “tangle” and “granulovacuolar” formation.

The characterization of all types of
spirochetes and co-infecting bacteria and viruses is needed, in order to develop
serological tests for the early detection of infection.

The pathological process is thought to begin long before the diagnosis of dementia is made therefore, an appropriate targeted treatment should start early in order to prevent dementia.

Persisting spirochetal infection and their persisting toxic components can initiate
and sustain chronic inflammatory processes through the activation of the innate and
adaptive immune system involving various signaling pathways.

In the affected brain the pathogens and their toxic components can be observed, along with host immunological responses.

The response itself is characteristic of chronic inflammatory processes associated with the site of tissue damage.

The outcome of infection is determined by the genetic predisposition of the patient, by the virulence and biology of the infecting agent
and by various environmental factors, such as exercise, stress and nutrition.

The accumulated knowledge, the various views, and hypotheses proposed to explain the pathogenesis of AD form together a comprehensive entity when observed in the light of a persisting chronic inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection.

As suggested by Hill, once the probability of a
causal relationship is established prompt action is needed. Similarly to syphilis, one may
prevent and eradicate dementia in AD.

The impact on healthcare costs and on the
suffering of the patients would be substantial.

Abstract: http://www.jneuroinflammation....tent/8/1/90/abstract

MUCH more info in the provisional pdf: http://www.jneuroinflammation....f/1742-2094-8-90.pdf
my LO has flossed three time a day for 50 years,never an infection in her mouth butdoes flossing below the gum line hide the infecton?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by john1943:
... but the work of Anderson and Graves' study of Cinnamon Verum in vitro was done with the WATER SOLUBLE part of the bark. Sounds like in vivo we should be taking all of it according to your comment on essential oils...


John, thanks for that thought. And I look forward to Swarfmaker's answer about the tea.

I'm trying to understand exactly what the options are for administering antibacterial agents such as cinnamon. Capsules, tea, what else?

I now see there are plenty of sites (including amazon I think) that sell "therapeutic oils."

One site warns that inhaling, and/or applying to the skin, oils that are insufficiently diluted can be very harmful.

Another site lists various combinations of oils that they say can be put into capsules and/or applied to the skin, and allegedly can be highly effective against various kinds of chronic infections. And of course there are compelling testimonials from customers. But this is all new to me.

I just finished reading an article entitled "Therapeutic Essential Oils - Nature's Antibiotic." Is there good science to back this up?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:
Along the lines of the above post, I was thinking about drinks. There has been some studies linking the consumption of things like red wine and green tea to a reduction in the incidence of dementia. What if there is an anti-spirochete property to something in red wine and green tea? Hmmm... This means that merely taking red wine or green tea supplements would not be of any use. One would have to swish these drinks around in the mouth to help.


Swarfmaker, interesting that you mention green tea.

In the comments section after one of the oral spirochete videos at youtube (referenced in the oral hygiene commentary), someone posted this:

"That is some important info. If these spirochetes do have some bearing on heart disease and also alzheimers, (in a previous video it is stated that these oral spirochetes have been found in the brains of alzheimer patients) this may be the key to these diseases.
For years I have read that drinking green/black tea inhibits the growth of plaque on teeth & the development of arterial plaque. Perhaps the ingredients in tea make an inhospitable environment for spirochetes, too."

_________


And I wonder if anyone has any thoughts on this: the person who posted the dental hygiene info (which I posted earlier) also posted this re speculations about AD treatment:

"We are looking at some over the counter methods that will raise the Chlorine level in the blood serum enough to kill spirochetes safely. When I know more, I will post it... but not before I know it's effective and safe."

My comment: Anyone have any guesses as to what that might be? (Obviously chlorine can be dangerous, so it's not something we want to be ingesting without knowing what we're doing.) And what's the difference between chloride and chlorine?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:

... If the infection is in the brain, then that would explain why even after fixing all the problems with bad teeth and gums that people still decline. I would explain why people seem to do better when the take antibiotics. It would explain why Embrel helps for a time, but since it also suppresses the immune system, long-term use is disappointing. It does not explain all cases, but there are probably many paths that lead to the same destination.

... But I'm always looking at the practical side: If this theory is correct, what does it allow us to do?

I wonder if methylene blue (Rember) actually kills off the bacteria?

I wonder if, when treating H.pylori, these other bugs are killed off in the process.


I wonder, too, about the use of so-called "natural antibiotics," and might they, perhaps used in combination, be of any help at all against multiple, entrenched, spirochete infections. Some of the OTC things touted as "natural" antibiotics are:

cinnamon
oregano
garlic
propolis
royal jelly
olive leaf extract
probiotics
essential oils

Here, for example, is an intriguing study:

__________________________________________



Comparison of bacteriostatic and bactericidal activity of 13 essential oils against strains with varying sensitivity to antibiotics

22 AUG 2008

Letters in Applied Microbiology
Volume 47, Issue 3, pages 167–173, September 2008


Abstract

Aims: To compare the bacteriostatic and bactericidal activity of 13 chemotyped essential oils (EO) on 65 bacteria with varying sensitivity to antibiotics.

Methods and Results:

Fifty-five bacterial strains were tested with two methods used for evaluation of antimicrobial activity (CLSI recommendations): the agar dilution method and the time-killing curve method.

EO containing aldehydes (Cinnamomum verum bark and Cymbopogon citratus), phenols (Origanum compactum, Trachyspermum ammi, Thymus satureioides, Eugenia caryophyllus and Cinnamomum verum leaf) showed the highest antimicrobial activity with minimum inhibitory concentration (MIC) <2% (v/v) against all strains except Pseudomonas aeruginosa.

Alcohol-based EO (Melaleuca alternifolia, Cymbopogon martinii and Lavandula angustifolia) exhibited varying degrees of activity depending on Gram status.

EO containing 1·8-cineole and hydrocarbons (Eucalyptus globulus, Melaleuca cajeputii and Citrus sinensis) had MIC90% ≥ 10% (v/v). Against P. aeruginosa, only C. verum bark and O. compactum presented MIC ≤2% (v/v).

Cinnamomum verum bark, O. compactum, T. satureioides, C. verum leaf and M. alternifolia were bactericidal against Staphylococcus aureus and Escherichia coli at concentrations ranging from to 0·31% to 10% (v/v) after 1 h of contact. Cinnamomum verum bark and O. compactum were bactericidal against P. aeruginosa within 5 min at concentrations <2% (v/v).

Conclusions: Cinnamomum verum bark had the highest antimicrobial activity, particularly against resistant strains.

Significance and Impact of the Study: Bacteriostatic and bactericidal activity of EO on nosocomial antibiotic-resistant strains.

http://onlinelibrary.wiley.com...5X.2008.02406.x/full

_____________________________________________

Kinda interesting, eh, that a certain type of cinnamon came out on top?

And here's a quote I found on a website promoting the use of "essential oils":

"Kurt Schnaubelt's book has a list of some basic research, including the following:

"1960: Maruzella demonstrated antibacterial and antifungal effects of hundreds of aromatic compounds
1987: Deininger and Lembke demonstrated antiviral activity of essential oils and their isolated components
1973: Wagner and Sprinkmeyer in 1973 did research on a 170 year old blend of distilled oils still available in Germany. The effects of melissa and the other oils in Kosterfrau Melissengeist had been empirically known since Paracelsus (about 1500). They concluded that, with varying degrees of intensity, there was an inhibiting influence on all the bacteria tested, (Pneumococcus, Klebsiella pneumoniae, Staphlococcus aureus haemolyticus, Neisseria catarrhalis, Streptococcus haemolyticus, Proteus vulgaris, Hemophilus influenza, Haemophilus pertussis, Candida albicans, Escherichia coli-Aerobacter group, various Corynnebacteria, and Listeria) and stated the large spectrum of this inhibitory action is as broad as or even greater than that of wide-spectrum antibiotics."

(I won't post a link because the page is promoting products they sell, but google it if you're interested. Much more info there.)

Of course there are always side effects to contend with, but at this point I don't know anything about "essential oils" and what the side effects may be.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:

Perhaps it is not the bacteria or infection itself, but rather some substance the body manufactures to fight the infection. One intriguing possibility is TNF-alpha. It might be possible to test this idea by blocking the action of TNF-alpha. The arthritis drug Enbrel, I think, is said to block TNF-alpha.

Of course, I think it would be better to remove the infection than to use Enbrel long-term to block the effect.



Going along with what you said, here's a quote from Ray Sahelian's site. (And I think this research has been touched on previously in another thread):

quote:
In a study of patients with mild to severe Alzheimer's disease, people who suffered acute or chronic infections, or even bumps and bruises from a fall, were much more likely to have high blood levels of a protein involved in inflammation and also experienced faster memory loss than people who did not have infections and who had low levels of this protein.

It's possible that finding a way to reduce inflammation in the body "could be beneficial for people with Alzheimer's disease," reports study chief Dr. Clive Holmes, from the University of Southampton, United Kingdom.

Over about 6 months, Dr. Clive Holmes measured the cognitive abilities and blood levels the inflammatory protein TNF-alpha of 222 people with Alzheimer's disease.

During follow up, roughly half of the study subjects experienced a sudden infection or injury that led to inflammation, and a spike in TNF-alpha levels.

These people, experienced memory loss that was at twice the rate of those who did not have infections or injuries.

People who had high levels of TNF-alpha in their blood at the beginning of the study, a sign of chronic, ongoing inflammation, had memory loss at four times the rate of those with low levels of the protein at the start of the study.

By contrast, subjects with low levels of TNF-alpha throughout the study showed no decline in brain function.


Neurology, September 8, 2009.




Here are some "natural" anti-TNF agents:


quote:
Anti-TNF agents in nature

TNF or the effects of TNF are also inhibited by a number of natural compounds, including curcumin (a compound present in turmeric), and catechins (in green tea).

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


Here's more:


quote:

Modulating TNF-a signaling with natural products

[excerpt]

Natural compounds as potential TNF-a inhibitors

Several protein-based TNF-a inhibitors, including Etanercept (Enbrel1), infliximab (Remicade1) and adalimumab (Humira1), have been approved (http://www.clinicaltrials.gov) for clinical use in various inflammatory diseases (Table 1).

As a class, these protein-based TNF-a inhibitors have demonstrated efficacy and several potentially serious adverse effects...

Thus, it has become important and essential to develop safer and perhaps more-cost-effective TNF-a inhibitors. In nature, many natural compounds belonging to various classes have been found to reduce TNF-a levels. These natural compounds (Figures 2 and 3; Table 2) have been found to interfere with various proinflammatory mediators and upstream targets, such as NF-kB and other signaling molecules, involved in TNF-a expression and, thus, could provide an alternative means of treating inflammatory disease by modulating production, rather than activity, of TNF-a.

See full article here:

http://people.mbi.ohio-state.e...ticles/2006-paul.pdf

Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: needs help

quote:
Originally posted by onward:
Needs-help: Sorry, I don't know the answer to your question.

__________________________________________


In case anyone's interested:

The article posted at the beginning of this thread ("Alzheimer's disease - a neurospirochetosis") was also posted (not by me) in another large discussion forum, generating an ongoing discussion with now more than 200 posts. (Needless to say, no one would agree with all that's posted there.)

Part of that discussion (see especially post 1, and also its follow-ups) is a commentary about oral spirochetes, their possible connection to AD, and suggestions about what does and doesn't work when one is trying to get rid of oral spirochetes.

Another part of the discussion is an informative, back-and-forth argument (still ongoing) over whether AD really is a spirochetosis or not.
My LO has been having blood tests every year can these tests show the spirochetes? and who can recommend the list of blood markers that should be in a healthy brain and what should not be ie. etc heavy metals
http://www.freerepublic.com/fo...f-chat/2769347/posts

Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:
Along the lines of the above post, I was thinking about drinks. There has been some studies linking the consumption of things like red wine and green tea to a reduction in the incidence of dementia. What if there is an anti-spirochete property to something in red wine and green tea? Hmmm... This means that merely taking red wine or green tea supplements would not be of any use. One would have to swish these drinks around in the mouth to help.


Interesting.

Not sure if you saw it, but in that lengthy discussion thread whose link I posted, there was the following exchange, fwiw:

Question:
"I wonder if this is directly related to the other thread, a drink a day keeps alzheimer’s away? Maybe the daily drink helps kill the little buggers."

Reply (from the person who started the thread):
"Well, Alcohol is antibacterial, but... it's not as effective, nor does it really get all of them. But something is better than nothing, I guess. I haven't heard of flossing with whiskey..."
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:
If it is true that some variant of these periodontal spirochetes invade our brains, what antibiotic targets them? What antibiotics ARE NOT effective?

I've read some on Lyme disease, and there are some physicians who think that an established case of Lyme should be treated for many, many months.


Thanks, swarf. As you already know, the article cited at the beginning of this thread identifies the specific spirochetes as follows:

quote:
Various types of spirochetes, including B. burgdorferi, and six periodontal pathogen spirochetes (T. socranskii, T. pectinovorum, T. denticola, T. medium, T. amylovorum and T. maltophilum) were detected in the brains of AD patients.


And, as you noted earlier, doxycycline is commonly used for B. burgdorferi (Lyme).

As for targeting the periodontal spirochetes, here's some info:

SUSCEPTIBILITY OF SMALL-SIZED ORAL SPIROCHETES TO EIGHT ANTIBIOTICS AND CHLORHEXIDINE
http://onlinelibrary.wiley.com...7.tb03133.x/abstract

ANTIBIOTIC ADJUNCTS TO PERIO DONTAL TREATMENT
http://www.slideshare.net/shab...s-to-perio-treatment

I haven't studied these yet and would appreciate any further input.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

quote:
The key thing, though, is whether this spirochete research and theorizing will lead us to treatments that will really help our loved ones. If indeed spirochetes truly are a central factor in AD, suppressing them in the mouth seems an important idea, and finding a way to safely suppress them in the blood seems even better.

I certainly want to help people who have AD symptoms, but on this one, I'm thinking of myself. Since the "brain changes" leading to AD start to happen maybe 50 years before symptoms, I'm constantly looking for simple things I can do to prevent AD if I can. So, I've switched to brushing with baking soda nightly. Nothing against regular toothpaste.

On the subject of green tea, I think it is a good thing to add to my diet. Before this "neurospirochetosis" article, I thought that all that was necessary was to get these supplements "into the system". I never thought about their possible effect in the mouth. Maybe it's important to have curcumin or even whole turmeric in food. Maybe one has to drink green tea.

Here are some articles about green tea:

Inhibition of periodontopathogen-derived proteolytic enzymes by a high-molecular-weight fraction isolated from cranberry
Journal of Antimicrobial Chemotherapy (2006) 57, 685–690
doi:10.1093/jac/dkl031
Advance Access publication 10 February 2006

Charles Bodet, Marilou Piche, Fatiha Chandad and Daniel Grenier

Results: NDM dose-dependently inhibited the proteinases of P. gingivalis, T. forsythia and T. denticola [a spirochete] as well as type I collagen and transferrin degradation by P. gingivalis.
http://jac.oxfordjournals.org/...nt/57/4/685.full.pdf

Improvement of periodontal status by green tea catechin using a local delivery system: a clinical pilot study.
J Periodontal Res. 2002 Dec;37(6):433-8.
Hirasawa M, Takada K, Makimura M, Otake S.
Source: Department of Microbiology, Nihon University School of Dentistry at Matsudo, Matsudo, Chiba Japan

Abstract

The purpose of this study was to determine the usefulness of green tea catechin for the improvement of periodontal disease. The minimum inhibitory concentration (MIC) and bactericidal activity of green tea catechin against black-pigmented, Gram-negative anaerobic rods (BPR) were measured. Hydroxypropylcellulose strips containing green tea catechin as a slow release local delivery system were applied in pockets in patients once a week for 8 weeks. The clinical, enzymatic and microbiological effects of the catechin were determined. Green tea catechin showed a bactericidal effect against Porphyromonas gingivalis and Prevotella spp. in vitro with an MIC of 1.0 mg/ml. In the in vivo experiment, the pocket depth (PD) and the proportion of BPR were markedly decreased in the catechin group with mechanical treatment at week 8 compared with the baseline with significant difference. In contrast, PD and BPR were similar to the baseline and the value at the end of the experimental period in the placebo sites of scaled groups. The peptidase activities in the gingival fluid were maintained at lower levels during the experimental period in the test sites, while it reached 70% of that at baseline in the placebo sites. No morbidity was observed in the placebo and catechin groups without mechanical treatment. Green tea catechin showed a bactericidal effect against BPR and the combined use of mechanical treatment and the application of green tea catechin using a slow release local delivery system was effective in improving periodontal status.
PMID:12472837[PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/12472837
http://ovoh.net/Files/PerioAndGreenTea.pdf

Green tea consumption and mortality due to cardiovascular disease, cancer, and all causes in Japan: the Ohsaki study.
http://www.ncbi.nlm.nih.gov/pubmed/16968850

Green tea consumption and cognitive function: a cross-sectional study from the Tsurugaya Project 1.
Am J Clin Nutr. 2006 Feb;83(2):355-61.

Kuriyama S, Hozawa A, Ohmori K, Shimazu T, Matsui T, Ebihara S, Awata S, Nagatomi R, Arai H, Tsuji I.

Division of Epidemiology, Department of Public Health and Forensic Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.

Abstract

BACKGROUND: Although considerable experimental and animal evidence shows that green tea may possess potent activities of neuroprotection, neurorescue, and amyloid precursor protein processing that may lead to cognitive enhancement, no human data are available.

OBJECTIVE: The objective was to examine the association between green tea consumption and cognitive function in humans.

DESIGN: We analyzed cross-sectional data from a community-based Comprehensive Geriatric Assessment (CGA) conducted in 2002. The subjects were 1003 Japanese subjects aged > or =70 y. They completed a self-administered questionnaire that included questions about the frequency of green tea consumption. We evaluated cognitive function by using the Mini-Mental State Examination with cutoffs of <28, <26, and <24 and calculated multivariate-adjusted odds ratios (ORs) of cognitive impairment.

RESULTS: Higher consumption of green tea was associated with a lower prevalence of cognitive impairment. At the <26 cutoff, after adjustment for potential confounders, the ORs for the cognitive impairment associated with different frequencies of green tea consumption were 1.00 (reference) for < or =3 cups/wk, 0.62 (95% CI: 0.33, 1.19) for 4-6 cups/wk or 1 cup/d, and 0.46 (95% CI: 0.30, 0.72) for > or =2 cups/d (P for trend = 0.0006). Corresponding ORs were 1.00 (reference), 0.60 (95% CI: 0.35, 1.02), and 0.87 (95% CI: 0.55, 1.3 (P for trend = 0.33) for black or oolong tea and 1.00 (reference), 1.16 (95% CI: 0.78, 1.73), and 1.03 (95% CI: 0.59, 1.80) (P for trend = 0.70) for coffee. The results were essentially the same at cutoffs of <28 and <24.

CONCLUSION: A higher consumption of green tea is associated with a lower prevalence of cognitive impairment in humans.

PMID: 16469995 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/16469995
Free article: American Journal of Clinical Nutrition, Vol. 83, No. 2, 355-361, February 2006
http://www.ajcn.org/content/83/2/355.long

Green Tea Has Rejuvenating Effect on Damaged Brain Cells
Researchers at the Technion Institute of Science in Haifa have shown that feeding green tea extract to mice with Parkinson's and Alzheimer's disease protects brain cells from dying, and helps 'rescue' already damaged neurons in the brain...
http://alzheimersweekly.com/co...-damaged-brain-cells


EGCG remodels mature alpha-synuclein and amyloid-beta fibrils and reduces cellular toxicity. Bieschke J, Russ J, Friedrich RP, Ehrnhoefer DE, Wobst H, Neugebauer K, Wanker EE.
Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7710-5.

Abstract

Protein misfolding and formation of beta-sheet-rich amyloid fibrils or aggregates is related to cellular toxicity and decay in various human disorders including Alzheimer's and Parkinson's disease. Recently, we demonstrated that the polyphenol (-)-epi-gallocatechine gallate (EGCG) inhibits alpha-synuclein and amyloid-beta fibrillogenesis. It associates with natively unfolded polypeptides and promotes the self-assembly of unstructured oligomers of a new type. Whether EGCG disassembles preformed amyloid fibrils, however, remained unclear. Here, we show that EGCG has the ability to convert large, mature alpha-synuclein and amyloid-beta fibrils into smaller, amorphous protein aggregates that are nontoxic to mammalian cells. Mechanistic studies revealed that the compound directly binds to beta-sheet-rich aggregates and mediates the conformational change without their disassembly into monomers or small diffusible oligomers. These findings suggest that EGCG is a potent remodeling agent of mature amyloid fibrils.
http://www.ncbi.nlm.nih.gov/pu...385841?dopt=Abstract
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

quote:
spirochetes

I am going to hazard a guess and say that using an antiseptic mouthwash, flossing, and brushing would eliminate a lot of periodontal disease.

As for Lyme disease, I don't believe there is a cure for that, is there? I have a son-in law who contracted it from a tick bite. He was given a lot of antibiotics to put it in remission, but it has recently come back.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

A recent paper:

Vitamin D, Cognitive Dysfunction and Dementia in Older Adults

Source: CNS Drugs, Volume 25, Number 8, 1 August 2011 , pp. 629-639(11)

Abstract:

The physiologically active form of vitamin D, 1,25-dihydroxyvitamin D3, is a fat-soluble steroid hormone with a well established role in skeletal health. A growing body of evidence suggests low vitamin D levels also play a role in the pathogenesis of a wide range of non-skeletal, age-associated diseases including cancer, heart disease, type 2 diabetes mellitus and stroke.

Low levels of serum 25-hydroxyvitamin D [25(OH)D], a stable marker of vitamin D status, are also associated with increased odds of prevalent cognitive dysfunction, Alzheimer's disease and all-cause dementia in a number of studies, raising the possibility that vitamin D plays a role in the aetiology of cognitive dysfunction and dementia.

To date, the majority of human studies reporting associations between vitamin D and cognition or dementia have been cross-sectional or case-control designs that do not permit us to exclude the possibility that such associations are a result of disease progression rather than being causal.

Animal and in vitro experiments have identified a number of neuroprotective mechanisms that might link vitamin D status to cognitive dysfunction and dementia, including vasoprotection and amyloid phagocytosis and clearance, but the clinical relevance of these mechanisms in humans is not currently clear.

Two recent, large, prospective studies go some way to establish the temporal relationship with cognitive decline. The relative risk of cognitive decline was 60% higher (relative risk = 1.6, 95% CI 1.2, 2.0) in elderly Italian adults with severely deficient 25(OH)D levels (<25 nmol/L) when compared with those with sufficient levels (≥75 nmol/L). Similarly, the odds of cognitive decline were 41% higher (odds ratio = 1.4, 95% CI 0.9, 2.2) when elderly US men in the lowest quartile (≤49.7 nmol/L) were compared with those in the highest quartile (≥74.4 nmol/L).

To our knowledge, no prospective studies have examined the association between 25(OH)D levels and incident dementia or neuroimaging abnormalities.

The possible therapeutic benefits of vitamin D have attracted considerable interest as over 1 billion people worldwide are thought to have insufficient 25(OH)D levels and these levels can be increased using inexpensive and well tolerated dietary supplements. However, no large randomized controlled trials have yet examined the effect of vitamin D supplements on cognitive decline or incident dementia.

Further studies are urgently needed to establish which mechanisms have clinical relevance in human populations and whether vitamin D supplements are effective at minimizing cognitive decline or preventing dementia.

http://www.ingentaconnect.com/...25/00000008/art00001
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

quote:
Originally posted by swarfmaker:
Perhaps it is not the bacteria or infection itself, but rather some substance the body manufactures to fight the infection. One intriguing possibility is TNF-alpha. It might be possible to test this idea by blocking the action of TNF-alpha. The arthritis drug Enbrel, I think, is said to block TNF-alpha.
Of course, I think it would be better to remove the infection than to use Enbrel long-term to block the effect.


Interesting thoughts. Thanks. Maybe the most effective approach would be to attack the disease process at multiple stages and levels - i.e., attack any infection as well as targeting specific products of the infection?

quote:
Isn't "Borrelia burgdorferi" Lyme Disease?


I believe you're right about that, and I think the drug doxycycline is commonly used to try to combat it, though other drugs may be more effective against other spirochetes.

Here, by the way, is an interesting study involving doxycycline and AD:

__________________________________________


J Am Geriatr Soc. 2004 Mar;52(3):381-7.

A randomized, controlled trial of doxycycline and rifampin for patients with Alzheimer's disease.

Abstract

OBJECTIVES: To assess whether doxycycline and rifampin have a therapeutic role in patients with Alzheimer's disease (AD).

DESIGN: Randomized, triple-blind, controlled trial.

SETTING: Three tertiary care and two community geriatric clinics in Canada.

PARTICIPANTS: One hundred one patients with probable AD and mild to moderate dementia.

INTERVENTION: Oral daily doses of doxycycline 200 mg and rifampin 300 mg for 3 months.

MEASUREMENTS: The primary outcome was a change in Standardized Alzheimer's Disease Assessment Scale cognitive subscale (SADAScog) at 6 months. Secondary outcomes were changes in the SADAScog at 12 months and tests of dysfunctional behavior, depression, and functional status.

RESULTS: There was significantly less decline in the SADAScog score at 6 months in the antibiotic group than in the placebo group, (-2.75 points, 95% confidence interval (CI)=-5.28 to -0.22, P=.034). At 12 months, the difference between groups in the SADAScog was -4.31 points (95% CI=-9.17-0.56, P=.079). The antibiotic group showed significantly less dysfunctional behavior at 3 months. There was no significant difference in adverse events between groups (P=.34). There were no differences in Chlamydia pneumoniae detection using polymerase chain reaction or antibodies (immunoglobulin (Ig)G or IgA) between groups.

CONCLUSION: Therapy with doxycycline and rifampin may have a therapeutic role in patients with mild to moderate AD. The mechanism is unlikely to be due to their effect on C. pneumoniae. More research is needed to investigate these agents.

http://www.ncbi.nlm.nih.gov/pubmed/14962152

___________________________________________


And here's something more recent:

Could low-dosage of Doxycycline be considered for Alzheimer's disease treatment?

July 2010

S.A. KAMER, and A.R. KAMER, New York University, New York, NY

Objectives: Alzheimer's disease (AD) is a neurodegenerative disease primarily of the elderly, and treatment modalities are limited. AD is characterized by the presence of senile plaques with its main component amyloid â , neurofibrillary tangles with phosphophorylated tau protein, and neuronal loss. These pathological components as well as inflammation are hypothesized to be involved in the pathogenesis of AD.

When considering potential treatment modalities for AD, this pathogenesis should be considered. Periostat is a drug containing low dosages of Doxycycline and is used in long-term administration to treat periodontal disease without the side effects characterizing the anti-microbial doses of this medication.

The objective of this study is to evaluate the possible use of Periostat for treating AD by critically analyzing the existing literature.

Methods: a Medline search was undertaken using combinations of the following terms: doxycycline, tetracycline, minocycline, Alzheimer's disease, cognition, mild impairment cognition, metalloproteinase (MMP), amyloid, and inflammation. Then, the relevant papers were reviewed manually.

Results: the database search resulted in a total 301 papers containing the search terms. Further evaluation resulted in 45 papers containing relevant data. The studies evaluated were based on in vitro, animal, and clinical data.

Only one randomized control study was found. The review study found that tetracycline derivatives, including doxycycline:

a) cross the brain blood barrier;
b) have neuroprotective effects;
c) destabilize the amyloid fibrils to make them susceptible to proteolysis;
d) inhibit caspase-3 that has a role in tau protein neurotoxicity;
e) inhibit the production of proinflammatory molecules; and
f) slow cognitive decline.

However, untoward effects have also been reported related to tetracyclines anti-MMPs activities.

Conclusion: the available data suggest that in selective cases low dosage doxycycline may be effective in treating AD.

http://iadr.confex.com/iadr/20.../abstract_140673.htm


Are there any OTC alternatives that might help?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Another addition to the list of "natural" TNF-a reducers:


VITAMIN D


quote:


"... The present data support earlier results of our study group of a vitamin D–induced suppression of TNF-α concentrations..."

http://www.ajcn.org/content/89/5/1321.full



and

quote:


"... we showed for the first time that a daily supplement of 50 µg vitamin D for 9 mo is able to increase serum concentrations of the antiinflammatory cytokine IL-10 and to prevent an increase in serum concentrations of the proinflammatory cytokine TNF-α in CHF patients... Our results agree with experimental data showing that vitamin D is able to suppress the release of TNF-α..."

http://www.ajcn.org/content/83/4/754.full


Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

Along the lines of the above post, I was thinking about drinks. There has been some studies linking the consumption of things like red wine and green tea to a reduction in the incidence of dementia. What if there is an anti-spirochete property to something in red wine and green tea? Hmmm... This means that merely taking red wine or green tea supplements would not be of any use. One would have to swish these drinks around in the mouth to help.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

By the way, when I was a teenager, I remember taking tetracycline and sometimes some other "-myacin" for years to prevent bad acne scars. It worked in that regard, so taking low dose Doxycycline, which I understand to be a synthetic tetracycline, shouldn't be too bad.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

And, re vitamin D for AD, also see:

http://alzheimers.infopop.cc/e...=717303573#717303573
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: needs help

Could toe nail fungus also be considered to attack the brain in AD?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: john1943

I looked up "Essential Oils On Wiki:

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

The references at the bottom did not show much in the way of a scientific study. That's a bit troubling.

They seem to be inhalants and are more like aromatic hydrocarbons than true oils.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: amelia99

I just read something about using Doxycycline in AD either in a clinical trial or as a treatment. I'll find the article and post it. I just can't remember exactly what they were using it for. I've always thought that a brain infection may be one of the first problems the brain encounters when it develops AD. Genes may be the main factor and a person may have to have the gene pathology first in order for the AD to start it's progression. There is just too much pointing to this scenario for it not to be a problem. Most of the things that we've seen help our LO's, all have an anti-bacterial, anti-fungal and anti-viral background.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

Here are some "natural" agents that can, allegedly, reduce TNF-a (and thus, potentially, improve memory??):

Resveratrol
quercetin
curcumin (turmeric)
catechins (green tea)
Devil’s claw
ginger
digestive enzymes
MSM
NAC
SAMe
zinc


I don't have links to studies for all of the above, but see, for example:

Zinc decreases C-reactive protein, lipid peroxidation, and inflammatory cytokines in elderly subjects...

http://www.ajcn.org/content/91/6/1634.abstract

And see also my post above, referencing the following article which lists many more of the "natural" TNF-a reducers:

http://people.mbi.ohio-state.e...ticles/2006-paul.pdf

So might taking a lot of these "natural TNF-a reducers," in combination, achieve a notable improvement in memory??
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

Foxycycline is a synthetic form of tetracycline. I suddenly had the urge to put "tetracycline" and "Alzheimer" into Google and see what popped up. The first thing is this article from 2001. This idea has been around for a while, and with all of the searching I've done, I'm really surprised I haven't run into this before:

FEBS Lett. 2001 Jan 5;487(3):404-7.
Anti-amyloidogenic activity of tetracyclines: studies in vitro.
Forloni G, Colombo L, Girola L, Tagliavini F, Salmona M.
Source

Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. forloni@irfmn.mnegri.it
Abstract

Cerebral deposition of beta-amyloid is a major neuropathological feature in Alzheimer's disease. Here we show that tetracyclines, tetracycline and doxycycline, classical antibiotics, exhibit anti-amyloidogenic activity. This capacity was determined by the exposure of beta 1-42 amyloid peptide to the drugs followed by the electron microscopy examination of the amyloid fibrils spontaneously formed and quantified with thioflavine T binding assay. The drugs reduced also the resistance of beta 1-42 amyloid fibrils to trypsin digestion. Tetracyclines not only inhibited the beta-amyloid aggregates formation but also disassembled the pre-formed fibrils. The results indicate that drugs with a well-known clinical profile, including activity in the central nervous system, are potentially useful for Alzheimer's therapy.

PMID: 11163366 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/11163366

My thought is, if as a teenager, my dermatologist can have me taking low dose tetracycline for 4 years to fight acne, why can't someone with dementia try it?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

I want to emphasize that the following is "anecdotal" & I don't know the identity of the person who wrote it, but I found it very interesting. It appears in the discussion linked in my previous post, and makes reference to the article I posted at the beginning of this thread: "Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria" by Judith Miklossy (Journal of Neuroinflammation 2011).


quote:



I am going to tell you what we have been telling our patients at my dental office for the past five years... Now that we have scientific PROOF that oral spirochetes DO INDEED CAUSE ALZHEIMER'S DISEASE and most likely also cause these other chronic plaque induced chronic diseases of heart disease and adult onset diabetes!


This is proof of an hypothesis that we have been pursuing in the dental office I manage and several other dental offices we are associated with. We started noticing that in very elderly patients who were alert, healthy, and did not have any chronic diseases of the heart, diabetes, or mental incapacity that their oral health was also exceedingly good. They also had something completely missing in their mouths. They had no oral spirochetes at all! There was a 100% correlation! Other dentists also were observing this fact. Oral spirochetes were observed in 85-90% of the population but about 10% of the population seems to naturally immune to them and in fact show none at all in their mouths.


One exception to this observation was the edentulous... those without teeth at all. Those who had had all teeth removed! They also were in excellent mental health at an old age, had far less chronic heart disease, and far less likelihood of adult onset diabetes... IF their teeth had been removed at an early age. Strange. Hmmmm.


Oral spirochetes are, we have been observing, associated very strongly with patients who have Alzheimer's Disease, age related dementia, chronic heart disease, and Type 2 Adult onset Diabetes, all diseases associated with plaques. This is the first peer reviewed paper that proves that oral spirochetes, the particular bacteria that we have been seeing under our phase contrast microscope, ARE indeed the cause of Alzheimer's disease.


The same researcher, Dr. Judith Miklossy, who is the president of the Alzheimer's Prevention Association of Europe, issued another peer reviewed paper in 2008, in which she reported that examination of the Islets of Langerhans in patients with Type 2 Diabetes were also rife with oral spirochetes—also further confirming our hypothesis—and mentioned in her 2008 paper that they should be investigated as a possible causal infection for diabetes along with other bacteria she noted.


Spirochetes are bad actors... they are the bacteria that cause syphisis, Yaws, Enug, Lyme disease, and a host of other very nasty diseases. The tertiary form of Syphilis the same dementia and is indistinguishable from Alzheimer's. Lyme disease can do the same dementia.


Oral Spirochete movie from Implant Dr DM at our office.
http://www.youtube.com/watch?v=hyof5QXflos


Another Spirochete movie from our office on youtube.
http://www.youtube.com/watch?v=iwP4e2LvmoE


We have seen a spirochete invade a Leukocyte (white blood cell) and kill it, then leave the dead Leukocyte and go on its way, in one of these movies! We have put up movies on YouTube where the doctor has mentioned the futility using of toothpaste and Youtube, being a part of Google has PULLED them every time! So we don't mention it, anymore... Advertising is king.


In our office, as part of our investigation of the linkage of oral spirochetes to these chronic diseases, our investigation has found that there is an historical progression of the advance of the spread of these chronic diseases in the population associated with the usage of toothpaste. It's a trailing indicator of about 20 years or so, because these diseases take about 20 years to actually appear after the bugs develop in the mouth and migrate into the blood vessels through bleeding gums. However, in the 1910s and 1920s the United States pioneered the use of sweetened pumice in the form of toothpaste to clean teeth, replacing the tooth powder that had been almost universally used prior to then. Sweetened pumice toothpaste has essentially no antibacterial effect even today, no matter what is claimed! Pumice is even harder than the enamel of the tooth surface. It did clean the teeth... but it did not kill bacteria. As a result, 20-30 years down the road, we can see an upsurge in the chronic heart disease, type 2 diabetes, and Alzheimer's start to grow in the populations that adopt toothpaste teeth cleaning... and it's consistent as toothpaste oral hygiene spread from America to Europe to Asia, Latin America, and else where in the world, replacing the former usage of Toothpowder.


You may be asking yourselves what was the Tooth Powder our ancestors used that was supplanted by toothpaste. Some of you may already know. It was essentially ordinary Baking Soda with a little bit of common table salt. The table salt is unnecessary! Baking Soda has a FIVE SECOND kill time on bacteria! It's like dumping a load of poisonous rocks on the bug's heads! It is a mild abrasive that will also clean your teeth and leave your mouth smelling far fresher than toothpaste will! It's CHEAP! You probably have a box in your kitchen! Brush your teeth with Arm and Hammer Baking Soda and floss it down into the gums—the nasty bugs LOVE to stay down in the gingeva. If you have bleeding gums, you have a superhighway for them to enter your blood stream! We have started giving each of our patients an 8oz. box of Arm & Hammer Baking Soda (we buy them for 47¢ each at WalMart by the case. You can buy it by the bag for a lot less per pound) instead of the free toothpaste we used to give.


The protocol is to take a heaping teaspoon of Baking Soda—I do it when I am in the shower—and load your toothbrush with the Soda. Then holding the toothbrush at a 45º angle to the tooth, brush into the gums, working the baking soda into the gums. Use all of the Baking soda and hit all off the gums line. Brush your tongue and the back of your tongue with a tongue brush. Leave the residue. Do not rinse. You will get to like the taste.


The second part of the protocol (this is not so palatable... but you can do it) is once or twice a week take a cap full of Clorox™ brand BLUE CAP bleach—do not use an off brand as we do not know the purity of any other brand—and put it in a glass. Add TWENTY caps fulls of water to make a 20 to 1 dilute mixture of water to bleach... and swish that around in your mouth like mouthwash. It is merely very strong "swimming pool water", called Dakin's Solution, but it will KILL any remaining bacteria in your mouth. It is also the only known substance that will dissolve plaque! Don't worry if you swallow any of it. It will convert to ordinary table salt in your stomach!


If you follow this protocol, you will kill the bacteria that live in your mouth and hopefully prevent any future infection that may cause Alzheimer's, Heart Disease, and adult onset Type 2 Diabetes. We do NOT yet know the life cycle of the Spirochetes... we think they have to reproduce in the mouth... but we are not certain. Dr Miklossy, and other scientists looking at this, hypothesizes the plaques in the brain, Islets of Langerhans, and in the arteries and blood vessels are the left over bodies of dead, twisted entertwined spirochetes... mixed with who knows what... and no one knows if the body can clean up the mess of twenty to thirty years of that build up... but we gotta start somewhere. Cleaning up the source in the mouth seems like a good place!


You can STILL brush your teeth with toothpaste if you like... the Fluoride is still a good idea... but don't be fooled: Even the Arm & Hammer Baking Soda Tooth Paste doesn't have enough baking soda in it to make a difference... Alcohol based mouthwashes don't do it, either.



Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

If it is true that some variant of these periodontal spirochetes invade our brains, what antibiotic targets them? What antibiotics ARE NOT effective?

I've read some on Lyme disease, and there are some physicians who think that an established case of Lyme should be treated for many, many months.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

I meant to type "Doxycycline", not "Foxycycline". Fat fingeritis.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

I talked this idea over with my dad's PCP, and to my surprise, he went along with it! He gave my dad a prescription for 100mg of doxycycline per day. I think it has helped stabilize the swings in his mental abilities, and most notably, his ability to walk. However, I still give him coconut/MCT oil (using Dr. Newport's reports about her husband as a guide). If he misses a dose, I really notice it! But, he was on the oils since April and they didn't seem to help much when he had an infection. (Pneumonia in April, infected cat bite in June followed by several urinary tract infections until prostrate surgery cleared up an obstruction.)

If his problems are due to a long-term infection then I don't expect a miraculous reversal of symptoms. I'm hoping to slow things down. I think that even if antibiotics work, the other things like the oils will still be necessary.
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: onward

In an article quoted above -
of 13 essential oils tested, "Cinnamomum verum bark" was found to have "the highest antimicrobial activity, particularly against resistant strains."


According to Wikipedia:

quote:
"Cinnamomum verum ("True cinnamon", Sri Lanka cinnamon or Ceylon cinnamon)"


So isn't it interesting that Ceylon cinnamon, which some on this discussion board have already chosen as the best cinnamon supplement for their AD LOs, turns out to have notable antimicrobial activity. Hmmm...

And cinnamon has been reported in a number of cases (on this discussion board) to produce at least a temporary improvement in AD symptoms.

And maybe this result is due to a variety of functions of cinnamon, antibacterial (anti-spirochete) being an important one of them?
Anonymous
Posted: Saturday, January 7, 2012 7:55 AM
Originally posted by: swarfmaker

I'm thinking that while an infection may be the root cause of some portion of cases, maybe even most of the cases, there will probably be other causes.

I'm also thinking that while having tooth/gum problems may be a sign of severe infection, it probably doesn't take a huge colony of the bacteria to cause AD, but rather a few getting into the wrong place. I'm thinking this because no doubt there will be people who say that their LO had dentures or never had a problem with their teeth or gums. This may also be where "genetic predisposition" comes into play, not a predisposition to AD, but to a spirochete infection. There are probably people who are immune.
 
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