The cause of diabetes, stroke, cancer, arthritis, alzheimers and more?

Laura

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Have we found the true cause of diabetes, stroke and Alzheimer's?

The diseases most people die of have been attributed to unhealthy lifestyles. But evidence now suggests bacteria are to blame, heralding a revolution in medicine
Health 7 August 2019
By Debora MacKenzie


FOR decades, health experts have been lecturing us about our bad habits, blaming them for the surge in “lifestyle diseases”. These often come on as we age and include heart disease, Alzheimer’s, type 2 diabetes and some cancers. Worldwide, 70 per cent of all deaths are now attributed to these conditions. In the UK, it is a whopping 90 per cent.


Too much red meat, too little fruit and veg, smoking, drinking, obesity and not enough exercise appear to make all these diseases more likely – and having any of them makes getting the others more likely. But no one really knows why, and we still haven’t worked out what causes any of them. Alzheimer’s is now one of the UK’s biggest killers, yet the main hypothesis for how it originates imploded this year after drugs based on it repeatedly failed. High blood cholesterol is blamed for heart attacks, except most people who have heart attacks don’t have it.

What we do know is that these conditions usually start causing symptoms later in life, and their prevalence is skyrocketing as we live longer. They all turn inflammation, the method our immune system uses to kill invaders, against us. And, by definition, these diseases aren’t communicable. They are down to bad habits and unlucky genes, not germs. Right?

Not necessarily. In disease after disease, we are finding that bacteria are covertly involved, invading organs, co-opting our immune systems to boost their own survival and slowly making bits of us break down. The implication is that we may eventually be able to defeat heart attacks or Alzheimer’s just by stopping these microbes.

Until now, bacteria’s involvement completely eluded us. That’s because they tend to work very slowly, stay dormant for long periods or hide inside cells. That makes them difficult to grow in culture, once the gold standard for linking bacteria to disease. But now DNA sequencing has revealed bacteria in places they were never supposed to be, manipulating inflammation in just the ways observed in these diseases.

The findings are so contrary to received wisdom and emerging in so many diseases, each with its own separate research community, that awareness of all this is only starting to hit the mainstream (See “Germ theory“). And predictably, as with any paradigm shift, there is resistance.

But some researchers, frustrated by years of failure to find causes, and therefore real treatments, for the diseases of ageing, are cautiously excited. And with reason: this could change everything.

The worst culprits, which seem to play a role in the widest range of ailments, are the bacteria that cause gum disease. This is the most widespread disease of ageing – in fact, “the most prevalent disease of mankind”, says Maurizio Tonetti at the University of Hong Kong. In the US, 42 per cent of those aged 30 or above have gum disease, but that rises to 60 per cent in those 65 and older. It has been measured at 88 per cent in Germany.

Strikingly, many of the afflictions of ageing – from rheumatoid arthritis to Parkinson’s – are more likely, more severe, or both, in people with gum disease. It is possible that some third thing goes wrong, leading to both gum disease and the other maladies. But there is increasing evidence that the relationship is direct: the bacteria behind gum disease help cause the others.

Circumstantial evidence is certainly damning. In the US, states that put federal Medicaid funds towards people’s dental costs, including those related to preventing or treating gum disease, ultimately pay between 31 and 67 per cent less than states that don’t, to help those people later with heart attacks, diabetes, strokes and cancer. Private insurance companies report similar patterns, says David Ojcius at the University of the Pacific in San Francisco.

But how can the bacteria that cause gum disease play a role in all these conditions? To answer that, we have to look at how they turn the immune system against us.

Your mouth hosts more than 1000 species of bacteria, in a stable community where potential bad actors are kept in check by peaceful bacteria around them. Elsewhere in the body, including on the skin or the lining of the gut, communities of bacteria live on a continuous sheet of cells, where the outermost layer is constantly shed, getting rid of invasive bacteria. But your teeth can’t cast off a layer like that, says Tonetti. There, the bacteria live on a hard surface, which pierces through the protective outer sheet of cells.

When the plaque the bacteria on your teeth live in builds up enough to harden and spread under the gum, it triggers inflammation: immune cells flood in and destroy both microbes and our own infected cells (see Diagram). If this goes on too long, an oxygen-poor pocket develops between gum and tooth. A handful of bacteria take advantage of this and multiply. One of them, Porphyromonas gingivalis, is especially insidious, disrupting the stable bacterial community and prolonging inflammation.



This might seem a strange thing to do. Most pathogens try to block or avoid inflammation, which normally kills them before it shuts down again. Starting in our 30s and 40s, this shutdown begins failing, leading to the chronic inflammation involved in diseases of ageing. No one knows why.

P. gingivalis may have a hand in it. It actually perpetuates inflammation by producing molecules that block some inflammatory processes, but not all of them, says Caroline Genco of Tufts University in Massachusetts. The resulting weakened inflammation never quite destroys the bacteria, but keeps trying, killing your own cells in the process. The debris is a feast for P. gingivalis, which, unlike most bacteria, needs to eat protein.

The destruction also liberates the iron that bacteria need and which the body therefore normally keeps locked up. “These bacteria manipulate their interaction with the host immune response to enhance their own survival,” says George Hajishengallis at the University of Pennsylvania.

Gum control

Eventually, the infected tooth falls out – but long before that P. gingivalis escapes into the bloodstream. There your immune system makes antibodies against it, which usually defend us from germs. But P. gingivalis antibodies seem to be more a mark of its passing than protection. People with these antibodies are actually more likely to die in the next decade than those with none, and more likely to get rheumatoid arthritis or have a heart attack or stroke.


This could be because, once in the blood, P. gingivalis changes its surface proteins so it can hide inside white blood cells of the immune system, says Genco. It also enters cells lining arteries. It remains dormant in these locations, occasionally waking to invade a new cell, but otherwise remaining hidden from antibiotics and immune defences. However, even hunkered down within our cells, P. gingivalis continues to activate or block different immune signals, even changing a blood cell’s gene expression to make it migrate to other sites of inflammation, where the bacteria can hop out and feast again.

One explanation for why gum disease makes you more likely to get conditions like diabetes and Alzheimer’s disease is that it adds to your general “inflammatory load”. But P. gingivalis may act more directly too: the bacteria have been detected in inflamed tissue in the brain, aorta, heart, liver, spleen, kidneys, joints and pancreas in mice and, in many cases, humans.

Master of concealment
If the bacterium Porphyromonas gingivalis is partly to blame for a wide range of inflammatory diseases such as Alzheimer’s and heart disease, why not just kill it? Unfortunately, it is brilliant at dodging our defences: lurking inside cells where antibodies can’t reach it, and often lying dormant, making it invisible to antibiotics, which mostly attack bacteria as they divide.

We could vaccinate against P. gingivalis, but vaccines work by inducing antibodies. People with gum disease already make antibodies against the bacteria, but these seem to do little to stop it.

It may be better to have the antibodies early and stop P. gingivalis invading our mouths when we are young. Eric Reynolds at the University of Melbourne is running a clinical trial of a vaccine that targets gingipains, the protein-digesting enzymes that P. gingivalis makes. Caroline Genco of Tufts University in Massachusetts is also working on an anti-gingipain vaccine. “The key is to prevent it ever colonising,” she says.

The trouble is, many of us already host the bacteria. Routine gum abrasion, through eating or brushing your teeth, can release the microbes into your bloodstream, even if you don’t have gum disease. There it can spread throughout the body and promote inflammation.

In studies by the company Cortexyme, antibiotics killed P. gingivalis in mice, but it rapidly became resistant. To limit resistance, instead of trying to kill the bacteria, it may be better to block its ability to cause disease. Cortexyme has a drug that does this by blocking gingipains. In mice, it reversed Alzheimer’s-like brain damage without driving resistance in P. gingivalis, and in a small trial in humans it improved inflammation and some measures of cognition. A large trial is now under way.

But as all these diseases involve inflammation, why not just block that? If we did, it could leave you open to the germs that this immune response does fight off or block other vital things that immune signals do. That’s why some companies are working on drugs to block only specific inflammatory signals. But tampering with our complex immune systems without doing damage – as P. gingivalis shows – will be a significant challenge.

The strongest case against P. gingivalis is as a cause of Alzheimer’s disease. This constitutes more than two-thirds of all dementia, now the fifth largest cause of death worldwide. It was long blamed on the build-up of two brain proteins, amyloid and tau. But that hypothesis is crumbling: people with dementia may lack this build-up, while people with lots of the proteins may have no dementia – and most damningly, no treatments reducing either have improved symptoms.

Then, in January, teams at eight universities and the San Francisco company Cortexyme found a protein-digesting enzyme called gingipain, produced only by P. gingivalis, in 99 per cent of brain samples from people who died with Alzheimer’s, at levels corresponding to the severity of the condition. They also found the bacteria in spinal fluid. Giving mice the bacteria caused symptoms of Alzheimer’s, and blocking gingipains reversed the damage.

“A bacterial cause could explain the genetic risk for Alzheimer’s”

Moreover, half of the brain samples from people without Alzheimer’s also had gingipain and amyloid, but at lower levels. That is as you would expect if P. gingivalis causes Alzheimer’s, because damage can accumulate for 20 years before symptoms start. People who develop symptoms may be those who accumulate enough gingipain damage during their lifetimes, says Casey Lynch at Cortexyme.

Still, dementia researchers have questioned how a bacterial cause can account for genetic risk factors for Alzheimer’s. But it may actually explain them, according to a team in Sweden. The people with the highest genetic risk produce a particular form of an immune protein called ApoE that is destroyed in the disease. Last year, Swedish researchers discovered that gingipains are better at destroying that particular ApoE than other forms.

P. gingivalis may literally break our hearts too. There is growing evidence for a causal link to atherosclerosis, or “hardening of the arteries”. Researchers have found P. gingivalis in the fatty deposits that line arterial walls and cause blood clots. When bits of clots clog blood vessels in hearts or brains, they cause heart attack and stroke.


The bacteria trigger the molecular changes in artery linings that are typical of atherosclerosis, says Genco. We have also found that P. gingivalis creates the lipoproteins thought to trigger atherosclerosis, causes it in pigs and affects arteries much like high fat diets. Lakshmyya Kesavalu at the University of Florida, who has cultured viable P. gingivalis from the atherosclerotic aortas of mice, calls the bacteria “causal”.

The American Heart Association agrees that gum disease is an “independent” risk factor for cardiovascular disease, but doesn’t call it causal. It argues that although treating gum disease improves hardened arteries, no studies have found that it reduces heart attacks or strokes. But, according to Steve Dominy at Cortexyme, that could be because, while gum treatment helps arteries by easing inflammatory load, it doesn’t eradicate the P. gingivalis already in the blood vessels. Clinical trials are needed to firm up the connection, but these are expensive and difficult – especially when the bacterial hypothesis is still in its early days.

The link is clearer for type 2 diabetes, in which people lose sensitivity to insulin and eventually can’t make enough to control blood sugar. It is currently a pandemic, blamed on the usual lifestyle suspects.

Diabetes worsens gum disease, because high blood sugar levels hurt immune cells. But gum disease also worsens diabetes, and treating it helps as much as adding a second drug to the regimen taken by someone with the condition, according to the American Academy of Periodontology. Treatment is now recommended by diabetes associations, yet none of them list gum disease as a risk factor. As with other conditions, there is evidence that P. gingivalis isn’t promoting diabetes just by adding to the body’s inflammatory load, but may also be acting directly in the liver and pancreas to cut insulin sensitivity.

“It is very hard to prove causation in a complex disease,” says Genco. We know that mice given a mouthful of P. gingivalis get gum disease – and diabetes, rheumatoid arthritis, atherosclerosis, fatty liver disease and Alzheimer’s-like symptoms. We know that, in humans, gum disease makes the other diseases more likely, and that P. gingivalis lurks in the affected tissues and makes the precise cellular changes typical of these conditions.


If these diseases actually share a more direct cause, it might finally suggest cures – as well as explaining just how the same bad habits bring them all on. People who drink more alcohol tend to have more P. gingivalis and are more susceptible to gum disease. Tobacco smoke helps the bacteria to invade gum cells. Exercise, the only known way to lower your risk of Alzheimer’s, improves gum disease by damping inflammation and ending P. gingivalis’s feast.

Then there is diet. Douglas Kell at the University of Manchester, UK, believes our blood contains many dormant bacteria, needing only a dose of free iron to awaken and cause disease. That could be why eating too much red meat and sugar or too little fruit and veg lead to these diseases: all increase your blood iron.

The long haul

No official medical advice for warding off these diseases includes “see your dentist”, at least not yet. “Periodontal disease should be better recognised by the community as a clearly established risk factor,” says Dominy. One of the clearest risks is for Alzheimer’s. But guidelines for avoiding Alzheimer’s published in May by the World Health Organization (WHO) say nothing about preventing gum disease.

“There is insufficient evidence to suggest that treating gum disease reduces the risk of dementia,” says Benoit Varenne at the WHO, echoing the verdict on heart disease, even though the same caveats probably apply. The guidelines recommend avoiding diabetes and high blood pressure, despite stating that there is little or no evidence that this stops Alzheimer’s.

“It’s perhaps too easy to mock the notion that flossing your teeth may contribute to good brain health,” says Margaret Gatz at the University of Southern California. And that may be part of why this idea hasn’t yet taken off in mainstream medicine. “There is a history of dental and medical doctors working apart and not cooperating,” says Thomas Kocher at the University of Greifswald, Germany.

But it also reflects the long-held belief that heart attacks and the other conditions are primarily the result of bad lifestyle, not bacteria. Such underlying paradigms in science can take decades to change. That happened when bacteria, not stress and stomach acid, were shown to cause stomach ulcers. After decades pursuing these explanations, many medical experts are reluctant to admit that amyloid may not cause Alzheimer’s and high cholesterol may not lead to heart disease.

With the world’s population ageing, we don’t have decades before these diseases become a health crisis severe enough to break health systems and societies. We need a new paradigm. That means facing the possibility that it may all be down to germs, after all.

Germ theory
A range of bacteria may play a role in supposedly non-communicable diseases. Propionibacterium acnes, for instance, is best known for causing acne, but also seems to damage the discs that cushion your spinal vertebrae, a common cause of severe back pain, says Ondrej Slab of Masaryk University in the Czech Republic. It has also been implicated in prostate cancer. But it is Porphyromonas gingivalis that has been linked to the widest array of conditions:

Rheumatoid arthritis
P. gingivalis is present in the joints of people who get this condition before symptoms appear and is the only bacterium known to make a chemical involved in the disease.

Parkinson’s disease
P. gingivalis and its protein-munching enzymes, gingipains, are found in the blood of people with Parkinson’s disease, and promote the inflammation and abnormal clotting seen in the condition.

Kidney disease
Gum disease is associated with chronic kidney disease and gum treatment seems to help the kidneys.

Fatty liver disease
There is far more P. gingivalis in affected livers than in healthy ones, and it worsens the disease in mice. Treating the gums helps.

Cancer
The bacteria has been found in early-stage cancers of the mouth, oesophagus, stomach and pancreas, and changes cell functions in ways typical of these cancers.

Macular degeneration
Injecting the bacteria into the retina seems to damage eyesight by producing age-related macular degeneration in mouse studies.

Preterm birth
Gum disease, caused by P. gingivalis, has been established as a risk for premature birth.

Source: https://www.newscientist.com/article/mg24332420-900-have-we-found-the-true-cause-of-diabetes-stroke-and-alzheimers/
 

Echo Blue

Jedi Master
FOTCM Member
This article is REALLY interesting to me. My baby sister passed recently from Alzheimers (or some form of dementia). She was a healthy woman until one day her brain stopped working correctly. She died at the age of 58.

I have read about Oil Pulling therapy (using coconut oil). It is supposed to help with detoxifying your body through oral cleansing. Dr. Bruce Fife has written much on the benefits of this form of detoxing. If anyone is interested, they could search with Dr. Bruce Fife's name and oil pulling.

I am just posting this information in case it could be of benefit. My sister did not do oil pulling. I try to do this as often as I can (sometimes it's hard to get used to the oil in your mouth). I find myself fortunate, at my age (71), to be free of any medical issues - with the exception of being somewhat tired after babysitting my grandaughter for 2 days each week! Also, I cannot say that the oil pulling has made any difference in my health.

And thanks for posting this article, Laura!
 

Julius

Jedi
Then there is diet. Douglas Kell at the University of Manchester, UK, believes our blood contains many dormant bacteria, needing only a dose of free iron to awaken and cause disease. That could be why eating too much red meat and sugar or too little fruit and veg lead to these diseases: all increase your blood iron.
This part reminds me of Ray Peat take on iron Iron's Dangers

"Q: Exactly how much iron do we need to eat?

Children's nutritional requirements are high, because they are growing, but there are indications that in the U.S. even children eat too much iron.
Some researchers are concerned that the iron added to cereals is contributing to the incidence of leukemia and cancers of the lymphatic tissues in children. [Goodfield, 1984.] During the time of rapid growth, children are less likely than adults to store too much iron. At birth, they have a large amount of stored iron, and this decreases as they "grow into it." It is after puberty, when growth slows and the sex hormones are high, that the storage of iron increases. [Blood, Sept., 1976.] In a study of the "malnourished" children of migrant fruit pickers in California, these children who were "seriously anemic" were actually more resistant to infectious diseases than were the "well nourished" middle class children in the same region."
 

LQB

The Living Force
FOTCM Member
Until now, bacteria’s involvement completely eluded us. That’s because they tend to work very slowly, stay dormant for long periods or hide inside cells. That makes them difficult to grow in culture, once the gold standard for linking bacteria to disease. But now DNA sequencing has revealed bacteria in places they were never supposed to be, manipulating inflammation in just the ways observed in these diseases.
Not exactly true. Throughout the first half of the 20th century, Edward Rosenow MD (head of experimental bacteriology for the Mayo foundation - 1915 to 1944) demonstrated in great detail how focal infections of the mouth/teeth invariably lead to the chronic infection conditions seen throughout the bodies of many sufferers. Rosenow found that these secondary infections could not be eliminated permanently without removal of the focal infection in the mouth. He found the worst focal offenders to be pulpless teeth, gum infections, and root canals. He proved that these bacteria (identified as a form of staph) change form as they travel in the body, and these forms adapt to the various oxygen gradients found in the various issues (organs, joints, heart, blood vessels, etc). Unless the focal infection of the mouth is found/eliminated, the chronic organ infection will always return - he (and many others) demonstrated this again and again ...

Rosenow's (and Weston Price and others) objections to root canals (due to extremely high infection rates) were defeated by a dental industry that saw great monetary potential in root canals. Rosenow's great work has come to be ignored in medical academia.

A must-read on Rosenow's work (and many others) is:

What's Eating You: Bacteria With Taste: Rosenow et al. on Microbial Infection, Variation, Localization (The Medical Guide Of The Future) (Volume 1)
by Stuart Shakman


Shakman has done us a great service with this book.
 

Helle

Jedi Master
I have been working as a dental assistant for 20 years, and we always administered antibiotics before deep cleansing teeth of a patient who had a known heartdisease., because of the bacteria getting into the bloodstream, and causing more strain on the heart.

So I'm not surprised the bacteria could be the source of a lot of other bad things as well.
 

Adaryn

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Against P. gingivalis and harmful bacteria in the mouth, a combination of manuka, tea tree and eucalyptus essential oils (plus a couple of others, but manuka seems to be the most potent one) looks like a promising treatment/preventive treatment:


Cariogenic bacteria and periodontopathic bacteria are present in dental plaque as biofilms. In this study, we investigated the antibacterial effects of essential oils on the following oral bacteria: Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, Streptococcus mutans, and Streptococcus sobrinus. We tested manuka oil, tea tree oil, eucalyptus oil, lavandula oil, and romarinus oil and determined their minimum inhibitory concentration and minimum bactericidal concentration. The essential oils inhibited the growth of the bacteria tested, manuka oil being the most effective. Minimum bactericidal concentration values showed that lavandula oil acts bacteriostatically, and the remaining oils, bactericidally. Periodontopathic bacterial strains tested were killed completely by exposure for 30 s to 0.2% manuka oil, tea tree oil or eucalyptus oil. Tea tree oil and manuka oil showed significant adhesion-inhibiting activity against P. gingivalis. All the essential oils tested inhibited the adhesion of S. mutans. This study showed that, among the essential oils tested, manuka oil and tea tree oil in particular had strong antibacterial activity against periodontopathic and cariogenic bacteria. From the viewpoint of safety, we also examined the effects of these essential oils on cultured human umbilical vein endothelial cells and found that, at a concentration of 0.2%, they had little effect on cultured cells.

Antimicrobial Efficacy of Various Essential Oils at Varying Concentrations against Periopathogen Porphyromonas gingivalis

There are increasing numbers of research paper on the antimicrobial efficacy of various essential oils for their prospective use as surface disinfectants, food preservatives and alternative medicinal therapy. However articles on their antibacterial efficacy against oral pathogens especially periopathogens are limited. Takarada et al., assessed the antimicrobial effect of essential oils on cariogenic and periodontopathic bacteria including P.gingivalis [30]. They found that periodontopathic bacteria were killed completely by exposure for 30 seconds to 0.2% manuka oil, tea tree oil and eucalyptus oil. Tea tree and manuka oil showed significant adhesion inhibiting activity against P.gingivalis [27]. These results are in accordance with our study. Among all the oils tested, manuka and tea tree oil had particular strong antibacterial activity against periodontopathic bacteria. In our study, we found eucylyptus oil to be more effective than tea tree oil against P.gingivalis.

Since periodontitis is highly prevalent disease, undesirable effects of several antimicroial agents presently being used in treatment of oral disease and augmented resistance of oral bacteria to antibiotics are a cause of concern. Alternate products that are safe but equally effective are required for the treatment as well as the prevention of disease. Essential oils such as those tested in this study could provide a good alternative to usual commercial antibiotics.
 

LQB

The Living Force
FOTCM Member
Since periodontitis is highly prevalent disease, undesirable effects of several antimicroial agents presently being used in treatment of oral disease and augmented resistance of oral bacteria to antibiotics are a cause of concern. Alternate products that are safe but equally effective are required for the treatment as well as the prevention of disease. Essential oils such as those tested in this study could provide a good alternative to usual commercial antibiotics.
Unfortunately, even antibiotics have a very hard time dealing with focal infections of the mouth/teeth. Often the infections are buried near the root in pulpless teeth and nearly 100% in root canals. The infection is chronic but there is no complaint of pain from the patient. Rosenow demonstrated this many times by using culture samples taken from the tips of extracted teeth, and using a special oxygen gradient culture to grow the various forms of bacteria across the oxygen gradient. The only condition he found for permanent cure of the secondary infection was verified removal of the focal infection of the mouth often requiring removal of many or all teeth.
 

Helle

Jedi Master
Unfortunately, even antibiotics have a very hard time dealing with focal infections of the mouth/teeth. Often the infections are buried near the root in pulpless teeth and nearly 100% in root canals. The infection is chronic but there is no complaint of pain from the patient. Rosenow demonstrated this many times by using culture samples taken from the tips of extracted teeth, and using a special oxygen gradient culture to grow the various forms of bacteria across the oxygen gradient. The only condition he found for permanent cure of the secondary infection was verified removal of the focal infection of the mouth often requiring removal of many or all teeth.
I have seen this many times on Xrays. An infection that spreads to the surrounding teeth and jawbone .A rootcanal treatment will only temporarily remove the symptoms. The only way to get rid of the infection completely, is to remove the tooth. But then, often you have to spend a lot off money, time and agony, replacing that missing tooth, otherwise you end up with a lot of other potentiel problems , teeth that wander / tilts, pain in the joint of the jaw , social stigmata.
 

LQB

The Living Force
FOTCM Member
I have seen this many times on Xrays. An infection that spreads to the surrounding teeth and jawbone .A rootcanal treatment will only temporarily remove the symptoms. The only way to get rid of the infection completely, is to remove the tooth. But then, often you have to spend a lot off money, time and agony, replacing that missing tooth, otherwise you end up with a lot of other potentiel problems , teeth that wander / tilts, pain in the joint of the jaw , social stigmata.
Thanks for your input Helle - I think you would really enjoy the book I mentioned above. Rosenow's work is fascinating and he essentially devoted his career to the focal infection source of so many chronic conditions that were slowly killing the patients. And its a pleasure to read so much good work that has since been ignored by the mainstream medical.
 

Helle

Jedi Master
Thanks for your input Helle - I think you would really enjoy the book I mentioned above. Rosenow's work is fascinating and he essentially devoted his career to the focal infection source of so many chronic conditions that were slowly killing the patients. And its a pleasure to read so much good work that Ihas since been ignored by the mainstream medical.
I'll definately look into it. I'm a little challenged, not being english native speaking, especially when it comes to medical terms. It makes my brain hurt.
 

Keyhole

The Living Force
FOTCM Member
Interestingly, I was recently notified of a new test by one of the labs I am signed up with. It is called OralEcologix, and it provides a snapshot of the oral bacterial population. I am not sure of its efficacy, but am probably going to test myself nonetheless.


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LQB

The Living Force
FOTCM Member
Well, I think that autohemotherapy might be part of an approach to this problem along with higher doses of Vit C with DMSO administered via IV.
That is addressed in the book. Autoblood can help temporarily with the chronic secondary infection but apparently, cannot deal with the focal infection. As a result, the secondary infection returns.
 

nicklebleu

The Living Force
FOTCM Member
That is addressed in the book. Autoblood can help temporarily with the chronic secondary infection but apparently, cannot deal with the focal infection. As a result, the secondary infection returns.
But Rosenow also said that if autohemotherapy is applied on a regular basis (every 5 - 7 days), it can help prevent further spread in the body, even though it cannot kill the cells already affected.

Interesting in this respect is that exercise can have a positive modifying effect. I was wondering, if one of the mechanism involved (apart from modifying your immune response, as quoted in the article), was to eliminate cells that are harboring pathogens in the cell itself, by stressing it - and because they are infected, their resistance might be limited (similar to the mechanism that can eliminate muscle cells with damaged mitochondria).

Just my musings!
 

Laura

Administrator
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FOTCM Member
But Rosenow also said that if autohemotherapy is applied on a regular basis (every 5 - 7 days), it can help prevent further spread in the body, even though it cannot kill the cells already affected.

Interesting in this respect is that exercise can have a positive modifying effect. I was wondering, if one of the mechanism involved (apart from modifying your immune response, as quoted in the article), was to eliminate cells that are harboring pathogens in the cell itself, by stressing it - and because they are infected, their resistance might be limited (similar to the mechanism that can eliminate muscle cells with damaged mitochondria).

Just my musings!
I wonder about an antibiotic mixed with DMSO, applied topically to the face/jaws? And iodine with DMSO as a mouth wash? Don't know what the percentages of such a solution should be, but maybe somebody could figure it out.
 
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