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Microbial Roots May Be Behind Most Disease

Alton

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Amazing discoveries!

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



Debora MacKenzie
New Scientist
Wed, 07 Aug 2019 00:01 UTC






© Kateryna Kon/Science Photo Library
Does this one microbe cause heart disease, stroke, Alzheimer's, diabetes, Parkinson's, pre-term birth, pancreatic cancer and kidney disease... and does that mean we can beat them?
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 orstroke.

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.


In fact, the build-up of beta amyloid plaques in the brain, rather than causing dementia, may be a natural defense mechanism against microbes. See: How an outsider in Alzheimer's research bucked the prevailing theory (and he's probably right)


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.

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 (see "Master of concealment") - 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.​
________________________________________________________________________________________________________________________​
My comments:

It is here you may want to stop and catch your breath before you run off to brush your teeth. Cleaning your teeth is helpful but you may want to do a search on what's called "Oil Pulling". Oil pulling is using various oils to clean your teeth and gums deeply and without a brush. This requires time and patience. You put a tablespon or three of of oil into your mouth and DO NOT SWALLOW! Instead you swish it around in your mouth for 5 to 20 minutes. Sounds impossible...right?!? Wrong! It IS possible and incredibly effective! Once you see what you spit out when you're done will quickly educate you in WHY you shouldn't swallow! What goes in as nice, clean looking oil comes out as a disgusting, ugly, really gross looking oily gak similar to stuff you might see at the edge of an oil slick. You can rinse and/or brush afterward to remove the taste and residue. Your WHOLE mouth will never feel so clean!
 

<SLV>

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Thanks for sharing this. I am in a journey to correct my biome. This adds a new dimension to the puzzle.
 

abeland1

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NEW BACTERIA DISCOVERED IN HUMAN BLOOD

Two new species of bacteria have been found in the blood of patients in China.



The bacteria were found in the blood of two human patients during blood tests as part of routine medical care. The new bacteria, both of which are in the Enterobacter genus, were found to be resistant to multiple antibiotics.

Enterobacter are not usually harmful and exist as part of the healthy gut microflora. However, when these bacteria enter the bloodstream, respiratory system or the urinary tract they can cause disease.

Enterobacter infection in the blood can lead to diseases including meningitis and bacteraemia, and Enterobacter in the lungs can lead to pneumonia. Bacteraemia is the presence of bacteria in the bloodstream and can lead to serious conditions including sepsis and septic shock.

The researchers named the newly discovered species Enterobacter huaxiensis and Enterobacter chuandaensis. The bacteria were named after the region in which they were discovered and Sichuan University, where the authors are based.

The discovery of E. huaxiensis and E. chuandaensis was reported in the International Journal of Systematic and Evolutionary Microbiology, along with a description of the new species and their antimicrobial resistance profiles.

The resistance of these newly discovered bacteria to antibiotics is a concern, as this would make the treatment of life-threatening infections more difficult. Both new species are resistant to penicillin and cephalosporin group antibiotics. These antibiotic groups are commonly used to treat bacterial infections.

Bacterial infections such as bacteraemia are usually with frontline antibiotics and a delay in treatment could cause progression to sepsis. Sepsis has a high mortality rate and so it is vital this condition is treated quickly.

The full scientific paper can be found on the International Journal of Systematic and Evolutionary Microbiology website here. (DOI: 10.1099/ijsem.0.003207)

Published by the Microbiology Society and owned by the International Committee on Systematics of Prokaryotes (ICSP), a committee of the Bacteriology and Applied Microbiology Division of the International Union of Microbiological Societies, International Journal of Systematic and Evolutionary Microbiology; is the leading forum for the publication of novel microbial taxa and the ICSP’s official journal of record for prokaryotic names.

In the five years between 2018 and 2022, the Microbiology Society’s principle goal is to develop, expand and strengthen the networks available to our members so that they can generate new knowledge about microbes and ensure that it is shared with other communities. The impacts from this will drive us towards a world in which the science of microbiology provides maximum benefit to society. Find out more at microbiologysociety.org

For more information, please contact: l.cox@microbiologysociety.org
 

TomD

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I've known for a while that a human body contains many times more bacteria cells than "human" cells with the relationship with most of the millions of strains inside the body being a symbiosis. I suspect that the true interplay between organisms is the least understood aspect of what we call "health".
 

GOLDBRIX

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Those of us who use Electrically Isolated Silver (EIS)/CS have known this for some time.
When you first use EIS/CS there is a very good chance you'll have a low grade headache that is usually remedied by your favorite OTC pain reliever. This headache is called the Herxhiemer [sp?] Effect.
This low grade headache is thought to be caused by the waste of dead bacteria as it is filtered out of the body. The bacterial death are caused by silver introduction into the body, and the main reason first time users should begin with only a teaspoonful of EIS/CS for the first few days of using EIS/CS.
Personally, I had the headache but continual use of EIS/CS ( 1t. twice a day sublingually and swallow Xs two days) and less than 12 hours of OTC Painkiller the Herxhiemer [sp?] Effect was over, For Me. ( I use ounces daily now)
CAUTION: There has been reports of some first time users have kept headaches longer and even fewer having to seek Medical care.
As a daily users of EIS we may have less issues with the above newly named bacteria simply due to our bodies having EIS/CS in our systems as a prophylactic nutrient which has reduced the bacterial population within out blood system.

Those who fear EIS/CS because of this effect on many bacteria can always supplement their diets with probiotics, Sweet Acidopholius [sp?] Milk, Yogurts, and cultured cottage cheese among other supplements.
I keep three gallons of filter water in my refrigerator. Each gallon gets a shot glass full of EIS/CS mixed in. I drink about a gallon to a gallon and a half of water daily.

DYODD,
WAOOR,
 

Zed

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I've been saying this is the case for years! It is all about your microbiome and your immune system! Gut health is so far and away more important than western medicine credits.
 

abeland1

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My first research on colloidal silver was by monitoring alternative medicine newsgroups. I was struck by the number of people claiming lifelong freedom from common ailments. My use of colloidal silver started because of a specific problem, sinusitis, so I didn't give these claims much credence. Do silver ions kill virtually all pathogens? Too good to be true? Is the "too good to be true" factor the reason we can't believe it? Is the presence of silver ions in their bloodstream the reason for these people's relative immunity to chronic disease?.

Posted by Mark Crislip
Mark Crislip, MD has been a practicing Infectious Disease specialist in Portland, Oregon, since 1990. He is a founder and the President of the Society for Science-Based Medicine where he blogs under the name sbmsdictator. He has been voted a US News and World Report best US doctor, best ID doctor in Portland Magazine multiple times, has multiple teaching awards and, most importantly, the ‘Attending Most Likely To Tell It Like It Is’ by the medical residents at his hospital. His growing multi-media empire can be found at edgydoc.com.
All Posts Website


“It’s just a theory”

https://sciencebasedmedicine.org/its-just-a-theory/
 
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Thecrensh

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I've begun to wonder if you can pass certain conditions on to your sexual partner...not just the classical STDs, but other ones like IBS, or allergies, or dimentia, etc.
 

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I've begun to wonder if you can pass certain conditions on to your sexual partner...not just the classical STDs, but other ones like IBS, or allergies, or dimentia, etc.

Yes. You share all your bugs. If your immune system isn't up to dealing with them you are toast. These bugs are everywhere, in the end its a healthy immune system that keeps them @ bay. While they are not all 'disease' they can cause a vast array of symptoms from arthritis, dietary intolerance through to depression and metal diseases. I'm convinced of it through my life experience. Have you ever met a couple and come away thinking that they are depressed in exactly the same kinda way... it's the damn bugs they shared I tell ya! Sounds a little mad but you will see in the years to come they will put almost everything down to wayward microbiology in your body. Hint --> When they die they create a toxic residue (basically a chemical release) just like any chemical it can impact mood or any number of things. Bug's with longer life cycles often match up with lunar phases, ie they die off around a full or new moon. So... now you know why the wife goes nuts @ the full moon... it's just damn chemistry!

This is some of what you learn fighting what they call 'chronic Lyme'... but it isn't a disease, its an immune system failure. Age + modern lifestyle is bringing myriad problems from basically the same source earlier and earlier as our food and environment changes. (chlorine, fluoride,antibiotics, electronics etc) Death by 1000 small cuts with no one cut being 'the problem'.

I'm trying to work out the best way to deal with this and I'm making some ground... if I 'win' I will tell you what I did and the theory it is based on. ---> Getting there slowly!

I know it sounds mad, one day I will try do a slow logical post covering what I have found out.
 

Thecrensh

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Yes. You share all your bugs. If your immune system isn't up to dealing with them you are toast. These bugs are everywhere, in the end its a healthy immune system that keeps them @ bay. While they are not all 'disease' they can cause a vast array of symptoms from arthritis, dietary intolerance through to depression and metal diseases. I'm convinced of it through my life experience. Have you ever met a couple and come away thinking that they are depressed in exactly the same kinda way... it's the damn bugs they shared I tell ya! Sounds a little mad but you will see in the years to come they will put almost everything down to wayward microbiology in your body. Hint --> When they die they create a toxic residue (basically a chemical release) just like any chemical it can impact mood or any number of things. Bug's with longer life cycles often match up with lunar phases, ie they die off around a full or new moon. So... now you know why the wife goes nuts @ the full moon... it's just damn chemistry!

This is some of what you learn fighting what they call 'chronic Lyme'... but it isn't a disease, its an immune system failure. Age + modern lifestyle is bringing myriad problems from basically the same source earlier and earlier as our food and environment changes. (chlorine, fluoride,antibiotics, electronics etc) Death by 1000 small cuts with no one cut being 'the problem'.

I'm trying to work out the best way to deal with this and I'm making some ground... if I 'win' I will tell you what I did and the theory it is based on. ---> Getting there slowly!

I know it sounds mad, one day I will try do a slow logical post covering what I have found out.

That's kind of how I feel things work...
 

GOLDBRIX

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Yes. You share all your bugs. If your immune system isn't up to dealing with them you are toast. These bugs are everywhere, in the end its a healthy immune system that keeps them @ bay. While they are not all 'disease' they can cause a vast array of symptoms from arthritis, dietary intolerance through to depression and metal diseases. I'm convinced of it through my life experience. Have you ever met a couple and come away thinking that they are depressed in exactly the same kinda way... it's the damn bugs they shared I tell ya! Sounds a little mad but you will see in the years to come they will put almost everything down to wayward microbiology in your body. Hint --> When they die they create a toxic residue (basically a chemical release) just like any chemical it can impact mood or any number of things. Bug's with longer life cycles often match up with lunar phases, ie they die off around a full or new moon. So... now you know why the wife goes nuts @ the full moon... it's just damn chemistry!

This is some of what you learn fighting what they call 'chronic Lyme'... but it isn't a disease, its an immune system failure. Age + modern lifestyle is bringing myriad problems from basically the same source earlier and earlier as our food and environment changes. (chlorine, fluoride,antibiotics, electronics etc) Death by 1000 small cuts with no one cut being 'the problem'.

I'm trying to work out the best way to deal with this and I'm making some ground... if I 'win' I will tell you what I did and the theory it is based on. ---> Getting there slowly!

I know it sounds mad, one day I will try do a slow logical post covering what I have found out.
Moms share antibodies with their babies through breast milk ( a body function of females) why would not other fluids contain some antibodies from the body that generated the fluid. Kissing involves saliva, sweating bodies in contact transfer body moisture....
 

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Amazing discoveries!

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



Debora MacKenzie
New Scientist
Wed, 07 Aug 2019 00:01 UTC






© Kateryna Kon/Science Photo Library
Does this one microbe cause heart disease, stroke, Alzheimer's, diabetes, Parkinson's, pre-term birth, pancreatic cancer and kidney disease... and does that mean we can beat them?
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 orstroke.

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.


In fact, the build-up of beta amyloid plaques in the brain, rather than causing dementia, may be a natural defense mechanism against microbes. See: How an outsider in Alzheimer's research bucked the prevailing theory (and he's probably right)


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.

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 (see "Master of concealment") - 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.​
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"My comments:

It is here you may want to stop and catch your breath before you run off to brush your teeth. Cleaning your teeth is helpful but you may want to do a search on what's called "Oil Pulling". Oil pulling is using various oils to clean your teeth and gums deeply and without a brush. This requires time and patience. You put a tablespon or three of of oil into your mouth and DO NOT SWALLOW! Instead you swish it around in your mouth for 5 to 20 minutes. Sounds impossible...right?!? Wrong! It IS possible and incredibly effective! Once you see what you spit out when you're done will quickly educate you in WHY you shouldn't swallow! What goes in as nice, clean looking oil comes out as a disgusting, ugly, really gross looking oily gak similar to stuff you might see at the edge of an oil slick. You can rinse and/or brush afterward to remove the taste and residue. Your WHOLE mouth will never feel so clean!
"

People sometimes ask… Why do I need 50 ppm EIS?
They had been told the 10 PPM is as much is anyone ever needs.
Porphyromonas gingivalis can be found at low levels in 25% of healthy individuals with no oral disease. Transmission to the bloodstream gingivalis can occur during ordinary activities such as brushing, flossing, and chewing, as well as during dental procedures. A research article on this common bacteria is available here:
https://advances.sciencemag.org/content/5/1/eaau3333
I guard against this bacteria by putting as much CS as I can in my mouth, not swallowing it, but swishing it around in my mouth as long as I can and then spit it out. By using 50 PPM, I have five times the chance of killing all of these bugs than would have been the case using 10 PPM. It's as simple as that.
 
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