One Theory to prove them all

[Jon_Tradicionali]

I believe the findings from the study linked below are perfectly linked to the case of CFS:

http://www.ncbi.nlm.nih.gov/m/pubmed/23268242/?i=2&from=herpes pharynx russian

A common virus e.g the infamous EBV, combined with pathogenic bacteria e.g Streptococci equals viral persistence.

Of course the study does not mention CFS specifically, as most studies of this kind do not. But the findings are of crucial importance for us. The study has focused on the viral-bacteria combo persistence in the pharynx, but of course this can occur in other parts of the body, e.g the human gut.

This links with:

-Lipkin, who says the action is in the gut (bacterial/viral)
-KDM who found abnormally high levels of Strep and Entero bacteria in PWCFS.
-Pridgen who has found evidence of HSV in patient guts
-The familial connection as bacteria is passed to us from our mothers which is the way we are 'predisposed' to CFS.
-Lerner who has for decades firmly believed in EBV causing CFS
-VZK who theorised the vagus nerve
-Loomis who believes in HHV6

Pathogenic Bacteria combined with A virus can lead to viral persistence and hence a chronic inflammatory state due to a chronically active immune system and hence the myriad of symptoms we call Chronic Fatigue Syndrome.

I've been doing nothing but reading and experimenting for the last decade and have had CFS since age 4, this is by far the definitive cause of CFS for the very large majority of us. I am positive this cause can also manifest itself as other syndromes, FM etc....

Eagerly awaiting Pridgens results as he claims his combo of drugs stop the PROCESS which leads to symptoms, such as detaching the virus and bacteria which persists. This is the next best thing to a cure. To achieve a cure, the bacteria must also be eliminated in order to remove the predisposition that we inherited.

I've focused on the bacterial side of this theory extensively in my thread for those interested:

Http://forums.phoenixrising.me/index.php?threads/gut-microbes-pathogenesis-of-cfs.27546/

I am writing this rushed at work. So correct me on any mistakes and I'll edit.

Jon.

 

[Antares in NYC]

This is a very interesting study that could explain CFS (or at least a subset), but it could also explain other similar debilitating conditions like chronic Lyme. Think about it. This study implies that a nasty virus like EBV and an intracellular bacterial infection can combine to wreak havoc in the immune system.

Maybe we should not be looking for one microbe/pathogen as the trigger to ME/CFS, but a very specific combo of infections that leads to the chronic immune disregulation. Take virus from column A, combine with bacterium from column B, (add certain genetic or environmental predispositions), and voila: ME/CFS happens.

At the very least, quite an interesting thought.

 

[Antares in NYC]

As I keep thinking about this theory, a lot of the usual suspects could fit the bill of a lethal combo:

Column A: Epstein-Barr, HHV6, Coxsackie enterovirus, Parvo, etc...
Column B: Streptococcus, cPN (chlamydia pneumonia), Lyme, brucellosis, mycobacteria, etc...
Add to it the exposure to mold biotoxins or other factors that mess up the immune system... and you have a devilish combination of factors, a trifecta that could precipitate the processes that we know as ME/CFS

Maybe this explains why they have not found ONE single pathogen responsible for CFS, but all CFS patients show random high titres of a number of the pathogens listed above and then some.

 

[alex3619]

I have been saying for some time now that a lot of pathogens have co-evolved to take advantage of each other. We have been thinking of pathogens in isolation, as invaders, but its more like an ecology. Having said that I have not read the paper yet, so I am reserving further comment.

 

[Gijs]

I do not think that certain bacteria or viruses cause ME. There is a problem with the immune system. Normally these infections remain dormant. In ME patients, there is somewhere a 'defect'. A problem with TLR7 and TLR9 for example could explain everything.

 

[lansbergen]

. A problem with TLR7 and TLR9 for example could explain everything.

And what causes these problems????

 

[Jon_Tradicionali]

I do not think that certain bacteria or viruses cause ME. There is a problem with the immune system. Normally these infections remain dormant. In ME patients, there is somewhere a 'defect'. A problem with TLR7 and TLR9 for example could explain everything.

May I ask why then would this 'defect' only show up in some people when they're in their 30's or 40's?

 

[adreno]

I do not think that certain bacteria or viruses cause ME. There is a problem with the immune system. Normally these infections remain dormant. In ME patients, there is somewhere a 'defect'. A problem with TLR7 and TLR9 for example could explain everything.

You can't explain a problem with another problem, this is circular reasoning. A problem has to have a cause.

 

[Gijs]

And what causes these problems????

Good question.

 

[Gijs]

You can't explain a problem with another problem, this is circular reasoning. A problem has to have a cause.

This work both ways.

 

[Gijs]

May I ask why then would this 'defect' only show up in some people when they're in their 30's or 40's?

Who says that this 'defect' only shows up in people in their 30's or 40's? Many people with ME are in their 20's or adolescent.

 

[Jon_Tradicionali]

Who says that this 'defect' only shows up in people in their 30's or 40's? Many people with ME are in their 20's or adolescent.

I know that...I've had it since age 4.

I didn't say all have it in their 30s or 40s.
It was an example. When a 36 year old woman contracts ME after a simple flu she had triggered it. Why didn't her 'defect' show up in the first 36 years of her life?

 

[caledonia]

It doesn't matter what virus you have. What matters is the stressor (virus, toxins, mold, etc.) more than your body can handle?

Genetic susceptibility + environmental stressors = multifactorial disease

The body will compensate or mask symptoms up until the tipping point of the final stressor.

See the Methylation Made Easy video #1 linked in my signature.

 

[Gijs]

I know that...I've had it since age 4.

I didn't say all have it in their 30s or 40s.
It was an example. When a 36 year old woman contracts ME after a simple flu she had triggered it. Why didn't her 'defect' show up in the first 36 years of her life?

I don't know if this 'defect' is genetic, maybe it can be acguired during our lives...

 

[tdog333]

Caledonia is right on the money. Once you overload the body and tip the balance it's a hard climb out, but it's possible. It's not about treating the specific strain of virus(most of the time) It's about finding the underlying cause. Why is the immune system malfunctioning?

 

[Antares in NYC]

I do not think that certain bacteria or viruses cause ME. There is a problem with the immune system. Normally these infections remain dormant. In ME patients, there is somewhere a 'defect'. A problem with TLR7 and TLR9 for example could explain everything.

I don't want to pile on, but a "genetic defect" is not exactly the answer to the ME/CFS puzzle. If anything, this would point even further towards a viral trigger that precipitates the immune dysfunction. All viruses (but particularly entero and retroviruses) can change your DNA in insidious ways. If it were a "genetic defect" (as in something you inherit genetically), it makes no sense people get ME/CFS at random times in their lives... usually after a major viral onset.

It makes more sense that a pathogen, combination of pathogens, or added toxic environmental factors would precipitate the immune overload, and it's plausible that genetic problems for ME/CFS people may be the consequence of an initial and nasty viral infection.

 

[MeSci]

I don't want to pile on, but a "genetic defect" is not exactly the answer to the ME/CFS puzzle. If anything, this would point even further towards a viral trigger that precipitates the immune dysfunction. All viruses (but particularly entero and retroviruses) can change your DNA in insidious ways. If it were a "genetic defect" (as in something you inherit genetically), it makes no sense people get ME/CFS at random times in their lives... usually after a major viral onset.

It makes more sense that a pathogen, combination of pathogens, or added toxic environmental factors would precipitate the immune overload, and it's plausible that genetic problems for ME/CFS people may be the consequence of an initial and nasty viral infection.

I think that we do have a high proportion of certain heritable genetic SNPs (single-nucleotide polymorphisms) from what I have read in the genetics forum. @Valentijn has been compiling some charts based on data provided by members and by non-ME people.

As illnesses tend to result from a combination of genes and environment ('Nature and nurture'), it is perfectly possible - indeed likely - that certain genes will increase susceptibility to environmental factors at certain times of life, and combinations of these. ('Environment' includes anything that happens to a person, e.g. exposure to pathogens, chemicals, psychological stress, allergens, medicines, diet, etc.) Age-related hormonal changes will change the physiological environment, and could be an important variable.

 

[Valentijn]

As illnesses tend to result from a combination of genes and environment ('Nature and nurture'), it is perfectly possible - indeed likely - that certain genes will increase susceptibility to environmental factors at certain times of life, and combinations of these. ('Environment' includes anything that happens to a person, e.g. exposure to pathogens, chemicals, psychological stress, allergens, medicines, diet, etc.) Age-related hormonal changes will change the physiological environment, and could be an important variable.

I think there are two basic issues which make both genes and an infection (or other physical stressor) necessary components:
1) We aren't born sick, so it can't be entirely genetic.
2) Not everyone exposed to the same infection has the same reaction.

5% of people with Q-fever end up with ME, but 95% don't. Similar for EBV, etc. So there must be some reason why those 5% end up with a serious problem. The anecdotal indication that many of us have family members with ME or similar problems would seem to argue for a genetic susceptibility.

That susceptibility is a huge unknown. Is it a problem with methylation? An anomaly in our immune reaction? An issue with vitamins, amino acids, or neurotransmitters?

 

[Vegas]

I think there are two basic issues which make both genes and an infection (or other physical stressor) necessary components:
1) We aren't born sick, so it can't be entirely genetic.
2) Not everyone exposed to the same infection has the same reaction.

5% of people with Q-fever end up with ME, but 95% don't. Similar for EBV, etc. So there must be some reason why those 5% end up with a serious problem. The anecdotal indication that many of us have family members with ME or similar problems would seem to argue for a genetic susceptibility.

That susceptibility is a huge unknown. Is it a problem with methylation? An anomaly in our immune reaction? An issue with vitamins, amino acids, or neurotransmitters?

While I tend to agree, and understand that your reference to "sick" applies to development of ME/CFS, I think a disproportionate number of us have features of immune dysfunction from very early childhood that are manifested by food intolerances, eczema, asthma, etc. The expansion of these conditions and "auto-immune" disease in the last twenty-five years to include ADHD, and ASD has me concerned about the prospects for a significant escalation in cases of ME/CFS, but more importantly, it suggests to me there is an epigenetic explanation for these disease processes, along with ME/CFS.

While genetic and environmental disease susceptibility, likely plays a part, we are witnessing an explosion in inflammatory diseases. I think the effect of microbial acquisition from birth/infancy, or the subsequent alteration of the microbiome later in life has to be considered given the rapidity in which microbial changes could alter genetic expression. Not only the speed of such changes, but the breadth of these epigenetic changes is what impresses me.

I also think genetic susceptibility is likely, but the historically recent epidemic of inflammatory disease suggests to me that there has to be an epigenetic underpinning of this phenomenon. There may be heritability of genetic expression instead of heritability of actual nucleotide sequence changes. My study of inflammatory bowel disease tells me that these are in large part mediated by changes in gene expression not gene sequence. These disease processes have now demonstrated epigentic patterns similar to what we are likely to see in ME/CFS, with very prominent interference in methylation. Methylation is both a means of rapidly influencing gene expression and it is critical in regulating energy metabolism. Inhibition down-regulates energy synthesis and hence cellular/DNA damage.

I would suggests that the use of antibiotics, vaccines, the use of glyphosate, and radical shifts in modern diets may be among some of the more prominent causal environmental factors, in part, because these modern developments would unfavorably modify the microbiome and disproportionately effect those with microbial inferiority. I think alterations of our intestinal microbiome can most readily explain Impaired methylation, amino acid metabolism and micronutrient availability, immune and neurotransmitter dysfunction.

These changes largely reflect combinations of adaptive responses to sustain life and genetic expression. They interact wth methylation, histone acetylation, etc. to limit ROS/NOS. The question is, how can we favorably impact epigentic expression. I think the answer for many involves restoring the microbiome; this I believe is the best way to limit ROS and impact gene expression.

Vasopressin, Leptin, Cortisol, etc., these things are known to be under epigenetic control because we are dynamic creatures with dynamic exposures to ROS, and we have to react quickly or we die.

 

[tdog333]

I don't want to pile on, but a "genetic defect" is not exactly the answer to the ME/CFS puzzle. If anything, this would point even further towards a viral trigger that precipitates the immune dysfunction. All virures (but particularly entero and retroviruses) can change your DNA in insidious ways. IF it were a "genetic defect" (as in something you inherit genetically), it makes no sense people get ME/CFS at random times in their lives... usually after a major viral onset.

The genetic defect generally pre-disposes the person for catastrophic failure. Methylation is key to create immune cells, DNA/RNA, and other vital functions. Eventually the body can't keep up due to oxidative stress, generally triggered by an infection(commonly viral). It's also important to note that not every case of CFS starts with a virus. Mine was due to crappy diet, over training and exertion, stress, and finally a tiny bacterial infection and one round of ABX paved the way for a larger infection and meltdown. At this point the balance is tipped and the body can't keep up enough energy to perform vital functions such as creating immune cells and detoxifying via the liver.