Dr Chia finds Double-stranded RNA in stomach biopsies

[natasa778]

In my family, there are several with CFS/ME and/or the usual co-morbid disorders. We grew up and live in different cities and countries. I also have a relative in the same branch of the family who battled lymphoma. This and related conditions are too prevalent in my family not to be genetic, especially without other common factors (such as local diet, places of birth, places of living). But I agree in part: microbiome will turn out to be one influential factor.

Basically, I think all of the physical prerequisites need to happen all together in genetically susceptible people to create the perfect immune storm. I realize now that @halcyon pointed out, that Dr, Chia has focused mostly on enteroviruses as the cause.

I will look at @halcyon 's Dr. Chia links and your micribiota/viral susceptibility link. I'm definitely curious to read them. I'm also reading through Dr. Chia's site and found this:


....
From this explanation, it seems he thinks there's an underlying immune problem, which makes patients more susceptible to the infections.

Family members share much more than just genes. Research into metagenome - bacteria, viruses etc, all non-human DNA, being passed from parents to children and interchanged between family members is in its infancy but one of the most exciting areas of 'general' modern science.

So when diseases (or susceptibility to diseases) are inherited or running in the family this does not automatically exclude infectious agents. On the contrary, those seem to be part of our family heirloom.


Regarding the question of genes vs gut microbiome playing a central part in immune reactions, there was a study recently that found past CMV infections played a much larger role than genes in one's immune responses.

 

[Mya Symons]

Does anyone know if a person who is susceptible to a chronic enterovirus infection would also be susceptible to an adenovirus infection? I'm asking because my son was in the hospital for a month for an adenovirus infection. While he was in there, a rheumatologist told us he had Fibromyalgia and CFS based on past and current symptoms including nerve pain, muscle pain and joint pain. He also had rheumatoid arthritis antibodies. This all happened when he was around 12. However, eventually all of his symptoms went away except for the migraines. All of the symptoms came back again his senior year of High School except for the rheumatoid arthritis and he had a really rough last year. The symptoms went away again after he graduated and now he is working and going to college. Everything is going well for now. However, this is similar to how I started out. When I turned 30 the symptoms stayed. I spend a lot of time worrying about him.

I have CFS (SEID) and Fibromyalgia. His father has Fibromyalgia. My husband's brother also has Fibromyalgia and he has a sister with ME/CFIDS. His sister is the worst case in the family.

I also wonder if some of us have some gene mutation or something else that is hereditary that makes us particularly susceptible to certain viruses. I wish they would approve treatment with ampligen or something similar.

 

[halcyon]

Does anyone know if a person who is susceptible to a chronic enterovirus infection would also be susceptible to an adenovirus infection?

It's hard to say exactly what makes one person more susceptible than another. Robust antibody production is very important in fighting enterovirus infections. I don't think it's a coincidence that a lot of people with ME have IgG subclass 1 and 3 deficiencies, which are the subclasses often produced against protein based antigens. Strong innate immunity is also probably required to help contain it to the respiratory and GI tract and limit it from going systemic. I'm not sure how important these same factors are in adenovirus infections.

 

[thegodofpleasure]

I reiterate the importance of understanding the specifics of dsRNA viruses in the context of Dr Chia's work:
http://en.wikipedia.org/wiki/Double-stranded_RNA_viruses

• A persistent dsRNA virus infection can cause the patient to become immuno-suppressed.
• dsRNA viruses are vulnerable to being degraded by the "DICER" enzyme - hence a properly functioning DICER1 gene is crucial to eradicating them.
• Several dsRNA viruses are known to contain chaperonin / HSP60 proteins that have the potential to cause autoimmunity in infected patients.

Nowhere near enough is known about this class of viruses and their pathogenic potential at present.

I see parallels with Marshall & Warren's discovery of Helicobacter Pylori (and it's role in causing stomach ulcers and stomach cancer) in Dr Chia's findings.

 

[Kati]

I reiterate the importance of understanding the specifics of dsRNA viruses in the context of Dr Chia's work:
http://en.wikipedia.org/wiki/Double-stranded_RNA_viruses

• A persistent dsRNA virus infection can cause the patient to become immuno-suppressed.
• dsRNA viruses are vulnerable to being degraded by the "DICER" enzyme - hence a properly functioning DICER1 gene is crucial to eradicating them.
• Several dsRNA viruses are known to contain chaperonin / HSP60 proteins that have the potential to cause autoimmunity in infected patients.

Nowhere near enough is known about this class of viruses and their pathogenic potential at present.

I see parallels with Marshall & Warren's discovery of Helicobacter Pylori (and it's role in causing stomach ulcers and stomach cancer) in Dr Chia's findings.

Thx for the @thegodofpleasure

 

[adreno]

If gut microbiota explain it, why don't people who have fecal transplants recover?

While many do seem to improve after fecal transplants, it might not be enough to randomly throw a bunch of bacteria up your bum. We need to know more about the microbiome and how it relates to disease. Lipkin would be looking into this, if anyone cared to fund him.

The "persistent infection" hypothesis seems circular and non-explanatory to me. It doesn't explain why some people get very sick with common pathogens, while others don't. And as I said, I doubt genetics on their own explain this variance, although I grant that they probably have an influence.

 

[cigana]

While many do seem to improve after fecal transplants, it might not be enough to randomly throw a bunch of bacteria up your bum. We need to know more about the microbiome and how it relates to disease. Lipkin would be looking into this, if anyone cared to fund him.

The "persistent infection" hypothesis seems circular and non-explanatory to me. It doesn't explain why some people get very sick with common pathogens, while others don't. And as I said, I doubt genetics on their own explain this variance, although I grant that they probably have an influence.

I've also often wondered about the possibility of biofilms, which presumably would allow problematic bacteria to survive despite a fecal transplant, and would explain why the improvements seen are only temporary. I think KDM believes there is an underlying immune dysfunction which is why the new microbiome does not persist after a transplant.

Personally, distention/bloating was my first symptom, and I feel sure that whatever will cure that will cure everything else...

 

[adreno]

I've also often wondered about the possibility of biofilms, which presumably would allow problematic bacteria to survive despite a fecal transplant, and would explain why the improvements seen are only temporary. I think KDM believes there is an underlying immune dysfunction which is why the new microbiome does not persist after a transplant.

Personally, distention/bloating was my first symptom, and I feel sure that whatever will cure that will cure everything else...

Diet is also an extremely important factor in this. The microbiome responds to diet in weeks, and bacteria will not survive or function without the substrates that feed them. So even if we transplant the right bacteria, we also need to keep feeding them. See for example:

The interaction shown by the research team is valuable because many bacteria are adept at utilizing carbohydrates such as fucose, which are abundant in the gut. Confronted with diets that have little or no complex plant sugars, these bacteria are forced to change their function, especially in hosts that lack fucose. This was seen with the altered metabolic gene expression of one of the key microbes in the gut -- Bacteroides thetaiotaomicron. Changes in microbial membership or function as demonstrated in this study may, in turn, foster a "digestive landscape" that can promote inflammatory conditions such as Crohn's disease.

http://www.sciencedaily.com/releases/2013/09/130925130613.htm

 

[lansbergen]

The "persistent infection" hypothesis seems circular and non-explanatory to me. It doesn't explain why some people get very sick with common pathogens, while others don't. And as I said, I doubt genetics on their own explain this variance, although I grant that they probably have an influence.

When a low virulent strain carrier gets infected with a high virulent strain it can cause an extremne response.

 

[Bob]

Our genes simply doesn't seem to be that different, compared with the normal population.

I suspect that our understanding of genetics is still too primitive too be able to make strong conclusions about hereditary risk factors. Mark Davis' recent research into the immune systems of twins suggests that most immune changes seen in the general population are non-hereditary, but some genetic differences (suggesting potential genetic risk factors for ME) were seen in ME/fibro patients in another recent research study.

 

[adreno]

I suspect that our understanding of genetics is to primitive too be able to make any conclusions, although Mark Davis' recent twin research suggests that most immune differences are non-hereditary. Although some generic differences (suggesting potential genetic risk factors) were seen in ME/fibro patients in some other recent research.

But would there be any evolutionary purpose to having genes predisposing you to ME from common pathogens? Why would such genes have survived through a human history where having ME would most likely equal being dead, or at least not reproducing?

 

[Valentijn]

But would there be any evolutionary purpose to having genes predisposing you to ME from common pathogens? Why would such genes have survived through a human history where having ME would most likely equal being dead, or at least not reproducing?

The HLA genes already do a similar thing with our immune system, from what I understand. Hence people end up nicely protected against one thing, and at increased risk of different problems.

Another example would be sickle-cell anemia. It can cause serious health problems, but also protects people from malaria.

 

[Bob]

But would there be any evolutionary purpose to having genes predisposing you to ME from common pathogens? Why would such genes have survived through a human history where having ME would most likely equal being dead, or at least not reproducing?

That question opens up a complex niche discussion about evolution that I don't have expert knowledge about. But not all evolutionary changes have to be beneficial. For example, consider HERVs; They become inserted into our genome (I believe) not usually because they are beneficial, but because they aren't harmful to those whom they don't kill. Also, there are many genetic mutations that get carried in a population that aren't beneficial but only get expressed from time to time, and the population as a whole can cope with a certain amount of unhelpful randomness in the gene pool.

 

[adreno]

That question opens up a complex niche discussion about evolution that I don't have expert knowledge about. But not all evolutionary changes have to be beneficial. For example, consider HERVs; They become inserted into our genome (I believe) not usually because they are beneficial, but because they aren't harmful to those whom they don't kill. Also, there are many genetic mutations that get carried in a population that aren't beneficial but only get expressed from time to time, and the population as a whole can cope with a certain amount of unhelpful randomness in the gene pool.

Well, there is certainly a difference between something being "not harmful" or "unhelpful randomness" and a predisposition towards ME. But I get your point, and agree that it is possible that such a predisposition would convey advantages unknown at this point. It is just very hard to see from where I stand.

 

[cigana]

But would there be any evolutionary purpose to having genes predisposing you to ME from common pathogens? Why would such genes have survived through a human history where having ME would most likely equal being dead, or at least not reproducing?

Couldn't you use the same argument to say that no diseases have a genetic component (which we know to be untrue)?

 

[adreno]

Couldn't you use the same argument to say that no diseases have a genetic component (which we know to be untrue)?

No. Not if the genes convey substantial advantages, along with the disadvantages, as discussed above.

 

[cigana]

No. Not if the genes convey substantial advantages, along with the disadvantages, as discussed above.

Why there would necessarily have to be an evolutionary advantage? Presumably some mutations that caused no particular advantage/disadvantage in our evolutionary past could now cause a disadvantage given that our environment has changed.

 

[adreno]

Why there would necessarily have to be an evolutionary advantage? Presumably some mutations that caused no particular advantage/disadvantage in our evolutionary past could now cause a disadvantage given that our environment has changed.

Well, lots of things in the environment can change gene expression. For example, the gut microbiota. Hence my point.

 

[Bob]

Well, there is certainly a difference between something being "not harmful" or "unhelpful randomness" and a predisposition towards ME. But I get your point, and agree that it is possible that such a predisposition would convey advantages unknown at this point. It is just very hard to see from where I stand.

Actually, the point that I was making was that a predisposition to ME could be due to a harmful genetic mutation (i.e. unhelpful randomness). As cigana says, not all mutations have to be beneficial. And any population can afford to carry some harmful genes if it affects only a small minority of the population. Cystic fibrosis seems like an obvious example of a harmful genetic mutation that has no obvious benefit.

 

[SDSue]

…….. randomly throw a bunch of bacteria up your bum.

Thanks for the laugh. You certainly do have a way with words.