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Video Dr. Byron Hyde - Enterovirus theory?

Hip

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@Forbin
Yes, looking at this further, I think you are right that it was Colin McEvedy's PhD thesis that Byron Hyde is talking about.

It seems that on 3 January 1970 Colin McEvedy published a paper in the British Medical Journal about his opinion that the Royal Free outbreak was mass hysteria (full paper here), which you linked to above. And also his PhD thesis issued in Oxford 1971 was on this same subject (full PhD thesis available here).

However, if you look at the cover of the 26th January 1970 issue of Time that you linked to above and which contains an article on supposed Royal Free mass hysteria (see the Time 1970s covers here), the cover is not about the outbreak, but about the Biafra war in Nigeria. However, as you say, the Canadian Edition of Time may have had a different cover.
 

Forbin

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@Hip
I think the idea of it being on the cover was likely a misapprehension on my part. Dr. Hyde repeatedly says that it was "on the front page of Time magazine." The "front page" may not be the cover, but rather the first interior page that displays the table of contents.
 

Hip

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I think the idea of it being on the cover was likely a misapprehension on my part. Dr. Hyde repeatedly says that it was "on the front page of Time magazine." The "front page" may not be the cover, but rather the first interior page that displays the table of contents.
Yes, I saw your comment, but it seems unlikely to me, because presumably all articles in the magazine will be listed in the table of contents; so then why would Dr Hyde mention this?

Also, what's confusing me is that Dr Hyde says the PhD student visited the Royal Free for half a day to see the patients affected by the epidemic; well, then why it take 15 years for him to publish his study and PhD?

Anyway, it's not that important. I would have just liked to have seen the artwork on the Time cover page depicting mass hysteria.
 

Thomas

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Dr. Hyde has told me this story many times over the years. And each time there are various different details or conflicting pieces of information that I just boil down to the fact that he is quite old and often forgets the little things.
He is also the only doctor I know of who has visited a member of each and every ME outbreak dating back to the one in the 20's in LA so he's definitely been around.

With respect to the cover of TIME magazine, perhaps the Canadian version is different. But there is also a chance that Dr. Hyde is confusing the Royal Free outbreak in the 50's with the Incline Village outbreak in the 80's that gave rise to the term CFS. I'm pretty sure that outbreak made the cover of TIME but I have not gone back to look into this to verify. This is just my assumption.
 
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for me it all started with Coxsackie B so I'm a Byron-fan and would've loved to have a chat with him (the association does chat sessions with all the other video participants) but there seem to be no dates scheduled this time, alas! also missed the chance to see him while in Holland, a friend got to go though
 

eljefe19

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Yes, I saw your comment, but it seems unlikely to me, because presumably all articles in the magazine will be listed in the table of contents; so then why would Dr Hyde mention this?

Also, what's confusing me is that Dr Hyde says the PhD student visited the Royal Free for half a day to see the patients affected by the epidemic; well, then why it take 15 years for him to publish his study and PhD?

Anyway, it's not that important. I would have just liked to have seen the artwork on the Time cover page depicting mass hysteria.
@Hip Yo hip I finally mustered the energy to come onto the forum to pick your brain about this enterovirus theory.
How do you reconcile the test results that myself and others like you have of positive Coxsackie and Echovirus tests (Mine were actually Coxsackie A7,A9,A11,A21. Very high titers too. Plus high nagalese), with the recent series of studies showing hypo metabolic function, with the possibility that the enterovirus may not be the causal factor of the disease?

I should say I follow your posts religiously. I am similarly over anxious and moody with no clear reason why, along with lots of neuro and body inflammation. I take NAG, Flax, Low dose amisulpride, etc.

I am also taking mega doses of the Equilibrant components separately. EQ made me considerably sicker when I first started but after a couple months, I began to slowly improve. I've been escalating the doses further than EQ levels to 800 mg Oxymatrine, for example, at night. My supplementation is extensive. I believe if I can either, kill the viruses while supporting the immune system with gcmaf and others, and also addressing metabolic deficiencies, the kill switch would be somehow getting the mitochondria to work properly again. The two nootropics I've found that have pro mitochondrial properties are Tianeptine and Super Dose Pomegranate Extract (Pomella). PQQ and some others might help and I figure the more the better anyways. I was hoping you might be able to put your research skills into finding a way to possibly get our mitochondria to begin to transition out of this "dauer state" as its been described.

Thank you so much for all you have written over the years. My ability to focus is destroyed by this illness, and so your well sourced and formatted posts are a tremendous help. I have to say, my extensive supplementation regimen wouldn't have been possible without your work, and it really has given me great improvements. I used to feel like I had a stomach flu all the time. Now I'm simply tired and hazy. But its a huge difference! You're the man.

Jeff
 

eljefe19

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@Hip Also I have another question. It's a pickle. How do you reconcile the is microglial activation harmful or helpful debate? The gcmaf researchers showed that LDN decreased the effectiveness of the gcmaf. Dr. Chia says he doesn't understand Dr Montoya using Valcyte (potent microglial deactivator) when we're dealing with enterovirus infection? Which is why I stopped taking LDN when I started gcmaf. I want to try Ibudilast, but its similarly a TLR4 inhibitor. What does your research show on this subject?
 

Hip

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How do you reconcile the test results that myself and others like you have of positive Coxsackie and Echovirus tests (Mine were actually Coxsackie A7,A9,A11,A21. Very high titers too. Plus high nagalese), with the recent series of studies showing hypo metabolic function, with the possibility that the enterovirus may not be the causal factor of the disease?
Hi @eljefe19, glad you decided to join the forum.

I think it could be reconciled if enterovirus, or other viruses linked to ME/CFS, such as EBV, are triggering an autoimmune response that targets and disables mitochondria, or some related area of the energy metabolism.

The rituximab studies indicate that there is likely autoimmunity going on in ME/CFS (and the two orthostatic intolerance conditions common found in ME/CFS, namely orthostatic hypotension and POTS, have also been linked to autoimmunity); so there is a good argument for an autoimmune basis of ME/CFS.

So actually what we need to do is reconcile three areas: the large amount of studies that have shown enterovirus is linked to ME/CFS, with the fact that ME/CFS likely involves autoimmunity, with the fact that energy metabolism seems to be dysfunctional in ME/CFS.

The idea that viruses may trigger an autoimmune response that targets the energy metabolism would reconcile these three areas, and explain a lot of what we already know about ME/CFS.



I am similarly over anxious and moody with no clear reason why, along with lots of neuro and body inflammation. I take NAG, Flax, Low dose amisulpride, etc.
Did these supplements help your anxiety to any degree?



My ability to focus is destroyed by this illness, and so your well sourced and formatted posts are a tremendous help.
Glad that these posts have been a help to you.

In fact it's only by slow methodical writing of my posts, and making a clear layout, that I am able to understand the material myself!

I have the same brain fog problems, and ADHD too, which makes reading text difficult for me, and I find the process of writing posts with a clear layout helps me get to grips with the material I am trying to learn.



How do you reconcile the is microglial activation harmful or helpful debate?
The three brain autopsies that so far have been conducted on deceased ME/CFS patients all showed some degree of enterovirus infection in the brain. So if brain infection is common in ME/CFS, you might expect some chronic microglial activation, just in order to keep the infection in check.

There are two main modes of microglial activation: the classical mode, which is the "kill" mode that destroys pathogens, but which is also neurodestructive and causes collateral damage. (One major destructive factor in the classical mode may arise when microglia activate an enzyme called NADPH oxidase. This enzyme generates superoxide in order to kill pathogens, but the superoxide probably also causes some mild collateral damage.)

There is also the alternative mode of microglial activation, which is the "repair and heal" mode, and presumably this alternative mode would normally kick after microglia in the classical mode have completely killed the brain infection.

But if the brain infection is chronic and cannot be fully eradicated, it's hard to say what might be going on. I have not seen any research on this. Perhaps the microglia might remain in the classical mode, but at a low level of activation, just to keep the infection in check.


I don't think neurological damage from microglial activation will be major factor in most cases of ME/CFS, as not many patients show brain lesions on their MRI scans.

Also, consider the fact that some patients report very occasional periods where they spontaneously obtain temporary but complete remission from symptoms for period of a few days. If ME/CFS were caused by major damage to the brain, such remissions would be hard to explain. Those remissions suggest that there is nothing much physically wrong with the brain.

It seems more likely that some chronic immunological dysfunction is driving the brain symptoms; then when you get a few day where the immune system rights itself for a short time, the temporary spontaneous remissions occur.


I compiled a large list of microglial activation inhibitors in this post. There is also section in that post for supplements that favor the neuroprotective alternative mode of microglial activation, over the neurodestructive classical mode.

Of particular interest is apocynin from the herb Picrorhiza kurroa, which is a potent NADPH oxidase inhibitor, and has been shown to promote the neuroprotective alternative microglial mode of activation.

It may be worth experimenting with these microglial activation inhibitor supplements; however, assuming there is a low level brain infection in many ME/CFS patients, I should think that you will always have some degree of classical microglial activation, as this will be needed just to keep the infection under control.



I should say I follow your posts religiously.
Not a good idea! Better to be a bit skeptical and questioning!
 
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halcyon

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How do you reconcile the test results that myself and others like you have of positive Coxsackie and Echovirus tests (Mine were actually Coxsackie A7,A9,A11,A21. Very high titers too. Plus high nagalese), with the recent series of studies showing hypo metabolic function, with the possibility that the enterovirus may not be the causal factor of the disease?
On the surface, the two hypotheses don't seem to be incompatible. Despite his assertions made outside the peer reviewed paper, Naviaux states in the paper:
The low sphingolipid profile in CFS appears to be an adaptive response that is opposite to the increased sphingolipids observed in metabolic syndrome (11) and the acute cell danger response (CDR) (7) and ultimately may represent a fundamental response to oppose the spread of persistent viral and intracellular bacterial infections.
If you look at the older literature, there were some ideas about what might be going on. From Behan et al. 1985:

The results reported here suggest that the syndrome is due to the interaction of viral infection and immunological processes which produce damage to intracellular enzymes and result in abnormal muscle metabolism, especially on exercise. Viral infections have already been shown to cause such enzyme abnormalities, e.g. depletion of adenylate deaminase. Another possibility is that an autoantibody, such as the anti-mitochondrial antibody recently identified in patients with viral myocarditis, might be involved.
Lane et al. 2003:
While the effects of ‘‘disuse’’ and lack of fitness cannot be excluded, previous studies, supported by the evidence presented here, show that some CFS patients have abnormal muscle energy metabolism which is related statistically to the presence of enterovirus sequences in muscle, and that the viruses involved are predominantly coxsackie-B-like.
 

eljefe19

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@Hip @halcyon Thanks for the thorough responses guys. So I guess I'm wondering then is a cure possible without finding a cure for the enteroviruses themselves? Can our immune system be supplemented just right so that remission is possible?

@Hip I went to my new doc here in Salt Lake City and he knows about Chia and he believes enterovirus is probable, but his only idea for treatment is Interferon Beta. If I recall correctly you said Chia used this but it caused intense depression right? When it comes to anxiety, for me, having to live with this bullshit illness, and dealing with bullshit doctors and pharmacy techs and insurance companies, and then having to try and take care of myself in the real world when the state is meanwhile denying my disability application, has just got me at a level of anxiety where I've been taking Etizolam on top of everything else to help cope.

Its crazy how extensive my supplement regimen is. I might have upwards of 75 supplements, herbs, nootropics, Research chems, prescription drugs and OTC drugs, and then my marijuana which is the most important of all 75 when it comes to symptom relief of my CFS/Fibro/IBS. This illness is crazy isn't it?

I enjoy it though. Having some semblance of control over my own body. Btw, I've read that post you wrote on Microglial activation inhibitors a few times. I had forgotten about the two modes. I guess I am skeptical of inhibiting microglial activation if we are trying to kill off a brain virus. How would Coxsackie and Echovirus ever even be killed off for good? This is why I am taking Gcmaf. To bolster my immune system's ability to fight enterovirus. They claim that LDN blocked progress in gcmaf patients. Why? Well they didn't know for sure, but they postulated it was because of LDN inhibiting microglial activation. So, I asked my doctor about this, and he told me that microglial activation is probably over active so to speak and inhibiting it would be beneficial. But I'm not sure I'm convinced just yet.

Anyways man I have a ton more to discuss. But my biggest point of research right now is trying to figure out possible ways to get our mitochondria working again, once our immune systems are healed enough to put the enterovirus away.[/USER]
 

Hip

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If I recall correctly you said Chia used this but it caused intense depression right?
Interferon does cause depression in some patients taking it, but not all. In my case, the virus I caught seemed to induce depression and anhedonia by some neurological or immunological mechanism, and so I would be a little wary of taking interferon myself, given that the virus created this propensity to depression.


Having said that, I am looking into trying Russian interferon alpha suppositories, which are extremely cheap in comparison to interferon injections.

In his ME/CFS study, Dr Chia used subcutaneous injections of 3 million IU of interferon alpha-2B, given to patients three times a week, for 2 to 6 months. Dr Chia said the cost of such interferon treatment was around $5,000 a month in the US. So that works out to one dose of interferon at 3 million IU costing around $400.

Whereas Russian suppositories containing 1 million IU of interferon alpha-2B cost around $5 each.

So I want to try Russian interferon alpha suppositories, but I am concerned with the possible depression side effect.

In Dr Chia's interferon studies, some patients were put into full remission for up to 14 months, but all patients treated eventually relapsed. But that may be because they did not keep taking the interferon indefinitely, but just took a course of interferon, and then stopped taking it.

Note that Dr Chia in his above study found interferon was effective for ME/CFS patients with coxsackievirus B3 or coxsackievirus B5. But in his presentation at the Invest in ME 2009 London Conference at timecode 42:31 says that interferon does not work for coxsackievirus B4:
Interestingly enough, my son also has coxsackie B4, and for coxsackie B4, the antibody titer did not change at all, which is what I usually see using ribavirin and interferon; it is ineffective against coxsackie B4.


As well as being hugely less expensive that interferon injections, interferon suppositories also have advantage of not creating anti-interferon antibodies even in long term use. Ref: 1 The problem with long term interferon injections is that after many months of treatment, anti-interferon antibodies can form, thereafter rendering the interferon ineffective.

Interferon suppositories are available at several pharmacies that specialize in Russian products:

otc-online-store.com
Interferon

medicinesdelivery.com
Genferon suppositories
Viferon suppositories

rupharma.com
Genferon suppositories

farmacy-houses.com
Viferon suppositories

wmmedicalsupply.com
Search interferon

pilloid.com
Search interferon

pillbuys.com
Genferon suppositories
Roferon-A
Kipferon suppositories
Viferon suppositories

Cost for 10 interferon suppositories of 1 million IU is typically around $50.



If the interferon suppositories did cure my ME/CFS, I would not stop taking them. I would continue to take them on a maintenance dose indefinitely, to ensure my ME/CFS never came back. The suppositories are cheap and easy enough to take indefinitely.

Rectally administered interferon routes itself into the body via the lymph system. Ref: 1 I am not sure about how interferon suppositories compare to interferon injections in terms of potency, though. Presumably the bioavailability is lower when administered by rectal suppository.
 
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eljefe19

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@Hip yo great info as always hip. Here's a philosophical question for you. If your propensity towards depression is caused by the enterovirus, then you would think remission would end that propensity towards depression, right?
 

Hip

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@Hip yo great info as always hip. Here's a philosophical question for you. If your propensity towards depression is caused by the enterovirus, then you would think remission would end that propensity towards depression, right?
Yes, if I could significantly reduce my viral loads, I would think the depression would disappear, as it was caused by the virus.
 

halcyon

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So I guess I'm wondering then is a cure possible without finding a cure for the enteroviruses themselves? Can our immune system be supplemented just right so that remission is possible?
In theory I believe yes, but I don't think the success rate will be very high.

I went to my new doc here in Salt Lake City and he knows about Chia and he believes enterovirus is probable, but his only idea for treatment is Interferon Beta.
There are no studies on inteferon beta for treatment of CFS as far as I know, but there are three studies on interferon alpha and all three showed a positive effect. Similar to hep C though, not every patient will respond, and even those that respond successfully can still relapse after treatment.
 

JES

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I enjoy it though. Having some semblance of control over my own body. Btw, I've read that post you wrote on Microglial activation inhibitors a few times. I had forgotten about the two modes. I guess I am skeptical of inhibiting microglial activation if we are trying to kill off a brain virus. How would Coxsackie and Echovirus ever even be killed off for good? This is why I am taking Gcmaf. To bolster my immune system's ability to fight enterovirus. They claim that LDN blocked progress in gcmaf patients. Why? Well they didn't know for sure, but they postulated it was because of LDN inhibiting microglial activation. So, I asked my doctor about this, and he told me that microglial activation is probably over active so to speak and inhibiting it would be beneficial. But I'm not sure I'm convinced just yet.
LDN works in quite many ways. Besides being a microglial inhibitor, it also boost/modulates the immune system through creating a temporary blockage of certain opioid receptors which eventually will upregulate endorphin production (this particular mechanism is explained quite well in this video).

I usually react quite badly to most immune suppressant supplements and microglial inhibitors. Within couple of days I get a fluish feeling and increased fatigue, which I presume is due to this chronic viral infection getting stronger. With LDN I had a different reaction, it didn't cause this feeling I usually got on microglial inhibitors. Instead I started sleeping slightly better and having slightly less pain, without feeling that my immune system was compromised.
 

eljefe19

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@JES LDN has done me well in the past as well. I could feel the upregulating opiod receptors as it had a strong antidepressant effect. It began to wear off eventually though and my doc suggested I cycle it.
 

eljefe19

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@Hip why does interferon alpha work hip? I've been trying to figure out, why microglial activation inhibitors would be efficacious in CFS if the underlying enterovirus was not addressed as well. Is that where interferon comes into play?
 

Hip

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@Hip why does interferon alpha work hip? I've been trying to figure out, why microglial activation inhibitors would be efficacious in CFS if the underlying enterovirus was not addressed as well. Is that where interferon comes into play?
Dr John Chia and other enterovirus researchers believe ME/CFS is likely driven by a particular mode of enterovirus infection, called a non-cytolytic infection. In these infections, enterovirus lives inside human cells on a long term basis, but without destroying the cell.

To kill these intracellular infections, you need to activate the intracellular immune system (the internal immune system inside cells). Interferons do precisely that.

The ME/CFS drug Ampligen works in a similar way to interferon, and also activates the intracellular immune system.
 

Hip

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@Hip https://examine.com/supplements/spirulina/

According to examine.com Spirulina was directly compared to the herb you mentioned and was found to be a much stronger inhibitor of NADPH oxidase
Thanks for the link. Very interesting. I have added phycocyanin to the NADPH oxidase inhibition section of the microglia activation inhibitors post.

Though I can't see in the examine.com article where it says phycocyanin (from spirulina) is more potent than apocynin (from Picrorhiza kurroa), in terms of NADPH oxidase inhibition.