Prednisone makes me feel good

[Wishful]

My hypothesis certainly isn't based on PhD level understanding, nor on the kind of studies that labs do. My personal observations are consistent with the core problem being neurological. The physical symptoms common to the majority of PWME could, I think, quite easily be caused by a single hard-to-find neurological dysfunction. One little change in a reaction rate can have cascading effects throughout the body.

I do feel that the existence of a subgroup without the common physical symptoms is reasonably strong evidence for those symptoms to be secondary, rather than primary. Those physical symptoms being secondary (or tertiary or whatever) seems much more likely than the subgroup having a defence or counter to physical symptoms while retaining the neurological ones.

 

[used_to_race]

I do feel that the existence of a subgroup without the common physical symptoms is reasonably strong evidence for those symptoms to be secondary, rather than primary. Those physical symptoms being secondary (or tertiary or whatever) seems much more likely than the subgroup having a defence or counter to physical symptoms while retaining the neurological ones.

Which physical symptoms are you referring to? What about the subgroup without neurological symptoms? I don't believe that I have the same disease process as someone who had a gradual onset, lacks sore throat and GI problems as symptoms, and has extreme cognitive symptoms.

 

[Wishful]

The physical symptoms common to ME seem to be loss of muscle strength and endurance. Some people lack the physical strength or endurance to get out of bed; for others it's just a slight loss. I haven't heard much discussion about ME without neurological symptoms, so I can't comment on that.

I don't have the sore throat or lymph nodes, or GI issues either. I have various other minor issues, such as double-vision--that I'm not sure are due to ME. My belief is that the core dysfunction of ME is one specific chemical reaction at the wrong rate somewhere in some cells, and all the other issues cascade down from that. There are probably cofactors in our susceptibility to ME, so that it might require a set of genes and epigenetic factors to be set in a certain way, which allows the core dysfunction to lock into a feedback loop. The symptoms arising from the core dysfunction depend on another set of factors, so many people get the muscle issues, some get the lymph node issues, and so forth. With all those factors affecting what the core dysfunction does, we also react differently to external factors, such as drugs or foods.

It does make research into ME tough...

 

[used_to_race]

The physical symptoms common to ME seem to be loss of muscle strength and endurance. Some people lack the physical strength or endurance to get out of bed; for others it's just a slight loss. I haven't heard much discussion about ME without neurological symptoms, so I can't comment on that.

I was a competitive athlete before I got sick, so maybe I'm not the best example. But even on a below average day for me, I could still smoke the average person in a running or cycling race of any distance. I've lost a lot of strength and conditioning in the 2+ years I've been sick, but I am sure I could still run close to a 5 minute mile on a track, especially if I had someone to race against. I have been doing a bit better in recent months and played on a soccer team with some people from work. At one point we had 4 games in a week and I was able to play a role in all of them. I'm not saying all this to brag, but more to illustrate that I too have questioned my diagnosis being ME/CFS. And yet I've seen two of the "famous" ME/CFS specialists on these boards, as well as some of the best rheumatology and immunology specialists in LA (and probably the United States). The only things I've been "diagnosed" with are ME/CFS by all these experienced doctors, and depression by one moronic psychiatrist.

It does make research into ME tough...

I agree completely, Dr. Davis has a very unenviable task coordinating all this, and I fear that a lot of the individual projects being explored are not going to yield much due to heterogeneous patient groups. Just the fact that some of us respond well to prednisone and others respond poorly, according to my rheumatologist, is evidence that these are separate disease processes, and I think I agree.

 

[Wishful]

Different downstream processes. For an example, let's assume that the core defect is a single RNA defect that produces fewer calcium channels in the microglial mitochondrial membrane. This affects dozens of chemical reactions, which affect the immune system, the HPA system, and whatever else. Patient A has an epigenetic bias for t-cells to overreact to cortisol . Patient B has a bias to underreaction. Do we describe this as a different disease process, or just a variation in downstream complications?

I too have lost some conditioning, but not the underlying potential. I haven't had an official diagnosis of ME (can't see the point in making the effort) but whenever I question my self-diagnosis, I end up convinced that it is ME. I fit the Canadian and International criteria. The PEM is definite. I have similar responses to other ME victims with such treatments as prednisone...and also inverse responses to other treatments. Thus I feel that ME just has a lot of variation in symptoms.

 

[samantha-g]

I'm guessing that you're asking about people other than me, since I reported that cumin had the same effect on my symptoms that prednisone had, at least for a few weeks after the second prednisone course. Then it stopped having that effect. I only recently discovered that it effectively blocks my PEM. I haven't had anyone else report to me that cumin had a definite effect on them.

Do you mean curcumin which is part of turmeric, or cumin which is a different plant - the seeds are used in cooking? Do you have a product link? Thanks

 

[Wishful]

I mean cumin (Cuminum cyminum), the spice common in curry. Definitely not curcumin; turmeric makes my symptoms worse. Also not black cumin (Nigella sativa). No product link; I just take a level tsp of ground cumin, and the cheap packages of no-name brand seem to work as well as freshly ground seeds. Cumin does go stale eventually, (seeds nearly ten years old had noticeable lost some potency).

Cumin is wonderfully effective at blocking my physically-induced PEM. However, as I said, no one else has reported a similar definite effect. I was very much hoping that it would work for at least some other PWME, so that researchers could figure out why, and then hopefully why we get PEM.

If you try it and it does work for you, please let me know.

 

[used_to_race]

Different downstream processes. For an example, let's assume that the core defect is a single RNA defect that produces fewer calcium channels in the microglial mitochondrial membrane. This affects dozens of chemical reactions, which affect the immune system, the HPA system, and whatever else. Patient A has an epigenetic bias for t-cells to overreact to cortisol . Patient B has a bias to underreaction. Do we describe this as a different disease process, or just a variation in downstream complications?

It would never be this simple though, because nobody is born with ME/CFS. We can't speculate about the underlying mechanism like this. Besides, what would an "epigenetic bias for T cells to overreact to cortisol" even look like? I would again say this is far too simplistic and doesn't get us anywhere in terms of understanding. Once we have basic information about immunological and metabolic processes in ME/CFS, we will hopefully be able to see how different patients group together. It doesn't make any sense to assume what the central disease process might be and decide that it must apply to everyone who fits the diagnostic criteria for such a poorly understood disease. Just as an example of another disease group that suffered because it was assumed to be one underlying mechanism, look up how many different processes can be diagnosed as Parkinson's disease. Now people get different treatments based on what is actually going on with them as individuals, and the situation is starting to improve. We need to support the basic science and learn all the facts or else we will never get any treatment that works.

 

[Lone Wolf]

My "remission" only lasted as long as I took the prednisone - ... and maybe 4/5 days later...
... I just loved the fact that I was "me" for a few weeks. It was an awesome feeling.

That is exactly what happened to me 10 years ago when I was prescribed Prednisone.
All my brain-fog disappeared and I thought that 20 years of illness was "cured".

My holistic doc said that the Pred STOPS ALL INFLAMMATION. Period.
He said "everyone feels great on it" for that reason. People with arthritis, etc.

I am sure there are granular reasons why it works that I don't understand, but brain inflammation is core to my issues so it all went "poof" for a little while.

I have a lot of auto-immune stuff including inflammatory bowel disease. So the Pred for me was a big dose then taper in preparation for longer term bowel med (Entocort) and the Pred stopped my inflammatory bowel immediately.

The brief remission from brain fog was amazing, and as others have said let me know I was not a permanent idiot.

My rheumatologist put me on a 10-day prednisone taper starting today - 20mg for 5 days, 10mg for 5 days.

I am not advocating anyone take a boatload of Pred, but for what it's worth my brief remission with Pred was at least twice that dose.
2 of the people on page one of this thread were starting at 40 mg a day.
If you do a search for "prednisone taper pack instructions" you will see mention of starting with high doses, one of them starts at 60 mg.
the concept is to HALT the inflammation. You take enough Pred and it will happen, but you wouldn't want to continue it - so it is not any kind of cure or lasting symptom relief.
In that search you will also see hits for Medrol, which is a bit stronger than Pred. and has very similar effect.

 

[Wishful]

@used_to_race , I guess you're right that there could be multiple core dysfunctions, producing multiple sets of symptoms that appear similar. Not all of us display PEM, for example.

BTW, my example was made up just for discussion purposes, not a real assumption of the actual cause. I am waiting for the understanding of the processes involved.

I do hope that finding a core dysfunction for a majority of PWME doesn't leave a subset of people with a new label, ignored by the medical profession. Sadly possible though.

 

[starlily88]

That is exactly what happened to me 10 years ago when I was prescribed Prednisone.
All my brain-fog disappeared and I thought that 20 years of illness was "cured".

My holistic doc said that the Pred STOPS ALL INFLAMMATION. Period.
He said "everyone feels great on it" for that reason. People with arthritis, etc.

I am sure there are granular reasons why it works that I don't understand, but brain inflammation is core to my issues so it all went "poof" for a little while.

I have a lot of auto-immune stuff including inflammatory bowel disease. So the Pred for me was a big dose then taper in preparation for longer term bowel med (Entocort) and the Pred stopped my inflammatory bowel immediately.

The brief remission from brain fog was amazing, and as others have said let me know I was not a permanent idiot.

I am not advocating anyone take a boatload of Pred, but for what it's worth my brief remission with Pred was at least twice that dose.
2 of the people on page one of this thread were starting at 40 mg a day.
If you do a search for "prednisone taper pack instructions" you will see mention of starting with high doses, one of them starts at 60 mg.
the concept is to HALT the inflammation. You take enough Pred and it will happen, but you wouldn't want to continue it - so it is not any kind of cure or lasting symptom relief.
In that search you will also see hits for Medrol, which is a bit stronger than Pred. and has very similar effect.

Yes I started at 40 mg Prednisone - but used it for only 14/15 days May 2018. My Hopkins Endocrinologist let me try it a second time a few months later - but the insomnia and speed were just too much for me, so I stopped after 4 days.
If you want to see how inflamed you are - do a blood word on Sedimentation Rate.
All of us are high, no doubt - but I was at >130 - highest I have ever been to my recollection.

 

[penny pitst0p]

hi everyone..just wanted to add in my experience with pred...first time I was pescribed I had an adverse reaction ..like a temporary paralysis with strange pschological effect of spaced out feelings..

.didnt take any more and reported to gp..about a year later was pescribed again and reluctantly decided to try again as was so desperate for some relief...

it was amazing..had the energy I had at 16 but also became argumentative slightly aggresive snd euphoric..and couldnt stop talking rapidly

..but thinking of trying again if I want to do something like a holiday or even just to get to hospital apts.

My thoughts keep returning to the pred and how energising it was it gives me hope..though it didnt take all my pain away..fatigue is my worst symptom.

 

[gbells]

I know how Prednisone ruins one's body - that is not the answer. Has anyone found anything to replace the "Prednisone" affect that I have gotten?

I contracted SEIDS first then developed systemic lupus erythematosis 4 years later. I have taken prednisone twice for lupus flares of pericarditis. I had a flare about 4 months ago and was able to avoid prednisone by dating max dose ibuprofen for about a week (not giving specifics because I don't want anyone trying it without a doctor). Prednisone gives weight gain and bone loss.

Prednisone makes you feel good because it is an anti-inflammatory. I believe SEIDS is a disease of co-infections that together lower immunity to the point that they are self-sustaining. Illnesses that your body could handle alone become superinfections together, called Russian doll diseases because they fit together like a Russian doll, sustaining themselves and hiding their presence.

Medicine doesn't know how to address them. Most of the time they rely on antibody tests that don't work for co-infections.

For example:

1. Epstein Barr Virus alone = mononucleosis which resolves in a few months

2. EBV + Bartonella = SEIDS, chronic

Once EBV gets going it suppresses the production of antibodies, giving false negatives on lab tests that rely on antibodies.

Part of this process is creating inflammation. So any treatment that lowers inflammation will give you some pain relief. However, because you aren't curing the underlying infections there is no real improvement in other areas (fatigue, enlarged lymph nodes, etc.). Many SEIDs patients feel better on megadoses of anti-oxidants and oregano oil because they buffer inflammation. The problem with doing this is that the body needs anti-oxidants in cancer defence. So if you follow this route you should have a higher cancer risk.

None of the treatments so far has been shown to be effective in curing SEIDS.

Because of the pro-cancer effect I would avoid taking large doses of antioxidants, oregano oil, etc. Curcumin ie. Long vida curcumin is an excellent supplement for reducing inflammation in a non-harmful way without relying on antioxidants.

 

[Wishful]

Prednisone gave me complete temporary remission the first two times, but I'm not convinced that it's effects involve viral infections. After the second prednisone course, I discovered that cumin (Cuminum cyminum) was just as effective at triggering remission as prednisone. Unfortunately, the effect faded within a few weeks of daily cumin, and neither it nor prednisone had any effect on the symptoms after that. It seems that both substances--prednisone and cuminaldehyde--had the same effect on ME. The likelihood of them having the same effect on multiple species of viruses seems unlikely. More likely that they both influenced one or more cytokines or other biochemicals.

For whatever it's worth, in the last year or so did I discover that cumin effectively blocked my physically-induced PEM. No one else has reported a similar response to cumin. Antioxidants generally make my ME symptoms worse.

 

[Wishful]

I've been thinking more about the hidden viral infections hypothesis, and I still don't think it fits ME. My alternative is that viral infections may trigger ME, and could increase the severity of ME (by increasing ME's chronic neuroinflammation), but aren't the ongoing cause of ME. Instead, our immune systems are stuck in a feedback loop, and it's that immune activation that is causing most of our symptoms, directly or indirectly. Our immune systems are supposed to have an 'off switch', but either that's not functioning properly or our 'on switches' are stuck in the on state. Mitochondria might be part of the feedback loop, and our microbiome might be part of the loop (though I don't believe it is) or just another factor that increases symptom severity or secondary problems, but the root cause is part of the immune system that is stuck in a feedback loop. The ability of some chemicals to trigger full remission within minutes, and lasting for hours, seems to point to chemical reaction rates at work, rather than viral activation/deactivation.

 

[gbells]

My experience is that the antioxidant usually lets me feel good for one day, I would exercise then my body would crash the next.

An easy way to identify the EBV without relying on antibodies is if you have EBV symptoms (swollen lymph nodes, sore throat, etc) ask your MD to order a nagalase blood test. You'll have to cover the cost ($100). If it is abnormal it is either a viral infection or cancer (most likely viral and EBV is a known immune inhibitor).

http://www.hdri-usa.com/tests/nagalase/

If you end up ordering it please post your results.

My initial test was 3x normal.

More tip offs for immunity problems are sudden periodontal disease, root canal re-infections and developing cellulitis from cuts that used to stay localized.

 

[gbells]

I've been thinking more about the hidden viral infections hypothesis, and I still don't think it fits ME. My alternative is that viral infections may trigger ME, and could increase the severity of ME (by increasing ME's chronic neuroinflammation), but aren't the ongoing cause of ME. Instead, our immune systems are stuck in a feedback loop, and it's that immune activation that is causing most of our symptoms, directly or indirectly. Our immune systems are supposed to have an 'off switch', but either that's not functioning properly or our 'on switches' are stuck in the on state. Mitochondria might be part of the feedback loop, and our microbiome might be part of the loop (though I don't believe it is) or just another factor that increases symptom severity or secondary problems, but the root cause is part of the immune system that is stuck in a feedback loop. The ability of some chemicals to trigger full remission within minutes, and lasting for hours, seems to point to chemical reaction rates at work, rather than viral activation/deactivation.

The hyperactivation still needs a cause and the most likely one is EBV infection.

By analyzing the blood of 192 people who had met one of the established criteria for CFS/ME diagnosis and 392 healthy individuals, the team found that the levels of 17 cytokines, substances produced by immune cells in response to infection, correlated with disease severity. They were higher in patients with the severest symptoms than in patients with milder symptoms or healthy people. In patients with the mildest symptoms, the levels of those same cytokines were lower than in healthy people, and in patients with moderate symptoms they were comparable to individuals with no disease. Of these 17 immune molecules, the vast majority is known to stimulate inflammation and produce flulike symptoms, the researchers report today in the Proceedings of the National Academy of Sciences.
https://www.sciencemag.org/news/201...une-system-imbalance-chronic-fatigue-syndrome

Other researchers have suggested that certain pathogens may, in predisposed people, trigger a chronic immune activation, which would create chronic inflammation and a cascade of problems. One of the main suspects in this scenario is the Epstein-Barr virus, which causes mononucleosis ("the kissing disease.")
https://www.verywellhealth.com/inflammation-autoimmunity-in-chronic-fatigue-syndrome-716122​

 

[knackers323]

@gbells how high does the nagalase have to be to be significant? Mine was slightly over the given normal range

 

[gbells]

@gbells how high does the nagalase have to be to be significant? Mine was slightly over the given normal range

If you have chronic EBV symptoms I would consider that significant. As the EBV load increases the nagalase result will worsen over time.

I would caution you when considering anti-EBV therapies. There is a lot of quackery out there that are using EBV to sell unproven products.

And the GcMAF approach normally recommended for high nagalase plus an effective EBV inhibitor regimen could give you systemic lupus which is how I contracted it. The body normally creates a lot of antibodies to fight early stage EBV. Once it gets to chronic the body doesn't have the capacity to fight it quickly and turns auto-immune.

 

[Wishful]

The hyperactivation still needs a cause and the most likely one is EBV infection.

The initial activation can be any type of immune system trigger: viral, bacterial, foreign substance, autoimmune, maybe others too. Once triggered in a predisposed body, it feeds back for a chronic activated state. The trigger doesn't need to create a special hyperactivation; ordinary activation is all that's required. Some triggers might be more likely to trigger the feedback loop.

We can occasionally force a temporary break in this feedback loop (temporary remission), but maybe there are slow-to-be-removed cytokines or some other long-term changes ready to push us back into the feedback state. Maybe there's some sort of 'monitor function' that is supposed to keep some cell activity at a certain level, and ME disrupts that in a way that it keeps trying to do its job, but at the wrong target setting.